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Welcome to the #1 online source of information for Diabetes Specialists! An international online community of more than 10,000 Diabetes Specialists.
CME on Diabetes is a website built to transmit top-level CME conferences given by international experts in endocrinology, insulin resistance, prediabetes, metabolic syndrome and type 2 diabetes. More than 2.6 million slides have been viewed since the website launch. Thank you for your continued support and commitment!
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PathophysiologyIn order to better understand the causes of Type 2 diabetes, certain fundamental studies are necessary. Many elements are presently being studied: production of insulin, method of hormonal action, signals produced by its production, chain reaction of cells when in contact with the hormone, receptors involved in the process of detection, causes of insulin insensitivity... The development of a better understanding of each of these factors may help prevent and treat Type 2 diabetes.
Presentations listing
Polyglandular Autoimmune Syndromes - Dr. Patricia Crock Autoimmune Diseases: Impact on Diabetes - Dr. Trisha O'Moore-Sullivan Relationship between hyperglycaemia and micro- and... - Prof. Timothy Davis Relationship between underlying causes of insulin... - Prof. Christopher Nolan Underlying Causes of Disease Progression: The Role of... - Prof. Nikolaus Marx Women, CHD & Diabetes - Dr. Pat Phillips « Is HDL Dysfunctional in Diabetes » ? - Prof. John Chapman Nox, Nox, Knocking: The Emerging Roles of NADPH Oxidases in... - Dr. Grant Drummond Mitochondria and the Pathogenesis of Type 2 Diabetes... - Prof. J.A. Maassen Pathophysiology of Type 2 Diabetes - The Critical Role of... - Prof. Steven Kahn The Clinical Implications of Advanced Glycation - Dr. Merlin C. Thomas The Clinical Value of ApoB - Dr. Allan D. Sniderman Diabetes Related Foot Complications - Dr. Paul Wraight Diabetic Autonomic Neuropathy: GI Tract: DX and RX -... - Dr. Terry Moore Quality of Life & Diabetes - Dr. Pat Phillips Interaction of Metabolic with Haemodynamic Factors in... - Prof. Mark E. Cooper Effects of fatty acids on glucose metabolism and the... - Dr. Meredith Hawkins 21 Years of Insulin Resistance - Targeted Drug Research:... - Dr. Stephen A. Smith Introduction - Prof. Jean-Pierre Després Natural History of ß-cell Decline in Type 2 Diabetes - Prof. Stefano Del Prato Adipose Tissue as an Inflammatory Organ (Endocrine Tumor)... - Prof. John N. Fain Muscle - Adipose Tissue "Crosstalk" :... - Prof. Edward W. Kraegen Resistin and Fasting-Induced Adipose Factor (FIAF) in the... - Dr. Russell Brown The ß-cell: Friend and Foe - Prof. Steven Kahn Vascular Disease and Insulin Resistance - Prof. Giancarlo Viberti Postprandial Hyperglycemia and Cardiovascular Disease - Prof. Antonio Ceriello Increased Risk of Coronary Events in Dysglycemic Patients:... - Dr. Richard W. Nesto Lessons from the UKPDS - Prof. Alastair Gray Effect of Fructose Overfeeding and Fish Oil Administration... - Dr. David Faeh Neural Control of Energy Balance - Prof. Stephen C. Woods Markers of Inflammation and Hypercoagulation in CAD - Dr. Russell P. Tracy Obesity, Dyslipidemia and Inflammation - Dr. Robert H. Eckel Adiponectin - Prof. John Prins Association of hsCRP with Later Stage ß-Cell Dysfunction... - Dr. A. Pfützner CRP, Inflammation, and its Relationship to Cardiovascular... - Dr. Paul M. Ridker What are the manifestations of beta-cell dysfunction and... - Dr. Steven V. Edelman Type 2 Diabetes Mellitus and Heart Failure: Implications... - Dr. Richard W. Nesto Impaired Microvascular Recruitment and Muscle Insulin... - Dr. Michael G. Clark Ectopic fat and oxidative stress: common denominators in... - Dr. Robin Buckingham Insulin Sensitivity in the Adiponectin Transgenic Mouse - Dr. Terry Combs A PPAR gamma Mutation and the Lipodystrophic Phenotype - A... - Dr. Thomas Ransom New Insights in Diabetic Retinopathy - Dr. Filiberto Altomare The Wheres and Whats of Body Fat Distribution - Prof. Steven Kahn Nuclear Receptor Diseases Mechanisms - Dr. Mitchell Lazar Beta Cell Failure in type 2 Diabetes: A Paradigm Revisited - Dr. Minna Woo
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"Polyglandular Autoimmune Syndromes"Dr. Patricia Crock (biography)
English - 2009-03-09 - 49 minutes
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Summary :
Dr. Crock starts with a case presentation of a boy with Addison's disease, glucocorticoid and mineralocorticoid deficiency, and a family history of polyglandular autoimmune disease.
Autoimmune endocrinopathies cluster, for example patients with type 1 diabetes may have Hashimoto's disease or coeliac disease. Although Addison's disease is rare it may be indicated by falling insulin...
Learning objectives :
After viewing this presentation the participant will be able to discuss:
- Autoimmune diseases which cluster with type 1 diabetes
- A classical case presentation of polyglandular autoimmune disease
- Target autoantigens and autoantibody markers
- How to avoid some diagnostic pitfalls
- Monogenic Autoimmunity Syndromes
- Polyglandular Autoimmune syndromes
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"Autoimmune Diseases: Impact on Diabetes"Dr. Trisha O'Moore-Sullivan (biography)
English - 2007-11-21 - 36 minutes
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Summary :
Autoimmune diseases are found more commonly in people with Type 1 Diabetes (T1DM) than amongst the general population. Dr. O'Moore-Sullivan discusses the implications of a diagnosis of autoimmune disease accompanying T1DM, which relate to the management of both conditions, as well as to the screening for other autoimmune diseases in the patient and his family.
A common...
Learning objectives :
After viewing this presentation the participant will be able to discuss:
-The association of Type 1 Diabetes with the following endocrine autoimmune diseases:
Autoimmune thyroid disease (AIT)
Autoimmune Addison's Disease (AD)
-The association of Type 1 Diabetes with a non-endocrine autoimmune disease, Coeliac Disease (CD)
-Autoimmune Polyendocrine Syndromes (APS)
Bibliographic references :
Jennifer M. Barker Type 1 Diabetes-Associated Autoimmunity: Natural History, Genetic Associations, and ScreeningThe Journal of Clinical Endocrinology & Metabolism Vol. 91, No. 4 1210-1217
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"Relationship between hyperglycaemia and micro- and macrovascular outcomes"Prof. Timothy Davis (biography)
English - 2007-11-10 - 34 minutes
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Summary :
Long-term randomised controlled trials have provided good evidence for the relationship between glycaemia and the risk of vascular complications of diabetes.
The DCCT study in type 1 diabetic patients showed that intensive treatment was associated with significant improvements in microvascular outcomes. There was a low number of cardiovascular events, however fewer events were seen...
Learning objectives :
After viewing this presentation the participant will be able to discuss:
- The relationship between glycaemia and vascular outcomes in type 1 and type 2 diabetes
- Evidence in support of a 'legacy' effect of good glycaemic control
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"Relationship between underlying causes of insulin resistance and beta-cell function"Prof. Christopher Nolan (biography)
English - 2007-11-10 - 34 minutes
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Summary :
Islet beta-cell failure is a key factor in type 2 diabetes pathogenesis. It is progressive, and occurs in the context of islets compensating for insulin resistance.
Beta-cell failure occurs in “susceptible” islets, and the mechanisms involved are of the initiation and progression types.
The factors that make islets susceptible to dysfunction need to be discovered,...
Learning objectives :
After viewing this presentation the participant will be able to discuss:
- GDM as an insulin resistant state
- Insulin secretion in women with previous GDM
- The influence of GDM on long-term control of glucose tolerance
- The islet beta-cell in T2DM
- Glucolipotoxicity as a proposed mechanism of beta-cell failure in T2DM
Bibliographic references :
Marc Prentki and Christopher J. NolanIslet β cell failure in type 2 diabetes J Clin Invest. 2006 July 3; 116(7): 1802–1812.
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"Underlying Causes of Disease Progression: The Role of PPAR-gamma and the Metabolic and Vascular Actions of the TZDs"Prof. Nikolaus Marx (biography)
English - 2006-12-04 - 28 minutes
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Summary :
Type 2 diabetes mellitus is a complex metabolic disorder associated with various risk factors like dyslipidaemia, inflammation and hypertension. Patients with insulin resistance and type 2 diabetes mellitus exhibit an increased propensity to develop arteriosclerosis with its sequelae acute myocardial infarction and stroke. Anti-diabetic, PARγ−activating, thiazolidinediones (TZDs,...
Learning objectives :
After viewing this presentation the participant will be able to discuss:
- Metabolic and vascular aspects of insulin resistance
- Mechanism of action of the insulin-sensitizing thiazolidinedione (TZD) drugs
- Metabolic effects of TZDs, including effects on HDL-C and LDL particle size
- Vascular action of TZDs: in vitro and in vivo evidence for anti-inflammatory and anti-atherogenic properties
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"Women, CHD & Diabetes"Dr. Pat Phillips (biography)
English - 2006-10-27 - 27 minutes
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Summary :
In this presentation Dr. Phillips talks about the importance of coronary heart disease (CHD) in diabetes, particularly in women.
Is diabetes a CHD risk equivalent? A well-known case-control study reported by Haffner et al. in 1998 suggested that diabetic patients without previous myocardial infarction have as high a risk of myocardial infarction as non-diabetic patients with...
Learning objectives :
After viewing this presentation, the participant will be able to discuss:
- Coronary heart disease is very common in those with type 2 diabetes and vice versa.
- In women the presence of diabetes increases coronary risk much more than in men and equalises coronary risk for men and women.
- Many women and their professionals do not appreciate the risk of coronary heart disease in women nor do they appreciate that diabetes increases a woman’s coronary risk as much as it does.
Bibliographic references :
1. Haffner SM, Lehto S, Ronnemaa T, Pyorala K, Laakso M.Mortality from coronary heart disease in subjects with type 2 diabetes and in nondiabetic subjects with and without prior myocardial infarction. N Engl J Med. 1998 Jul 23;339(4):229-34.
2. S Lehto, T Ronnemaa, SM Haffner, K Pyorala, V Kallio and M LaaksoDyslipidemia and hyperglycemia predict coronary heart disease events in middle-aged patients with NIDDM Diabetes. 1997 Aug;46(8):1354-9.
3. Juutilainen A, Kortelainen S, Lehto S, Ronnemaa T, Pyorala K, Laakso M.Gender Difference in the Impact of Type 2 Diabetes on Coronary Heart Disease Risk Diabetes Care 27:2898-2904, 2004.
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"« Is HDL Dysfunctional in Diabetes » ?"Prof. John Chapman (biography)
English - 2006-10-04 - 62 minutes
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Summary :
In this presentation Prof. Chapman talks about high density lipoprotein (HDL) dysfunction in insulin-resistant states including type 2 diabetes. Not only HDL cholesterol (HDL-C) concentrations are reduced, but it has recently come to light that HDL particles themselves are dysfunctional in insulin-resistant states.
The atherogenic dyslipidemia of insulin-resistant states including...
Learning objectives :
After viewing this presentation, the participant will be able to discuss
- Epidemiological data supporting the concept that elevated levels of HDL-cholesterol are atheroprotective
- Epidemiological data that low levels of HDL-C are a major CV risk factor in diabetics and in non-diabetics
- Mechanisms underlying perturbed HDL metabolism in insulin-resistant states associated with hypertriglyceridemia
- Anti– atherogenic activities of HDL and defects in Type 2 diabetes
Bibliographic references :
1. Chieko Mineo, Hiroshi Deguchi, John H. Griffin, Philip W. Shaul Endothelial and Antithrombotic Actions of HDL Circulation Research. 2006;98:1352.
2. Barbara V. Howard; David C. Robbins; Maurice L. Sievers; Elisa T. Lee; Dorothy Rhoades; Richard B. Devereux; Linda D. Cowan; R. Stuart Gray; Thomas K. Welty; Oscar T. Go; Wm. James Howard. LDL Cholesterol as a Strong Predictor of Coronary Heart Disease in Diabetic Individuals With Insulin Resistance and Low LDL: The Strong Heart Study Arteriosclerosis, Thrombosis, and Vascular Biology. 2000;20:830.
3. Kontush A, Chapman MJ.Antiatherogenic small, dense HDL--guardian angel of the arterial wall? Nat Clin Pract Cardiovasc Med. 2006 Mar;3(3):144-53.
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"Nox, Nox, Knocking: The Emerging Roles of NADPH Oxidases in Vascular Physiology & Disease"Dr. Grant Drummond (biography)
English - 2006-09-16 - 48 minutes
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Summary :
"Despite the bad press about reactive oxygen species, they are not always that bad," says Dr. Drummond. "In fact they are critical for cell signaling processes." What happens when oxygen free radicals/reactive oxygen species are overproduced, and what are the potential implications for lowering oxidative stress in the vasculature?
All of the known cardiovascular risk factors are...
Learning objectives :
After viewing this presentation the participant will be able to discuss:
- What are reactive oxygen species?
- Effects of overproduction of reactive oxygen species in disease states
- Clinical trials with antioxidants
- NADPH oxidase isoforms and superoxide production
- Proposed mechanisms of vascular free radical production
Bibliographic references :
1. Young-Ah Suh, Rebecca S. Arnold, Bernard Lassegue, Jing Shi, Xiangxi Xu, Dan Sorescu, Andrew B. Chung, Kathy K. Griendling and J. David LambethCell transformation by the superoxide-generating oxidase Mox1 Nature 1999;401:79.
2. Bernard Lassègue, Dan Sorescu, Katalin Szöcs, QiQin Yin, Marjorie Akers, Yong Zhang, Sharon L. Grant, J. David Lambeth, Kathy K. Griendling Novel gp91phox Homologues in Vascular Smooth Muscle Cells: nox1 Mediates Angiotensin II–Induced Superoxide Formation and Redox-Sensitive Signaling Pathways Circulation Research. 2001;88:888.
3. Cornelius F.H. Mueller; Karine Laude; J. Scott McNally; David G. Harrison Redox Mechanisms in Blood Vessels Arteriosclerosis, Thrombosis, and Vascular Biology. 2005;25:274.
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"Mitochondria and the Pathogenesis of Type 2 Diabetes Mellitus"Prof. J.A. Maassen (biography)
English - 2006-09-15 - 57 minutes
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Summary :
In this presentation Prof. Maassen talks about the role of mitochondria in the development of glucose intolerance, in tissues such as adipose tissue, liver, muscle and pancreatic beta cells.
Mitochondria have their own DNA (mtDNA), which is about 16.5kb in length. This DNA is maternally inherited, and a number of clinical syndromes are associated with mtDNA mutations. One mutation...
Learning objectives :
After viewing this presentation, the participant will be able to discuss:
- The life style factors that contribute to the development of common type 2 diabetes
- Why triglycerides and in particular fatty acids are major players in the development of type 2 diabetes
- The role of mitochondria in the pathogenesis of the metabolic syndrome and the development of type 2 diabetes
- Why hyperglycemia is a late event in the metabolic syndrome and why thiazolidinediones (TZDs, glitazones) and physical exercise have a beneficial effect in slowing down the disease process
Bibliographic references :
1. van den Ouweland JM, Lemkes HH, Ruitenbeek W, Sandkuijl LA, de Vijlder MF,
Struyvenberg PA, van de Kamp JJ, Maassen JA.Mutation in mitochondrial tRNALeu(UUR) gene in a large pedigree with maternally transmitted type II diabetes mellitus and deafness Nature Genetics 1, 368 - 371 (1992).
2. Takashi Kadowaki, Hiroko Kadowaki, Yasumichi Mori, Kazuyuki Tobe, Ryoichi Sakuta, Yoshihiko Suzuki, Yuzo Tanabe, Hiroshi Sakura, Takuya Awata, Yu-ichi Goto, Takaki Hayakawa, Kenpei Matsuoka, Ryuzo Kawamori, Takenobu Kamada, Satoshi Horai, Ikuya Nonaka, Ryoko Hagura, Yasuo Akanuma, and Yoshio YazakiA Subtype of Diabetes Mellitus Associated with a Mutation of Mitochondrial DNA N Engl J Med. 1994 Apr 7;330(14):962-8.
3. Mootha VK, Lindgren CM, Eriksson KF, Subramanian A, Sihag S, Lehar J, Puigserver
P, Carlsson E, Ridderstrale M, Laurila E, Houstis N, Daly MJ, Patterson N,
Mesirov JP, Golub TR, Tamayo P, Spiegelman B, Lander ES, Hirschhorn JN,
Altshuler D, Groop LC.PGC-1alpha-responsive genes involved in oxidative phosphorylation are coordinately downregulated in human diabetes Nature Genetics 34, 267 - 273 (2003).
4. Petersen KF, Dufour S, Befroy D, Garcia R, Shulman GI.Impaired Mitochondrial Activity in the Insulin-Resistant Offspring of Patients with Type 2 Diabetes N Engl J Med. 2004 Feb 12;350(7):664-71.
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"Pathophysiology of Type 2 Diabetes - The Critical Role of the Beta-Cell"Prof. Steven Kahn (biography)
English - 2006-09-13 - 40 minutes
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Summary :
The beta-cell is critical in the maintenance of glucose tolerance and a marked decrease in beta-cell function is clearly associated with the development of hyperglycaemia in type 2 diabetes. Understanding the importance of insulin sensitivity in modulating beta-cell function has demonstrated that the beta-cell is capable of dramatically increasing insulin release in response to increased...
Learning objectives :
After viewing this presentation the participant will be able to discuss:
- Loss of the acute insulin response in T2DM
- Beta-cell adaptation to insulin sensitivity
- Beta-cell function in relation to fasting plasma glucose
- Beta-cell volume in IFG and T2DM
Bibliographic references :
1. Kahn SE.The relative contributions of insulin resistance and b-cell dysfunction to the pathophysiology of type 2 diabetes.Diabetologia 46:3-19, 2003
2. Utzschneider KM, Prigeon RL, Carr DB, Hull RL,Tong J, Shofer JB, Retzlaff BM, Knopp RH, Kahn SE. Impact of differences in fasting glucose and glucose tolerance on the hyperbolic relationship between insulin sensitivity and insulin responses.Diabetes Care 29:356-362, 2006
3. Holman RR. Assessing the potential for alpha-glucosidase inhibitors in prediabetic states. Diabetes Res Clin Pract 40 (Suppl):S21-S25, 1998
4. Leung N, Sakaue T, Carpentier A, Uffelman K, Giacca A, Lewis GF. Prolonged increase of plasma non-esterified fatty acids fully abolishes the stimulatory effect of 24 hours of moderate hyperglycaemia on insulin sensitivity and pancreatic b-cell function in obese men. Diabetologia 47:204-213, 2004
5. Kloppel G, Lohr M, Habich K,Oberholzer M, Heitz PU. Islet pathology and the pathogenesis of type 1 and type 2 diabetes mellitus revisited. Surv Synth Pathol Res 4:110-125, 1985
6. Butler AE, Janson J, Bonner-Weir S, Ritzel R, Rizza RA, Butler PC. b-cell deficit and increased b-cell apoptosis in humans with type 2 diabetes.Diabetes 52:102-110, 2003
7. Hull RL,Westermark GT,Westermark P, Kahn SE. Islet amyloid: a critical entity in the pathogenesis of type 2 diabetes. J Clin Endocrinol Metab 89:3629-3643, 2004
8. Barroso I.Genetics of type 2 diabetes.Diabet Med 22:517-535, 2005
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"The Clinical Implications of Advanced Glycation"Dr. Merlin C. Thomas (biography)
English - 2006-09-13 - 43 minutes
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Summary :
In this presentation Dr. Merlin Thomas of the Baker Heart Research Institute talks about the relevance of advanced glycation in diabetic patients. A number of haemodynamic and metabolic factors operate in chronic hyperglycemia, says Dr. Thomas, however, one pivotal pathway appears to be the formation and accumulation of advanced glycation end-products (AGEs).
AGEs are formed by ...
Learning objectives :
After viewing this presentation the participant will be able to discuss:
- What are AGEs?
- Experimental evidence for AGEs as downstream mediators of hyperglycemic injury
- Ten reasons why AGEs are important in the clinic
Bibliographic references :
1. Josephine M. Forbes, Mark E. Cooper, Matthew D. Oldfield and Merlin C. Thomas Role of Advanced Glycation End Products in Diabetic Nephropathy J Am Soc Nephrol 14:S254-S258, 2003.
2. Helen Vlassara. The AGE-receptor in the pathogenesis of diabetic complications Diabetes/Metabolism Research and Reviews. Volume 17, Issue 6 , Pages 436 - 443.
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"The Clinical Value of ApoB"Dr. Allan D. Sniderman (biography)
English - 2006-05-27 - 45 minutes
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Summary :
"Lowering the level of atherogenic lipoproteins in plasma is unquestionably the single most important step that can be taken to reduce the complications of vascular disease," says Dr. Sniderman. How should this be done and does measurement of LDL-C provide an accurate picture of risk in all cases?
The apoB value represents the total number of circulating atherogenic lipoproteins,...
Learning objectives :
After viewing this presentation the participant will be able to discuss:
- Limitations of LDL-C for risk assessment
- The value of apoB vs LDL-C for estimating cardiovascular risk and guiding therapy
- New data from CARDS: On-treatment apoB as a predictor of outcome in type 2 diabetic patients
- Approach to lowering apoB
Bibliographic references :
Barter PJ, Ballantyne CM, Carmena R, Castro Cabezas M, Chapman MJ, Couture P, de Graaf J, Durrington PN, Faergeman O, Frohlich J, Furberg CD, Gagne C, Haffner SM, Humphries SE, Jungner I, Krauss RM, Kwiterovich P, Marcovina S, Packard CJ, Pearson TA, Reddy KS, Rosenson R, Sarrafzadegan N, Sniderman AD, Stalenhoef AF, Stein E, Talmud PJ, Tonkin AM, Walldius G, Williams KM. Apo B versus cholesterol in estimating cardiovascular risk and in guiding therapy: report of the thirty-person/ten-country panel. J Intern Med. 2006 Mar;259(3):247-58.
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"Diabetes Related Foot Complications"Dr. Paul Wraight (biography)
English - 2006-05-06 - 33 minutes
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Summary :
Approximately 20 percent of the diabetic population will develop a foot complication during their lifetime, says Dr. Wraight. These complications come in different kinds, such as pressure lesions or burns in a neuropathic foot, neuropathic ulcers due to ill-fitting shoes and other more serious conditions. These conditions are usually precipitated by neuropathy, trauma or foot deformity, and the...
Learning objectives :
After viewing this presentation the participant will be able to discuss:
- Different kinds of diabetic foot complications
- The pathogenesis of diabetic foot complications
- Diabetic pedal osteomyelitis: diagnosis and treatment strategies
Bibliographic references :
1. Morrison WB, Schweitzer ME, Wapner KL, Hecht PJ, Gannon FH, Behm WR.Osteomyelitis in feet of diabetics: clinical accuracy, surgical utility, and cost-effectiveness of MR imaging. Radiology. 1995 Aug;196(2):557-64.
2. G Ha Van, H Siney, JP Danan, C Sachon and A GrimaldiTreatment of osteomyelitis in the diabetic foot. Contribution of conservative surgery Diabetes Care. 1996 Nov;19(11):1257-60.
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"Diabetic Autonomic Neuropathy: GI Tract: DX and RX - Conclusions of a Careful Clinician or Frustrations of an Impatient Patient"Dr. Terry Moore (biography)
English - 2006-04-28 - 38 minutes
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Summary :
Gastrointestinal (GI) complaints are common in diabetic patients, and in this presentation Dr. Moore discusses the more common GI symptoms in diabetes and their underlying mechanisms, as well as diagnostic and therapeutic approaches.
Diabetic patients may experience upper GI symptoms such as epigastric fullness, nausea and heartburn, and lower GI symptoms such as constipation,...
Learning objectives :
After viewing this presentation the participant will be able to discuss:
- The upper and lower gastrointestinal symptoms that are more common in diabetes
- The mechanisms especially the neuropathies, that promote these symptoms
- Based on these mechanisms, a diagnostic and therapeutic approach to GI symptoms in the diabetic patient
Bibliographic references :
1. J Arts, P Caenepeel, K Verbeke and J TackInfluence of erythromycin on gastric emptying and meal related symptoms in functional dyspepsia with delayed gastric emptying Gut 2005;54:455-460.
2. Prakash C, Lustman PJ, Freedland KE, Clouse RE.Tricyclic Antidepressants for Functional Nausea and Vomiting (Clinical Outcome in 37 Patients) Dig Dis Sci. 1998 Sep;43(9):1951-6.
3. Brian E. Lacy, PHD, MD, Michael D. Crowell, PHD, Ann Schettler-Duncan, RN, Carole Mathis, PHD and Pankaj J. Pasricha, MDThe Treatment of Diabetic Gastroparesis With Botulinum Toxin Injection of the Pylorus Diabetes Care 27:2341-2347, 2004.
4. Abell T, McCallum R, Hocking M, Koch K, Abrahamsson H, Leblanc I, Lindberg G, Konturek J, Nowak T, Quigley EM, Tougas G, Starkebaum W.Gastric electrical stimulation for medically refractory gastroparesis Gastroenterology. 2003 Aug;125(2):421-8.
5. Celik AF, Osar Z, Damci T, Pamuk ON, Pamuk GE, Ilkova H. "How important are the disturbances of lower gastrointestinal bowel habits in diabetic outpatients?" Am J Gastroenterol. 2001 Apr;96(4):1314-6.
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"Quality of Life & Diabetes"Dr. Pat Phillips (biography)
English - 2006-02-21 - 39 minutes
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Summary :
In this presentation Dr. Phillips talks about why it's important to understand quality of life (QoL) in diabetes, some of the measurements used, and the quality of life continuum in diabetes.
It is important to understand QoL in the context of individual choices of the patient, and to understand the health impact of QoL. QoL is also used in guiding public health choices and...
Learning objectives :
After viewing this presentation the participant will be able to discuss:
QOL and Diabetes:
- Why bother?
- Measurement of QoL
- The QoL continuum in diabetes
Bibliographic references :
1. UK Prospective Diabetes Study Group.Tight blood pressure control and risk of macrovascular and microvascular complications in type 2 diabetes: UKPDS 38 BMJ 1998;317:703-713.
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"Interaction of Metabolic with Haemodynamic Factors in Diabetic Nephropathy"Prof. Mark E. Cooper (biography)
English - 2006-02-16 - 40 minutes
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Summary :
In this presentation Prof. Cooper discusses the pathogenesis of diabetic nephropathy, current treatments, and future directions for the development of new and better treatments.
Elevated glucose and blood pressure levels are both associated with the development of diabetic complications, as seen in the UKPD study. With regards to the pathogenesis of diabetic nephropathy, there...
Learning objectives :
After viewing this presentation the participant will be able to discuss:
- A paradigm for the pathogenesis of diabetic nephropathy
- Efficacy of currently used antiproteinuric therapies and predictors of renal outcomes
- Potential therapeutic targets in diabetic nephropathy
Bibliographic references :
1. M. E. Cooper.Interaction of metabolic and haemodynamic factors in mediating experimental diabetic nephropathy Diabetologia, Volume 44, Issue 11, Nov 2001, Pages 1957 - 1972.
2. Barry M. Brenner, M.D., Mark E. Cooper, M.D., Ph.D., Dick de Zeeuw, M.D., Ph.D., William F. Keane, M.D., William E. Mitch, M.D., Hans-Henrik Parving, M.D., Giuseppe Remuzzi, M.D., Steven M. Snapinn, Ph.D., Zhonxin Zhang, Ph.D., Shahnaz Shahinfar, M.D., for the RENAAL Study Investigators. Effects of Losartan on Renal and Cardiovascular Outcomes in Patients with Type 2 Diabetes and Nephropathy N Engl J Med. 2001 Sep 20;345(12):861-9.
3. de Zeeuw D, Remuzzi G, Parving HH, Keane WF, Zhang Z, Shahinfar S, Snapinn S, Cooper ME, Mitch WE, Brenner BM.Proteinuria, a target for renoprotection in patients with type 2 diabetic nephropathy: Lessons from RENAAL Kidney International (2004) 65, 2309–2320.
4. Doublier S, Salvidio G, Lupia E, Ruotsalainen V, Verzola D, Deferrari G, Camussi G.Nephrin Expression Is Reduced in Human Diabetic Nephropathy: Evidence for a Distinct Role for Glycated Albumin and Angiotensin II Diabetes 52:1023-1030, 2003.
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"Effects of fatty acids on glucose metabolism and the metabolic syndrome"Dr. Meredith Hawkins (biography)
English - 2005-11-08 - 42 minutes
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Summary :
In this presentation Dr. Hawkins talks about the role of increased free fatty acids in various clinical manifestations of insulin resistance, including increased glucose production, the lack of its regulation by hyperglycemia, insulin resistance per se and a procoagulant state.
Beginning with the role of increased free fatty acids in increasing glucose production, elevated insulin...
Learning objectives :
After viewing this presentation the participant will be able to discuss:
The role of increased free fatty acid levels in the following manifestations of insulin resistance:
- Increased glucose production and its lack of regulation by hyperglycemia
- Reduced insulin action
- Increased PAI-1 circulating levels and gene expression
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"21 Years of Insulin Resistance - Targeted Drug Research: Redefining the Pathophysiology of Type 2 Diabetes"Dr. Stephen A. Smith (biography)
English - 2005-11-08 - 36 minutes
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Summary :
Type 2 diabetes has been seen principally as a disorder of glucose metabolism resulting from insulin resistance and beta-cell dysfunction, but recent findings suggest there is a major lipid disorder component to the pathophysiology as well. In this talk Dr. Smith discusses how knowledge of the effects of thiazolidinediones have contributed to this changing view.
Thiazolidinedione...
Learning objectives :
After viewing this presentation the participant will be able to discuss:
- Development of the thiazolidinedione drugs
- Mechanisms of insulin sensitisation due to PPARγ activation by thiazolidinediones
Bibliographic references :
1. S. A. Smith. Central role of the adipocyte in the insulin-sensitising and cardiovascular risk modifying actions of the thiazolidinediones Biochimie 2003;85(12):1219-1230.
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"Introduction"Prof. Jean-Pierre Després (biography)
English - 2005-10-25 - 16 minutes
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Summary :
In this introduction, Prof. Després talks about the “toxic” environment in today's society which promotes obesity, the development of type 2 diabetes and an increased risk of cardiovascular disease.
Hyperglycemia management is only the tip of the iceberg when it comes to preventing first or recurrent myocardial infarction in diabetic patients. The underlying metabolic abnormalities...
Learning objectives :
After viewing this presentation the participant will be able to discuss:
- The contribution of modern lifestyle choices towards increased diabetes and heart disease risk
- The impact of metabolic syndrome on CHD risk in diabetic patients
Bibliographic references :
1. Alexander CM, Landsman PB, Teutsch SM, Haffner SM; Third National Health and Nutrition Examination Survey (NHANES III); National Cholesterol Education Program (NCEP).NCEP-Defined Metabolic Syndrome, Diabetes, and Prevalence of Coronary Heart Disease Among NHANES III Participants Age 50 Years and Older Diabetes 52:1210-1214, 2003.
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"Natural History of ß-cell Decline in Type 2 Diabetes"Prof. Stefano Del Prato (biography)
English - 2005-09-14 - 44 minutes
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Summary :
In this presentation Prof. Del Prato answers Dr. Leiter's question on the role of beta-cell failure in the pathogenesis of type 2 diabetes.
In the natural history of type 2 diabetes, the notion has long been held of healthy beta-cells being challenged by insulin resistance to undergo compensatory hypersecretion of insulin till the point of exhaustion, and this would be followed by...
Learning objectives :
After viewing this presentation the participant will be able to discuss:
- The natural history of type 2 diabetes: traditional and emerging views
- The role of beta-cell dysfunction in the progression to diabetes
- Inherent and acquired factors promoting beta-cell dysfunction
Bibliographic references :
1. U.K. Prospective Diabetes Study GroupU.K. prospective diabetes study 16. Overview of 6 years' therapy of type II diabetes: a progressive disease.Diabetes 1995; Vol 44, Issue 11 1249-1258.
2. Stefano Del Prato, Piero Marchetti, and Riccardo C. BonadonnaPhasic Insulin Release and Metabolic Regulation in Type 2 Diabetes Diabetes 51:S109-S116, 2002.
3. Piero Marchetti, Roberto Lupi, Massimo Federici, Lorella Marselli, Matilde Masini, Ugo Boggi, Silvia Del Guerra, Giovanni Patanè, Salvatore Piro, Marcello Anello, Ettore Bergamini, Francesco Purrello, Renato Lauro, Franco Mosca, Giorgio Sesti, and Stefano Del PratoInsulin Secretory Function Is Impaired in Isolated Human Islets Carrying the Gly972->Arg IRS-1 Polymorphism Diabetes 51:1419-1424, 2002.
4. Anello M, Lupi R, Spampinato D, Piro S, Masini M, Boggi U, Del Prato S, Rabuazzo AM, Purrello F, Marchetti P.Functional and morphological alterations of mitochondria in pancreatic beta cells from type 2 diabetic patients Diabetologia. 2005 Feb;48(2):282-9. Epub 2005 Jan 15.
5. Sesti G, Cardellini M, Marini MA, Frontoni S, D'Adamo M, Del Guerra S, Lauro D, De Nicolais P, Sbraccia P, Del Prato S, Gambardella S, Federici M, Marchetti P, Lauro R.A Common Polymorphism in the Promoter of UCP2 Contributes to the Variation in Insulin Secretion in Glucose-Tolerant Subjects Diabetes 52:1280-1283, 2003.
6. Lupi R, Del Guerra S, Marselli L, Bugliani M, Boggi U, Mosca F, Marchetti P, Del Prato S.Rosiglitazone prevents the impairment of human islet function induced by fatty acids: evidence for a role of PPAR{gamma}2 in the modulation of insulin secretion Am J Physiol Endocrinol Metab 286: E560-E567, 2004.
7. D'Alessandris C, Andreozzi F, Federici M, Cardellini M, Brunetti A, Ranalli M, Del Guerra S, Lauro D, Del Prato S, Marchetti P, Lauro R, Sesti G.Increased O-glycosylation of insulin signaling proteins results in their impaired activation and enhanced susceptibility to apoptosis in pancreatic beta-cells FASEB J. 2004 Jun;18(9):959-61. Epub 2004 Apr 1.
8. Silvia Del Guerra, Roberto Lupi, Lorella Marselli, Matilde Masini, Marco Bugliani, Simone Sbrana, Scilla Torri, Maria Pollera, Ugo Boggi, Franco Mosca, Stefano Del Prato, and Piero MarchettiFunctional and Molecular Defects of Pancreatic Islets in Human Type 2 Diabetes Diabetes 54:727-735, 2005.
9. Lister CA et al. Diabetologia 1999;42(suppl 1):A150.
10. Loredana Farilla, Hongxiang Hui, Cristina Bertolotto, Elizabeth Kang, Angela Bulotta, Umberto Di Mario and Riccardo Perfetti Glucagon-Like Peptide-1 Promotes Islet Cell Growth and Inhibits Apoptosis in Zucker Diabetic Rats Endocrinology Vol. 143, No. 11 4397-4408.
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"Adipose Tissue as an Inflammatory Organ (Endocrine Tumor) in Human Obesity"Prof. John N. Fain (biography)
English - 2005-06-10 - 55 minutes
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Summary :
We postulate that many of the deleterious effects of obesity in humans may involve enhanced formation of cytokines by the non-fat cells in adipose tissue. Cytokines are factors that are involved in the response to infections but also appear to promote heart disease as well as diabetes. We compared the release of cytokines by the adipose tissue of morbidly obese women with a body fat weight of 123...
Learning objectives :
After viewing this presentation the participant will be able to discuss:
- The specific parts of adipose tissue that inflammatory factors come from
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"Muscle - Adipose Tissue "Crosstalk" : Implications for Insulin Action"Prof. Edward W. Kraegen (biography)
English - 2005-06-10 - 53 minutes
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Summary :
In this presentation Prof. Kraegen discusses the link between muscle insulin resistance and free fatty acids (FFAs), buffering of the FFA supply by adipose tissue, and adipokine targets in muscle.
An overload of supply of fatty acids to muscle may be a major factor in the pathogenesis of muscle insulin resistance, says Prof. Kraegen. Cytosolic lipid accumulation leading to muscle...
Learning objectives :
After viewing this presentation the participant will be able to discuss:
- Muscle Insulin Resistance – Link to FFAs
- Buffering of FFA supply by adipose tissue
- Adipokines and targets in muscle
Bibliographic references :
1. K. Frayn. Adipose tissue as a buffer for daily lipid flux Diabetologia, Volume 45, Issue 9, Sep 2002, Pages 1201 - 1210.
2. D.R. Laybutt, D.J. Chisholm and E.W. Kraegen
Specific adaptations in muscle and adipose tissue in response to chronic systemic glucose oversupply in ratsAm J Physiol Endocrinol Metab 273: E1-E9, 1997.
3. Carey DG, Jenkins AB, Campbell LV, Freund J, Chisholm DJ.Abdominal fat and insulin resistance in normal and overweight women: Direct measurements reveal a strong relationship in subjects at both low and high risk of NIDDM.Diabetes. 1996 May;45(5):633-8.
4. Seng Khee Gan, Katherine Samaras, Campbell H. Thompson, Edward W. Kraegen, Andrew Carr, David A. Cooper, and Donald J. Chisholm Altered Myocellular and Abdominal Fat Partitioning Predict Disturbance in Insulin Action in HIV Protease Inhibitor-Related Lipodystrophy Diabetes 51:3163-3169, 2002.
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"Resistin and Fasting-Induced Adipose Factor (FIAF) in the Brain and Pituitary: Implications for Insulin Resistance and Obesity"Dr. Russell Brown (biography)
English - 2005-05-06 - 29 minutes
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Summary :
In this presentation Russell Brown discusses experimental evidence for expression of the adipokines resistin and fasting-induced adipose factor (FIAF) in non-adipose tissues, and studies providing insights into the nature of expression of these genes.
Insulin and leptin are examples of hormones from the periphery that have been found to act in the brain, affecting food intake,...
Learning objectives :
Key Discussion Points:
- The brain and pituitary gland express adipokines including resistin and fasting-induced adipose factor (FIAF);
- RNA interference is an effective tool to study adipokines;
- These brain-derived adipokines may prove to be therapeutic targets for obesity and brain development, cell signaling and angiogenesis.
Bibliographic references :
1. Schwartz MW, Porte D Jr. Diabetes, obesity, and the brainScience. 2005 Jan 21;307(5708):375-9.
2. Schwartz MW and Morton GJ. “Keeping Hunger at Bay.” Nature 2002 Aug 8; 418:596-597.
3. Barbara A. Morash, Diane Willkinson, Ehud Ur and Michael Wilkinson. Resistin expression and regulation in mouse pituitary FEBS Lett. 2002; 526(1-3):26-30.
4. Michael Wilkinson, Diane Wilkinson, Glen Wiesner, Barbara Morash, Ehud UrHypothalamic Resistin Immunoreactivity Is Reduced b y Obesity in the Mouse: Co-Localization with (alpha)-Melanostimulating Hormone Neuroendocrinology 2005;81:19-30.
5. G Wiesner, BA Morash, E Ur, and M Wilkinson. Food restriction regulates adipose-specific cytokines in pituitary gland but not in hypothalamus Journal of Endocrinology, Vol 180, Issue 3, R1-R6.
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"The ß-cell: Friend and Foe"Prof. Steven Kahn (biography)
English - 2005-05-06 - 100 minutes
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Summary :
The islet ß-cell is a critical player in the maintenance of euglycemia and the development of the hyperglycemia of type 2 diabetes. When frank hyperglycemia is present, ß-cell function is markedly diminished. However, with the recognition that insulin sensitivity is an important modulator of the insulin response, it has become clear that individuals at high risk of developing type 2 diabetes...
Learning objectives :
After viewing this presentation the participant will be able to discuss:
- Assessment of beta-cell function in humans
- The role of islet amyloid in loss of beta-cell function
Bibliographic references :
1. Steven E. Kahn.The Importance of ß-Cell Failure in the Development and Progression of Type 2 Diabetes The Journal of Clinical Endocrinology & Metabolism Vol. 86, No. 9 4047-4058.
2. Christian Weyer, Clifton Bogardus, David M. Mott and Richard E. PratleyThe natural history of insulin secretory dysfunction and insulin resistance in the pathogenesis of type 2 diabetes mellitus J Clin Invest, September 1999, Volume 104, Number 6, 787-794.
3. Christine C. Jensen, Miriam Cnop, Rebecca L. Hull, Wilfred Y. Fujimoto, Steven E. Kahn, and the American Diabetes Association GENNID Study Groupß-Cell Function Is a Major Contributor to Oral Glucose Tolerance in High-Risk Relatives of Four Ethnic Groups in the U.S.Diabetes 51:2170-2178, 2002.
4.Kloppel G, Lohr M, Habich K, Oberholzer M, Heitz PU.Islet pathology and the pathogenesis of type 1 and type 2 diabetes mellitus revisited.Surv Synth Pathol Res. 1985;4(2):110-25.
5. Alexandra E. Butler, Juliette Janson, Susan Bonner-Weir, Robert Ritzel, Robert A. Rizza, and Peter C. Butlerß-Cell Deficit and Increased ß-Cell Apoptosis in Humans With Type 2 Diabetes Diabetes 52:102-110, 2003.
6. Rebecca L. Hull, Gunilla T. Westermark, Per Westermark and Steven E. Kahn Islet Amyloid: A Critical Entity in the Pathogenesis of Type 2 DiabetesThe Journal of Clinical Endocrinology & Metabolism 2004;Vol. 89, No. 8 3629-3643.
7. Rebecca L. Hull, Sofianos Andrikopoulos, C. Bruce Verchere, Josep Vidal, Feng Wang, Miriam Cnop, Ronald L. Prigeon, and Steven E. KahnIncreased Dietary Fat Promotes Islet Amyloid Formation and ß-Cell Secretory Dysfunction in a Transgenic Mouse Model of Islet Amyloid Diabetes 52:372-379, 2003.
8. Shen Z, Hull RL, Kodama K, et al. "Long term rosiglitazone and metformin treatment reduce the severity of islet amyloid but do not prevent its formation." Diabetes 2003; 52(Suppl 1):A338.
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"Vascular Disease and Insulin Resistance"Prof. Giancarlo Viberti (biography)
English - 2005-05-06 - 51 minutes
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Summary :
Insulin resistance increases the risk of cardiovascular disease, and Prof. Viberti describes data showing the relationships between traditional and non-traditional CVD risk factors and insulin resistance, as well as their associated risks.
PPAR gamma agonists affect the metabolic pathways of insulin signaling by improving insulin sensitivity, and also the trophic pathways mainly...
Learning objectives :
After viewing this presentation the participant will be able to discuss:
- CVD risk factors and insulin resistance
- The effects of PPAR gamma agonists
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"Postprandial Hyperglycemia and Cardiovascular Disease"Prof. Antonio Ceriello (biography)
English - 2005-04-16 - 31 minutes
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Summary :
Increasing evidence suggests that the postprandial state is a contributing factor to the development of atherosclerosis. In diabetes, the postprandial phase is characterized by a rapid and large increase in blood glucose levels, and the possibility that the post-prandial hyperglycemic spikes may be relevant to the onset of cardiovascular complications has received recently much attention....
Learning objectives :
After viewing this presentation, participants will be able to discuss:
- The relevance of postprandial hyperglycemia and hypertriglyceridemia on oxidative stress generation and endothelial dysfunction.
- The relationship of postprandial and fasting glucose levels with HbA1c levels
Bibliographic references :
The DECODE study group on behalf of the Europe an Diabetes Epidemiology GroupGlucose tolerance and mortality: comparison of WHO and American Diabetic Association diagnostic criteria Lancet Volume 354, Issue 9179 , 21 August 1999, Pages 617-621
M Tominaga, H Eguchi, H Manaka, K Igarashi, T Kato, and A SekikawaImpaired glucose tolerance is a risk factor for cardiovascular disease, but not impaired fasting glucose. The Funagata Diabetes StudyDiabetes Care 22: 920-924.
B Balkau, M Shipley, RJ Jarrett, K Pyorala, M Pyorala, A Forhan, and E EschwegeHigh blood glucose concentration is a risk factor for mortality in middle-aged nondiabetic men. 20-year follow-up in the Whitehall Study, the Paris Prospective Study, and the Helsinki Policemen StudyDiabetes Care 21: 360-367
E Barrett-Connor and A FerraraIsolated postchallenge hyperglycemia and the risk of fatal cardiovascular disease in older women and men. The Rancho Bernardo StudyDiabetes Care 21: 1236-1239
Markolf Hanefeld, Jean Louis Chiasson, Carsta Koehler, Elena Henkel, Frank Schaper, and Theodora Temelkova-Kurktschiev Acarbose Slows Progression of Intima-Media Thickness of the Carotid Arteries in Subjects With Impaired Glucose Tolerance Stroke 2004 35: 1073 - 1078
M. Hanefeld, M. Cagatay, T. Petrowitsch, D. Neuser, D. Petzinna, and M. RuppAcarbose reduces the risk for myocardial infarction in type 2 diabetic patients: meta-analysis of seven long-term studiesEur. Heart J., January 2004; 25: 10 - 16.
Katherine Esposito, Dario Giugliano, Francesco Nappo, Raffaele Marfella for the Campanian Postprandial Hyperglycemia Study Group Regression of Carotid Atherosclerosis by Control of Postprandial Hyperglycemia in Type 2 Diabetes Mellitus Circulation 2004 110: 214 - 219
Francesco Perticone, Roberto Ceravolo, Arturo Pujia, Giorgio Ventura, Saverio Iacopino, Angela Scozzafava, Alessandro Ferraro, Massimo Chello, Pasquale Mastroroberto, Paolo Verdecchia, and Giuseppe SchillaciPrognostic Significance of Endothelial Dysfunction in Hypertensive PatientsCirculation, Jul 2001; 104: 191 - 196.
Antonio CerielloNew Insights on Oxidative Stress and Diabetic Complications May Lead to a "Causal" Antioxidant TherapyDiabetes Care 26: 1589-1596
Irene M Stratton, Amanda I Adler, H Andrew W Neil, David R Matthews, Susan E Manley, Carole A Cull, David Hadden, Robert C Turner, and Rury R HolmanAssociation of glycaemia with macrovascular and microvascular complications of type 2 diabetes (UKPDS 35): prospective observational studyBMJ, Aug 2000; 321: 405 - 412.
Louis Monnier, Hélène Lapinski, and Claude ColetteContributions of Fasting and Postprandial Plasma Glucose Increments to the Overall Diurnal Hyperglycemia of Type 2 Diabetic Patients: Variations with increasing levels of HbA1c Diabetes Care 26: 881-885
Curt L. Rohlfing, Hsiao-Mei Wiedmeyer, Randie R. Little, Jack D. England, Alethea Tennill, and David E. GoldsteinDefining the Relationship Between Plasma Glucose and HbA1c: Analysis of glucose profiles and HbA1c in the Diabetes Control and Complications Trial Diabetes Care 25: 275-278.
EJ Bastyr, CA Stuart, RG Brodows, S Schwartz, CJ Graf, A Zagar, and KE RobertsonTherapy focused on lowering postprandial glucose, not fasting glucose, may be superior for lowering HbA1c. IOEZ Study GroupDiabetes Care 23: 1236-1241
Writing Team for the Diabetes Control and Complications Trial/Epidemiology of Diabetes Interventions and Complications Research GroupSustained Effect of Intensive Treatment of Type 1 Diabetes Mellitus on Development and Progression of Diabetic Nephropathy: The Epidemiology of Diabetes Interventions and Complications (EDIC) StudyJAMA. 2003;290:2159-2167
The Diabetes Control and Complications Trial/Epidemiology of Diabetes Interventions and Complications Research Group Intensive Diabetes Therapy and Carotid Intima–Media Thickness in Type 1 Diabetes MellitusNEJM 2003 (348):2294
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"Increased Risk of Coronary Events in Dysglycemic Patients: Mechanisms, and Reasons for Poor Outcomes"Dr. Richard W. Nesto (biography)
English - 2005-04-16 - 32 minutes
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Summary :
In recent years the early in-hospital mortality of diabetic patients after MI has been substantially reduced due to improvements in the medical management of these patients within the first 24 hours (1), however diabetes and hyperglycaemia itself still confer an increased risk of long-term mortality after MI which can be explained by a higher risk of congestive heart failure (2).
Learning objectives :
After viewing this presentation the participant will be able to discuss:
- Studies relating admission blood glucose levels to in-hospital and long-term mortality after MI in diabetic and non-diabetic patients
- Mechanisms whereby hyperglycaemia in AMI leads to poor outcomes
- The role of metabolic modulators in AMI: GIK infusion therapy
- Remaining questions
Bibliographic references :
1. Oliver Schnell, MD, Oliver Schäfer, Sonja Kleybrink, Wittich Doering, MD, Eberhard Standl, MD and Wolfgang Otter, MDIntensification of Therapeutic Approaches Reduces Mortality in Diabetic Patients With Acute Myocardial Infarction: The Munich registryDiabetes Care 27:455-460, 2004.
2. Ischa Stranders, MD; Michaela Diamant, MD, PhD; Rogier E. van Gelder, MD; Hugo J. Spruijt, MSEE; Jos W. R. Twisk, PhD; Robert J. Heine, MD, PhD, FRCP; Frans C. Visser, MD, PhD. Admission Blood Glucose Level as Risk Indicator of Death After Myocardial Infarction in Patients With and Without Diabetes Mellitus Arch Intern Med. 2004;164:982-988.
3. Nazneem N. Wahab MD, Elizabeth A. Cowden MD, Neil J. Pearce MD, Martin J. Gardner MD, Heather Merry MSc, Jafna L. Cox MD and ICONS Investigators. Is blood glucose an independent predictor of mortality in acute myocardial infarction in the thrombolytic era? JACC.20 November 2002, Volume 40, Issue 10 Pages 1748-1754.
4. John A. Colwell, MD, PHD and Richard W. Nesto, MD.The Platelet in Diabetes: Focus on prevention of ischemic eventskjhkhkhDiabetes Care 26:2181-2188, 2003.
5. Jorik R. Timmer, Jan Paul Ottervanger, Menko-Jan de Boer, Jan-Henk E. Dambrink, Jan C.A. Hoorntje, A.T. Marcel Gosselink, Harry Suryapranata, Felix Zijlstra, Arnoud W.J. van't HofHyperglycemia is an important predictor of impaired coronary flow before reperfusion therapy in ST-segment elevation myocardial infarctionJACC.5 April 2005, Volume 45, Issue 7 Pages 999-1002.
6. Katsuomi Iwakura MD, Hiroshi Ito MD, FACC, Masashi Ikushima MD, Shigeo Kawano MD, Atsushi Okamura MD, Katsuaki Asano MD, Tadashi Kuroda MD, Koji Tanaka MD, Tohru Masuyama MD, Masatsugu Hori MD and Kenshi Fujii MDAssociation between hyperglycemia and the no-reflow phenomenon inpatients with acute myocardial infarctionJACC.1 January 2003, Volume 41, Issue 1 Pages 1-7.
7. Raffaele Marfella, MD, PHD, Mario Siniscalchi, MD, PHD, Katherine Esposito, MD, Ausilia Sellitto, MD, Umberto de Fanis, MD, Ciro Romano, MD, PHD, Michele Portoghese, MD, Silvio Siciliano, MD, Francesco Nappo, MD, PHD, Ferdinando Carlo Sasso, MD, PHD, Nicola Mininni, MD, Federico Cacciapuoti, MD, Giacomo Lucivero, MD, PHD, Riccardo Giunta, MD, Mario Verza, MD and Dario Giugliano, MD, PHDEffects of Stress Hyperglycemia on Acute Myocardial Infarction: Role of inflammatory immune process in functional cardiac outcome Diabetes Care 26:3129-3135, 2003.
8. Oliver MF, Opie LH. Effects of glucose and fatty acids on myocardial ischaemia and arrhythmiasLancet. 1994 Jan 15;343(8890):155-8.
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"Lessons from the UKPDS"Prof. Alastair Gray (biography)
English - 2005-04-15 - 33 minutes
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Summary :
In this presentation Prof. Gray descibes results from UKPDS 61 and 68, which looked at fasting plasma glucose (FPG) levels at diagnosis of diabetes in relation to clinical outcomes, and the UKPDS Outcomes Model, respectively.
UKPDS 61 found that those with lower FPG levels at diagnosis of diabetes had fewer complications but similar rates of deterioration in glycemic control...
Learning objectives :
After viewing this presentation the participant will be able to discuss:
- The relationship between FPG level at diagnosis of diabetes and clinical outcomes
- The UKPDS Outcomes Model
Bibliographic references :
Stephen Colagiuri, FRACP, Carole A. Cull, PHD and Rury R. Holman, FRCP For the UKPDS Group. Are Lower Fasting Plasma Glucose Levels at Diagnosis of Type 2 Diabetes Associated With Improved Outcomes? - U.K. Prospective Diabetes Study 61 Diabetes Care 25:1410-1417, 2002.
P. M. Clarke, A. M. Gray, A. Briggs, A. J. Farmer, P. Fenn, R. J. Stevens, D. R. Matthews, I. M. Stratton, R. R. Holman and on behalf of the UK Prospective Diabetes Study (UKPDS) Group. A model to estimate the lifetime health outcomes of patients with Type 2 diabetes: the United Kingdom Prospective Diabetes Study (UKPDS) Outcomes Model (UKPDS no. 68)Diabetologia. 2004; 47(10):1747 - 1759.
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"Effect of Fructose Overfeeding and Fish Oil Administration on De Novo Lipogenesis and Insulin Sensitivity in Healthy Males"Dr. David Faeh (biography)
English - 2005-04-15 - 23 minutes
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Summary :
High fructose diets (Hfr) may stimulate hepatic de novo lipogenesis (DNL), and cause hypertriglyceridemia and insulin resistance in rodents. It can therefore be hypothesized that fructose-induced insulin resistance is secondary to alterations of hepatic and extra-hepatic lipid metabolism. Since fish oil supplementation (FO) is known to suppress lipogenic enzymes and to decrease TG, it may improve...
Learning objectives :
After viewing this presentation the participant will be able to discuss:
- Animal and human studies relating to the metabolic effects of fructose overfeeding and fish oil supplementation
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"Neural Control of Energy Balance"Prof. Stephen C. Woods (biography)
English - 2005-04-14 - 32 minutes
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Summary :
Knowledge of the hormones, neurotransmitters and neural pathways that regulate energy homeostasis is increasing at a rapid pace. Food intake was historically thought to occur in response to acute energy demands; however, current evidence suggests that meals occur based on habit and convenience rather than on metabolic need. Most individuals maintain stable body weights over long intervals by...
Learning objectives :
After viewing this presentation, participants will be able to discuss:
• The satiety system of energy balance
• The adiposity system of energy balance
• The central integrators of energy balance
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"Markers of Inflammation and Hypercoagulation in CAD"Dr. Russell P. Tracy (biography)
English - 2004-10-25 - 43 minutes
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Summary :
Inflammation is recognized as playing a major role in atherosclerosis (1), and markers of inflammation have been associated with the risk of future cardiovascular disease.
With regards to the clinical application of inflammatory markers, the American Heart Assocation and the Centers for Disease Control and Prevention have endorsed the optional use of high-sensitivity CRP testing...
Learning objectives :
After viewing this presentation the participant will be able to discuss:
- Inflammatory markers and cardiovascular risk: clinical utility of the hsCRP test
- Inflammation and thrombosis markers in the prediction of diabetes
- Studies on inflammation and thrombosis biomarkers in young and old patients
- Future epidemiological research possibilities using assays based on cellular function
Bibliographic references :
1. Peter Libby, MD Current Concepts of the Pathogenesis of the Acute Coronary Syndromes Circulation. 2001;104:365.
2. Thomas A. Pearson, MD, PhD (Co-Chair); George A. Mensah, MD (Co-Chair); R. Wayne Alexander, MD, PhD; Jeffrey L. Anderson, MD; Richard O. Cannon, III, MD; Michael Criqui, MD; Yazid Y. Fadl, MD; Stephen P. Fortmann, MD; Yuling Hong, MD, PhD; Gary L. Myers, PhD; Nader Rifai, PhD; Sidney C. Smith, Jr, MD; Kathryn Taubert, PhD; Russell P. Tracy, PhD; Frank Vinicor, MD Markers of Inflammation and Cardiovascular Disease: Application to Clinical and Public Health Practice: A Statement for Healthcare Professionals From the Centers for Disease Control and Prevention and the American Heart Association Circulation. 2003;107:499.
3. Andreas Festa, Ralph D’Agostino, Jr, Russell P. Tracy, and Steven M. HaffnerElevated Levels of Acute-Phase Proteins and Plasminogen Activator Inhibitor-1 Predict the Development of Type 2 Diabetes - The Insulin Resistance Atherosclerosis StudyDiabetes 51:1131-1137, 2002.
4. Andreas Festa, MD; Anthony J.G. Hanley, PhD; Russell P. Tracy, PhD; Ralph D’Agostino, Jr, PhD; Steven M. Haffner, MD Inflammation in the Prediabetic State Is Related to Increased Insulin Resistance Rather Than Decreased Insulin SecretionCirculation. 2003;108:1822.
5. Earl S. Ford, MD, MPH C-Reactive Protein Concentration and Cardiovascular Disease Risk Factors in Children: Findings From the National Health and Nutrition Examination Survey 1999–2000 Circulation. 2003;108:1053.
6. MA Ferguson, B Gutin, S Owens, M Litaker, RP Tracy and J AllisonFat distribution and hemostatic measures in obese childrenAmerican Journal of Clinical Nutrition. 1998. Vol 67, 1136-1140.
7. Mikko J. Järvisalo; Aimo Harmoinen; Maarit Hakanen; Ulla Paakkunainen; Jorma Viikari; Jaakko Hartiala; Terho Lehtimäki; Olli Simell; Olli T. Raitakari Elevated Serum C-Reactive Protein Levels and Early Arterial Changes in Healthy Children
Arteriosclerosis, Thrombosis, and Vascular Biology. 2002;22:1323.
8. Allen P. Burke, MD; Russell P. Tracy, PhD; Frank Kolodgie, PhD; Gray T. Malcom, PhD; Arthur Zieske, MD; Robert Kutys, MS; Joseph Pestaner, MD; John Smialek, MD; Renu Virmani, MDElevated C-Reactive Protein Values and Atherosclerosis in Sudden Coronary Death: Association With Different Pathologies Circulation. 2002;105:2019.
9. Tamara B. Harris MD, MS, Luigi Ferrucci MD, PhD, Russell P. Tracy PhD, M. Chiara Corti MD, PhD, Sholom Wacholder PhD, Walter H. Ettinger Jr MD, MBA, Harley Heimovitz MS, Harvey J. Cohen MD and Robert Wallace MD, Msc.Associations of elevated Interleukin-6 and C-Reactive protein levels with mortality in the elderlyAm J Med. 1999; 106(5): 506.
10. Mary Cushman; Rozenn N. Lemaitre; Lewis H. Kuller; Bruce M. Psaty; Elizabeth M. Macy; A. Richey Sharrett; Russell P. Tracy Fibrinolytic Activation Markers Predict Myocardial Infarction in the Elderly: The Cardiovascular Health Study ATVB. 1999; 19:493-498.
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"Obesity, Dyslipidemia and Inflammation"Dr. Robert H. Eckel (biography)
English - 2004-10-23 - 43 minutes
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Summary :
In this presentation Dr. Eckel discusses various pathways involved in the genesis of metabolic syndrome and options for the treatment of obesity, dyslipidemia and inflammation.
The metabolic syndrome is thought of as a disorder of insulin resistance, which in turn is related to high free fatty acid levels. Beyond the components listed in the NCEP ATP III definition of the metabolic...
Learning objectives :
After viewing this presentation the participant will be able to discuss
- The prevalence of obesity in the U.S. and projected diabetes rates globally
- The dependence of hs-CRP levels on body fat distribution and insulin sensitivity
- The importance of chronic inflammation in fat in the development of obesity-related insulin resistance
- How hs-CRP levels relate to the metabolic syndrome
- Therapeutic options for obesity, dyslipidemia and inflammation
Bibliographic references :
1. Dzien A, Dzien-Bischinger C, Hoppichler F, Lechleitner M.The metabolic syndrome as a link between smoking and cardiovascular diseaseDiabetes Obes Metab. 2004 Mar;6(2):127-32.
2. Ken Williams MS, Allan D. Sniderman MD, Naveed Sattar MD, Ralph D’Agostino Jr PhD, Lynne E. Wagenknecht PhD, and Steven M. Haffner MDComparison of the Associations of Apolipoprotein B and Low-Density Lipoprotein Cholesterol With Other Cardiovascular Risk Factors in the Insulin Resistance Atherosclerosis Study (IRAS)Circulation 2003;108:2312.
3. W. Timothy Garvey, Soonho Kwon, Deyi Zheng, Sara Shaughnessy, Penny Wallace, Amy Hutto, Kimberly Pugh, Alicia J. Jenkins, Richard L. Klein, and Youlian LiaoEffects of Insulin Resistance and Type 2 Diabetes on Lipoprotein Subclass Particle Size and Concentration Determined by Nuclear Magnetic Resonance Diabetes 52:453-462, 2003
4. V. Sigurdardottir, B. Fagerberg & J. HultheCirculating oxidized low-density lipoprotein (LDL) is associated with risk factors of the metabolic syndrome and LDL size in clinically healthy 58-year-old men (AIR study)Journal of Internal Medicine. Volume 252 Issue 5 Page 440 - November 2002.
5. Mercedes R. Carnethon, Stephen P. Fortmann, Latha Palaniappan, Bruce B. Duncan, Maria I. Schmidt and Lloyd E. Chambless.Risk Factors for Progression to Incident Hyperinsulinemia: The Atherosclerosis Risk in Communities Study, 1987–1998 Am J Epidemiol 2003; 158:1058-1067.
6. Latha Palaniappan, Mercedes Carnethon and Stephen P. FortmannAssociation between microalbuminuria and the metabolic syndrome: NHANES IIIAmerican Journal of Hypertension. Volume 16, Issue 11 , November 2003, Pages 952-958.
7. Chitturi S, Abeygunasekera S, Farrell GC, Holmes-Walker J, Hui JM, Fung C, Karim R, Lin R, Samarasinghe D, Liddle C, Weltman M, George J. NASH and insulin resistance: Insulin hypersecretion and specific association with the insulin resistance syndrome.
Hepatology. 2002 Feb;35(2):373-9.
8. Apridonidze T, Essah PA, Iuorno MJ, Nestler JE.
Prevalence and characteristics of the metabolic syndrome in women with polycystic ovary syndrome.
J Clin Endocrinol Metab. 2004 Dec 28.
9. Pamela A. Sakkinen, Patricia Wahl, Mary Cushman, Michael R. Lewis and Russell P. TracyClustering of Procoagulation, Inflammation, and Fibrinolysis Variables with Metabolic Factors in Insulin Resistance Syndrome American Journal of Epidemiology Vol. 152, No. 10 : 897-907.
10. Hoieggen A, Fossum E, Moan A, Enger E, Kjeldsen SE.Whole-blood viscosity and the insulin-resistance syndrome.J Hypertens. 1998 Feb;16(2):203-10.
11. Stuhlinger MC, Abbasi F, Chu JW, Lamendola C, McLaughlin TL, Cooke JP, Reaven GM, Tsao PS.
Relationship between insulin resistance and an endogenous nitric oxide synthase inhibitor.JAMA. 2002 Mar 20;287(11):1420-6.
12. James B. Meigs, MD, MPH, Paul F. Jacques, PHD, Jacob Selhub, PHD, Daniel E. Singer, MD, David M. Nathan, MD, Nader Rifai, PHD, Ralph B. D’Agostino, Sr., PHD and Peter W.F. Wilson, MDFasting Plasma Homocysteine Levels in the Insulin Resistance Syndrome: The Framingham Offspring Study Diabetes Care 24:1403-1410, 2001.
13. Johannes Hulthe, Lillemor Mattsson Hultén and Björn FagerbergLow adipocyte-derived plasma protein adiponectin concentrations are associated with the metabolic syndrome and small dense low-density lipoprotein particles: Atherosclerosis and insulin resistance study
Metabolism. December 2003 Volume 52 Number 12.
14. Urpu Salmenniemi, MD; Eija Ruotsalainen, MD; Jussi Pihlajamäki, MD; Ilkka Vauhkonen, MD; Sakari Kainulainen, MD; Kari Punnonen, MD; Esko Vanninen, MD; Markku Laakso, MD Multiple Abnormalities in Glucose and Energy Metabolism and Coordinated Changes in Levels of Adiponectin, Cytokines, and Adhesion Molecules in Subjects With Metabolic Syndrome Circulation. 2004;110:3842-3848.
15. Andreas Festa, MD; Ralph D’Agostino, Jr, PhD; George Howard, DrPH; Leena Mykkänen, MD, PhD; Russell P. Tracy, PhD; Steven M. Haffner, MD.Chronic Subclinical Inflammation as Part of the Insulin Resistance Syndrome Circulation. 2000;102:42.
16. Isabelle Lemieux; Agnès Pascot; Denis Prud’homme; Natalie Alméras; Peter Bogaty; André Nadeau; Jean Bergeron; Jean-Pierre Després. Elevated C-Reactive Protein: Another Component of the Atherothrombotic Profile of Abdominal Obesity Arteriosclerosis, Thrombosis, and Vascular Biology. 2001;21:961.
17. Tracey McLaughlin, MD; Fahim Abbasi, MD; Cindy Lamendola, RN, MSN; Lynn Liang, PhD; Gerald Reaven, MD; Patricia Schaaf, MS, RD; Peter Reaven, MD.Differentiation Between Obesity and Insulin Resistance in the Association With C-Reactive Protein Circulation. 2002;106:2908.
18. Stuart P. Weisberg, Daniel McCann, Manisha Desai, Michael Rosenbaum, Rudolph L. Leibel and Anthony W. Ferrante, Jr.Obesity is associated with macrophage accumulation in adipose tissue J. Clin. Invest. 112:1796-1808 (2003).
19. Haiyan Xu, Glenn T. Barnes, Qing Yang, Guo Tan, Daseng Yang, Chieh J. Chou, Jason Sole, Andrew Nichols, Jeffrey S. Ross, Louis A. Tartaglia and Hong Chen.Chronic inflammation in fat plays a crucial role in the development of obesity-related insulin resistance J. Clin. Invest. 112:1821-1830 (2003).
20. J Bolinder, L Kager, J Ostman and P Arner. Differences at the receptor and postreceptor levels between human omental and subcutaneous adipose tissue in the action of insulin on lipolysisDiabetes. 183; Vol 32, Issue 2 117-123.
21. CT Montague, JB Prins, L Sanders, JE Digby and S O'Rahilly
Depot- and sex-specific differences in human leptin mRNA expression: implications for the control of regional fat distributionDiabetes. 1997; Vol 46, Issue 3 342-347.
22. Arner P.Catecholamine-induced lipolysis in obesity.Int J Obes Relat Metab Disord. 1999 Feb;23 Suppl 1:10-3.
23. Mavri A, Alessi MC, Bastelica D, Geel-Georgelin O, Fina F, Sentocnik JT, Stegnar M, Juhan-Vague I.
Subcutaneous abdominal, but not femoral fat expression of plasminogen activator inhibitor-1 (PAI-1) is related to plasma PAI-1 levels and insulin resistance and decreases after weight loss.Diabetologia. 2001 Nov;44(11):2025-31.
24. Giacchetti G, Faloia E, Mariniello B, Sardu C, Gatti C, Camilloni MA, Guerrieri M, Mantero F.
Overexpression of the renin-angiotensin system in human visceral adipose tissue in normal and overweight subjects.Am J Hypertens. 2002 May;15(5):381-8.
25. Fain JN, Madan AK, Hiler ML, Cheema P, Bahouth SW.
Comparison of the release of adipokines by adipose tissue, adipose tissue matrix, and adipocytes from visceral and subcutaneous abdominal adipose tissues of obese humans.
Endocrinology. 2004 May;145(5):2273-82.
26. Julie K. Plenge, MD; Teri L. Hernandez, RN, BSN; Kathleen M. Weil, RN, MSS; Paul Poirier, MD; Gary K. Grunwald, PhD; Santica M. Marcovina, PhD; Robert H. Eckel, MD Simvastatin Lowers C-Reactive Protein Within 14 Days: An Effect Independent of Low-Density Lipoprotein Cholesterol Reduction Circulation. 2002;106:1447.
27. I. Jialal, MD, PhD; D. Stein, MD; D. Balis, MD; S. M. Grundy, MD, PhD; B. Adams-Huet, MS; S. Devaraj, PhD Effect of Hydroxymethyl Glutaryl Coenzyme A Reductase Inhibitor Therapy on High Sensitive C-Reactive Protein LevelsCirculation. 2001;103:1933.
28. Chiquette E, Ramirez G, Defronzo R.
A meta-analysis comparing the effect of thiazolidinediones on cardiovascular risk factors.
Arch Intern Med. 2004 Oct 25;164(19):2097-104.
29. Boden G, Cheung P, Mozzoli M, Fried SK.
Effect of thiazolidinediones on glucose and fatty acid metabolism in patients with type 2 diabetes.
Metabolism. 2003 Jun;52(6):753-9.
30. Willa A. Hsueh; Dennis Bruemmer Peroxisome Proliferator-Activated Receptor (gamma): Implications for Cardiovascular DiseaseHypertension. 2004;43:297.
31. Tontonoz P, Nagy L.
Regulation of macrophage gene expression by peroxisome-proliferator-activated receptor gamma: implications for cardiovascular disease.Curr Opin Lipidol. 1999 Dec;10(6):485-90.
32. Paul M Ridker, MD; Julie E. Buring, ScD; Nancy R. Cook, ScD; Nader Rifai, PhD C-Reactive Protein, the Metabolic Syndrome, and Risk of Incident Cardiovascular Events Circulation 2003;107: 391-7.
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"Adiponectin"Prof. John Prins (biography)
English - 2004-09-23 - 22 minutes
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Summary :
Adiponectin is an important adipokine having endocrine effects in the liver, muscle and vasculature.
Most adipokines are secreted at higher than normal levels in obesity and the metabolic syndrome, but adiponectin is an exception as its secretion is decreased in these states. Adiponectin promotes insulin sensitivity and has anti-inflammatory effects. Prof. Prins describes these...
Learning objectives :
After viewing this presentation the participant will be able to discuss:
- The characteristics and regulation of adiponectin;
- Improvement of insulin sensitivity via adiponectin action in muscle and the liver;
- Anti-inflammatory effects of adiponectin in the vasculature;
- The clinical implications of adiponectin deficiency in obesity and the metabolic syndrome.
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"Association of hsCRP with Later Stage ß-Cell Dysfunction and Insulin Resistance in Patients with Type 2 Diabetes"Dr. A. Pfützner (biography)
English - 2004-09-08 - 30 minutes
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Summary :
High-sensitivity C-reactive protein (hsCRP) was shown in large epidemiological studies to predict the risk of cardiovascular disease in apparently healthy individuals (1). In this presentation Dr. Pfutzner presents data from the IRIS-II study showing that hsCRP may also be a good marker of macrovascular risk in type 2 diabetic patients.
In the state of pathologically increased...
Learning objectives :
After viewing this presentation the participant will be able to discuss:
- Evidence for intact proinsulin as a marker of insulin resistance
- The pathophysiological staging of type 2 diabetes based on beta-cell secretion
- Data from the IRIS-II study on the prevalence of macrovascular disease in type 2 diabetics in relation to hsCRP levels and stage of beta-cell dysfunction and insulin resistance.
Bibliographic references :
1. Paul M. Ridker, M.D., Nader Rifai, Ph.D., Lynda Rose, M.S., Julie E. Buring, Sc.D., and Nancy R. Cook, Sc.D.Comparison of C-Reactive Protein and Low-Density Lipoprotein Cholesterol Levels in the Prediction of First Cardiovascular EventsNEJM.2002;347:1557-1565.
2. Andreas Pfützner, MD, PHD, Thomas Kunt, MD, Cloth Hohberg, MD, Agnes Mondok, MD, Sabine Pahler, MSC, Thomas Konrad, MD, Georg Lübben, MD and Thomas Forst, MD.Fasting Intact Proinsulin Is a Highly Specific Predictor of Insulin Resistance in Type 2 Diabetes Diabetes Care.2004;27:682-687.
3. Andreas Pfützner ; Anke H. Pfützner ; Martin Larbig ; Thomas Forst.Role of Intact Proinsulin in Diagnosis and Treatment of Type 2 Diabetes MellitusDiabetes Technology & Therapeutics.2004;6(3):405-412.
4. T. Forst, E. Standl, C. Hohberg, T. Konrad, J. Schulze, H. J. Strotmann, G. Lübben, S. Pahler, A. Bachinger, M. Langenfeld and A. Pfützner.IRIS II study: the IRIS II scoreassessment of a new clinical algorithm for the classification of insulin resistance in patients with Type 2 diabetesDiabetic Medicine.2004;21(10):1149.
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"CRP, Inflammation, and its Relationship to Cardiovascular Disease, Metabolic Syndrome and Type 2 Diabetes"Dr. Paul M. Ridker (biography)
English - 2004-06-25 - 45 minutes
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Summary :
In this presentation Dr Ridker reviews the use of high-sensitivity C-Reactive Protein (hs-CRP) as a prognostic indicator of myocardial infarction, stroke and type 2 diabetes; the added prognostic information CRP provides in patients with the metabolic syndrome, the role of CRP in atherothrombosis, and how some antidiabetic agents have been shown to lower levels of inflammatory markers including...
Learning objectives :
The participant will learn about CRP in relation to CVD, metabolic syndrome and type 2 diabetes.
Bibliographic references :
1. Paul M. Ridker, M.D., Mary Cushman, M.D., Meir J. Stampfer, M.D., Russell P.Tracy, Ph.D., and Charles H. Hennekens, M.D. Inflammation, Aspirin, and the Risk of Cardiovascular Disease in Apparently Healthy Men. NEJM 1997;336:973-79.
2. Paul M. Ridker, M.D., Charles H. Hennekens, M.D., Julie E. Buring, Sc.D., and Nader Rifai, Ph.D. C-Reactive Protein and Other Markers of Inflammation in the Prediction of Cardiovascular Disease in Women NEJM 2000;342:836-43.
3. Paul M. Ridker, M.D., Nader Rifai, Ph.D., Lynda Rose, M.S., Julie E. Buring, Sc.D., and Nancy R. Cook, Sc.D. Comparison of C-Reactive Protein and Low-Density Lipoprotein Cholesterol Levels in the Prediction of First Cardiovascular Events NEJM 2002;347: 1557-65.
4. Paul M Ridker, MD; Julie E. Buring, ScD; Nancy R. Cook, ScD; Nader Rifai, PhD C-Reactive Protein, the Metabolic Syndrome, and Risk of Incident Cardiovascular Events Circulation 2003;107: 391-7.
5. John S. Yudkin; C. D. A. Stehouwer; J. J. Emeis; S. W. Coppack C-Reactive Protein in Healthy Subjects: Associations With Obesity, Insulin Resistance, and Endothelial Dysfunction ATVG 1999;19:972-978 .
6. Aruna D. Pradhan, MD,MPH; JoAnn E. Manson, MD,DrPH; Nader Rifai, PhD; Julie E. Buring, ScD; Paul M. Ridker, MD,MPH C-Reactive Protein, Interleukin 6, and Risk of Developing Type 2 Diabetes Mellitus JAMA. 2001;286:327-334.
7. Frank B. Hu, James B. Meigs, Tricia Y. Li1, Nader Rifai, and JoAnn E. Manson Inflammatory Markers and Risk of Developing Type 2 Diabetes in Women Diabetes 53:693-700,2004.
8. Steven M. Haffner, MD; Andrew S. Greenberg, MD; Wayde M. Weston, PhD; Hongzi Chen, PhD; Ken Williams, MS; Martin I. Freed, MD Effect of Rosiglitazone Treatment on Nontraditional Markers of Cardiovascular Disease in Patients With Type 2 Diabetes Mellitus Circulation.2002;106:679.
9. Nikolaus Marx, MD; Armin Imhof, MD; Johannes Froehlich, MS; Laila Siam, MS; Jochen Ittner, MD; Gerhard Wierse, MD; Arnold Schmidt, MD; Winfried Maerz, MD; Vinzenz Hombach, MD; Wolfgang Koenig, MD Effect of Rosiglitazone Treatment on Soluble CD40L in Patients With Type 2 Diabetes and Coronary Artery Disease Circulation. 2003;107:1954.
10. Noriko Satoh, MD, PHD, Yoshihiro Ogawa, MD, PHD, Takeshi Usui, MD, PHD, Tetsuya Tagami, MD, PHD, Shigeo Kono, MD, PHD, Hiroko Uesugi, MD, PHD, Hiroyuki Sugiyama, MD, PHD, Akira Sugawara, MD, PHD, Kazunori Yamada, MD, PHD, Akira Shimatsu, MD, PHD, Hideshi Kuzuya, MD, PHD and Kazuwa Nakao, MD, PHD. Antiatherogenic Effect of Pioglitazone in Type 2 Diabetic Patients Irrespective of the Responsiveness to Its Antidiabetic Effect Diabetes Care 26:2493-2499, 2003.
11. BART STAELS, WOLFGANG KOENIG, AÏDA HABIB, RÉGINE MERVAL, MARILYNE LEBRET, INÉS PINEDA TORRA, PHILIPPE DELERIVE, ABDESSAMAD FADEL, GIULIA CHINETTI, JEAN-CHARLES FRUCHART, JAMILA NAJIB, JACQUES MACLOUF & ALAIN TEDGUIActivation of human aortic smooth-muscle cells is inhibited by PPAR (alpha) but not by PPAR (gamma) activatorsNature 393, 790 - 793 (25 June 1998).
12. Howard D. Sesso, ScD, MPH; Julie E. Buring, ScD; Nader Rifai, PhD; Gavin J.Blake, MD, MPH; J. Michael Gaziano, MD, MPH; Paul M. Ridker, MD, MPH C-Reactive Protein and the Risk of Developing Hypertension JAMA. 2003;290:2945-2951.
13. Ridker PM; JUPITER Study Group. Rosuvastatin in the primary prevention of cardiovascular disease among patients with low levels of low-density lipoprotein cholesterol and elevated high-sensitivity C-reactive protein: rationale and design of the JUPITER trial
Circulation. 2003 Nov 11;108(19):2292-7.
14. Paul A, Ko KW, Li L, Yechoor V, McCrory MA, Szalai AJ, Chan L. C-reactive protein accelerates the progression of atherosclerosis in apolipoprotein E-deficient mice. Circulation. 2004 Feb 10;109(5):647-55. Epub 2004 Jan 26.
15. Danenberg HD, Szalai AJ, Swaminathan RV, Peng L, Chen Z, Seifert P, Fay WP, Simon DI, Edelman ER. Increased thrombosis after arterial injury in human C-reactive protein-transgenic mice. Circulation. 2003 Aug 5;108(5):512-5. Epub 2003 Jul 21.
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"What are the manifestations of beta-cell dysfunction and insulin resistance?"Dr. Steven V. Edelman (biography)
English - 2004-06-04 - 12 minutes
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Summary :
In the natural history of type 2 diabetes, the development of insulin resistance, impaired glucose tolerance and finally type 2 diabetes occurs over several years, with no apparent symptoms. This period is significant as insulin resistance is associated with cardiovascular abnormalities. Compensatory hyperinsulinemia maintains blood glucose levels until the point of beta cell exhaustion, when...
Learning objectives :
After viewing these slides the participant will be able to discuss:
- The natural history of type 2 diabetes
- UKPDS data showing the decline in beta cell function over time
Bibliographic references :
UKPDS Group (UKPDS 16).U.K. prospective diabetes study 16. Overview of 6 years' therapy of type II diabetes: a progressive disease. U.K. Prospective Diabetes Study Group Diabetes 1995;44(11):1249-1258.
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"Type 2 Diabetes Mellitus and Heart Failure: Implications for the Use of TZDs"Dr. Richard W. Nesto (biography)
English - 2004-06-04 - 68 minutes
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Summary :
Diabetes increases the risk of congestive heart failure, and this effect is more prominent in women (1). Diabetes has been found to exert effects on cardiac structure and function including increased left ventricular (LV) mass (2). Furthermore, the Framingham Heart Study showed that women had greater LV mass than men across the range of glucose tolerance, and insulin resistance was associated...
Learning objectives :
After viewing this presentation the participant will be able to discuss:
- Sex related differences in the risk of CHF in diabetes
- Diabetes-related changes in cardiac structure and function
- Recommendations for the use of TZDs in patients with diabetes mellitus and CHD
Bibliographic references :
1. D. Levy, M. G. Larson, R. S. Vasan, W. B. Kannel and K. K. Ho
The progression from hypertension to congestive heart failureJAMA. 1996;275(20):1557.
2. Richard B. Devereux, MD; Mary J. Roman, MD; Mary Paranicas, BA; Michael J. O’Grady, BA; Elisa T. Lee, PhD; Thomas K. Welty, MD, MPH; Richard R. Fabsitz, MA; David Robbins, MD; Everett R. Rhoades, MD; Barbara V. Howard, PhD Impact of Diabetes on Cardiac Structure and Function: The Strong Heart Study Circulation. 2000;101:2271.
3. Martin K. Rutter, MB, ChB; Helen Parise, ScD; Emelia J. Benjamin, MD, ScM; Daniel Levy, MD; Martin G. Larson, ScD; James B. Meigs, MD, MPH; Richard W. Nesto, MD; Peter W.F. Wilson, MD; Ramachandran S. Vasan, MD Impact of Glucose Intolerance and Insulin Resistance on Cardiac Structure and Function: Sex-Related Differences in the Framingham Heart Study Circulation. 2003;107:448.
4. Ischa Stranders, MD; Michaela Diamant, MD, PhD; Rogier E. van Gelder, MD; Hugo J. Spruijt, MSEE; Jos W. R. Twisk, PhD; Robert J. Heine, MD, PhD, FRCP; Frans C. Visser, MD, PhD.Admission Blood Glucose Level as Risk Indicator of Death After Myocardial Infarction in Patients With and Without Diabetes Mellitus Arch Intern Med. 2004;164:982-988.
5. Michael N. Sack MD, PhD and Derek M. Yellon PhD, DSc, Hon FRCP, FACC.Insulin therapy as an adjunct toreperfusion after acute coronary ischemia: A proposed direct myocardial cell survival effect independent of metabolic modulation Journal of the American College of Cardiology. Volume 41, Issue 8 , 16 April 2003, Pages 1404-1407.
6. Dandona P, Aljada A, Mohanty P. "The anti-inflammatory and potential anti-atherogenic effect of insulin: a new paradigm." Diabetologia. 2002 Jun;45(6):924-30.
7. Tetsuya Shiomi, MD; Hiroyuki Tsutsui, MD; Shunji Hayashidani, MD; Nobuhiro Suematsu, MD; Masaki Ikeuchi, MD; Jing Wen, MD; Minako Ishibashi, MD; Toru Kubota, MD; Kensuke Egashira, MD; Akira Takeshita, MD Pioglitazone, a Peroxisome Proliferator–Activated Receptor-(gamma) Agonist, Attenuates Left Ventricular Remodeling and Failure After Experimental Myocardial Infarction Circulation. 2002;106:3126.
8. Tian-li Yue, PhD; Jun Chen, MS; Weike Bao, MD; Padma K. Narayanan, PhD; Antoine Bril, PhD; Wen Jiang, MD; Paul G. Lysko, PhD; Juan-Li Gu, MD; Rogely Boyce, PhD; Dawn M. Zimmerman, MS; Timothy K. Hart, PhD; Robin E. Buckingham, PhD; Eliot H. Ohlstein, PhD In Vivo Myocardial Protection From Ischemia/Reperfusion Injury by the Peroxisome Proliferator–Activated Receptor-(gamma) Agonist Rosiglitazone Circulation. 2001;104:2588.
9. Thomas J. Wang, MD; Jane C. Evans, DSc; Emelia J. Benjamin, MD, ScM; Daniel Levy, MD; Elizabeth C. LeRoy, BS; Ramachandran S. Vasan, MD Natural History of Asymptomatic Left Ventricular Systolic Dysfunction in the Community Circulation. 2003;108:977.
10. Richard W. Nesto, MD; David Bell, MD; Robert O. Bonow, MD; Vivian Fonseca, MD; Scott M. Grundy, MD, PhD; Edward S. Horton, MD; Martin Le Winter, MD; Daniel Porte, MD; Clay F. Semenkovich, MD; Sidney Smith, MD; Lawrence H. Young, MD; Richard Kahn, PhD Thiazolidinedione Use, Fluid Retention, and Congestive Heart Failure: A Consensus Statement From the American Heart Association and American Diabetes Association Circulation. 2003;108:2941.
11. Richard W. Nesto, MD, David Bell, MD, Robert O. Bonow, MD, Vivian Fonseca, MD, Scott M. Grundy, MD, PHD, Edward S. Horton, MD, Martin Le Winter, MD, Daniel Porte, MD, Clay F. Semenkovich, MD, Sidney Smith, MD, Lawrence H. Young, MD and Richard Kahn, PHD Thiazolidinedione Use, Fluid Retention, and Congestive Heart Failure: A consensus statement from the American Heart Association and American Diabetes Association Diabetes Care 27:256-263, 2004.
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"Impaired Microvascular Recruitment and Muscle Insulin Resistance"Dr. Michael G. Clark (biography)
English - 2004-05-15 - 53 minutes
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Summary :
Apart from increasing glucose uptake into muscle, in vivo insulin induces nitric oxide-dependent recruitment of muscle capillaries. In this presentation Dr. Clark speaks about insulin-mediated capillary recruitment, how it is affected by insulin resistant states, and how it affects glucose uptake in muscle.
Copyright © 2004 E-medHosting.com Inc.
Learning objectives :
The participant will learn about:
- Rate-limiting steps in muscle glucose uptake in vivo
- Status of capillary flow in muscle at rest
- Measurement of capillary recruitment
- Effects of insulin and exercise on capillary recruitment
- Insulin resistance
Bibliographic references :
Poulin RA, Steil GM, Moore DM, Ader M, Bergman RN. Dynamics of glucose production and uptake are more closely related to insulin in hindlimb lymph than in thoracic duct lymph. PMID: 8288041 [PubMed - indexed for MEDLINE]
Sjostrand M, Gudbjornsdottir S, Holmang A, Lonn L, Strindberg L, Lonnroth P. Delayed transcapillary transport of insulin to muscle interstitial fluid in obese subjects. Diabetes. 2002 Sep;51(9):2742-8.
Halseth AE, Bracy DP, Wasserman DH. Limitations to basal and insulin-stimulated skeletal muscle glucose uptake in the high-fat-fed rat. Am J Physiol Endocrinol Metab. 2000 Nov;279(5):E1064-71.
Rattigan S, Clark MG, Barrett EJ. Hemodynamic actions of insulin in rat skeletal muscle: evidence for capillary recruitment. PMID: 9287035 [PubMed - indexed for MEDLINE]
Vincent MA, Clerk LH, Lindner JR, Klibanov AL, Clark MG, Rattigan S, Barrett EJ. Microvascular recruitment is an early insulin effect that regulates skeletal muscle glucose uptake in vivo. Diabetes. 2004 Jun;53(6):1418-23.
Zhang N, Richter A, Suriawinata J, Harbaran S, Altomonte J, Cong L, Zhang H, Song K, Meseck M, Bromberg J, Dong H. Elevated vascular endothelial growth factor production in islets improves islet graft vascularization. Diabetes. 2004 Apr;53(4):963-70.
Vincent MA, Barrett EJ, Lindner JR, Clark MG, Rattigan S. Inhibiting NOS blocks microvascular recruitment and blunts muscle glucose uptake in response to insulin. Am J Physiol Endocrinol Metab. 2003 Jul;285(1):E123-9.
Youd JM, Rattigan S, Clark MG. Acute impairment of insulin-mediated capillary recruitment and glucose uptake in rat skeletal muscle in vivo by TNF-alpha. Diabetes. 2000 Nov;49(11):1904-9.
S Rattigan, MG Clark, and EJ Barrett Acute vasoconstriction-induced insulin resistance in rat muscle in vivo Diabetes 48: 564-569.
Lucy H. Clerk, Stephen Rattigan, and Michael G. Clark Lipid Infusion Impairs Physiologic Insulin-Mediated Capillary Recruitment and Muscle Glucose Uptake In Vivo Diabetes 51: 1138-1145.
Michelle G. Wallis, Catherine M. Wheatley, Stephen Rattigan, Eugene J. Barrett, Andrew D.H. Clark, and Michael G. Clark Insulin-Mediated Hemodynamic Changes Are Impaired in Muscle of Zucker Obese Rats Diabetes 2002 51: 3492-3498.
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"Ectopic fat and oxidative stress: common denominators in the 'Metabolic Syndrome' and its vascular sequelae"Dr. Robin Buckingham (biography)
English - 2004-05-14 - 55 minutes
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Summary :
In this presentation Dr. Buckingham describes how ectopic fat storage and oxidative stress are implicated in the metabolic syndrome and type 2 diabetes. Excess fat is unstable and pervasive, according to Dr. Buckingham. This fat may radiate out from established storage sites such as visceral depots and into skeletal muscle, liver and the heart. The effects of ectopic deposition of triglycerides...
Learning objectives :
The participant will learn about:
- Oxidative enzyme activity and lipid concentrations in skeletal muscle in obesity and type 2 diabetes
- Effects of fatty liver in type 2 diabetes
- Importance of fat cell size in the development of type 2 diabetes
- Fat as a source of inflammation
- Epicardial fat: association with metabolic syndrome parameters
- Mechanism underlying endothelial dysfunction in type 2 diabetes
Bibliographic references :
Joseph L. Evans, Ira D. Goldfine, Betty A. Maddux and Gerold M. Grodsky. Oxidative Stress and Stress-Activated Signaling Pathways: A Unifying Hypothesis of Type 2 Diabetes Endocrine Reviews 2002; 23(5): 599-622.
Tomasz J. Guzik, MD PhD; Shafi Mussa, MA MRCS; Daniela Gastaldi, MD; Jerzy Sadowski, MD PhD; Chandi Ratnatunga, FRCS; Ravi Pillai, FRCS; Keith M. Channon, MD MRCP. Mechanisms of Increased Vascular Superoxide Production in Human Diabetes Mellitus Circulation 2002;105:1656.
David E. Kelley, Therese M. McKolanis, Refaat A. F. Hegazi, Lewis H. Kuller, and Satish C. Kalhan. Fatty liver in type 2 diabetes mellitus: relation to regional adiposity, fatty acids, and insulin resistance Am J Physiol Endocrinol Metab 2003; 285: E906-E916.
Tomasz Mazurek, MD*; LiFeng Zhang, PhD*; Andrew Zalewski, MD; John D. Mannion, MD; James T. Diehl, MD; Hwyda Arafat, MD, PhD; Lea Sarov-Blat, PhD; Shawn O’Brien, PhD; Elizabeth A. Keiper, BS; Anthony G. Johnson, MD; Jack Martin, MD; Barry J. Goldstein, MD, PhD; Yi Shi, MD, PhD. Human Epicardial Adipose Tissue Is a Source of Inflammatory Mediators Circulation 2003;108:2460.
James B. Meigs, MD, MPH; Frank B. Hu, MD, PhD; Nader Rifai, PhD; JoAnn E. Manson, MD, DrPH. Biomarkers of Endothelial Dysfunction and Risk of Type 2 Diabetes Mellitus JAMA. 2004;291:1978-1986.
Paolisso G, Tataranni PA, Foley JE, Bogardus C, Howard BV, Ravussin E. A high concentration of fasting plasma non-esterified fatty acids is a risk factor for the development of NIDDM. Diabetologia. 1995 Oct;38(10):1213-7.
Paul M Ridker, MD; Julie E. Buring, ScD; Nancy R. Cook, ScD; Nader Rifai, PhD. C-Reactive Protein, the Metabolic Syndrome, and Risk of Incident Cardiovascular Events An 8-Year Follow-Up of 14 719 Initially Healthy American Women Circulation 2003;107:391.
Hideki Urakawa, Akira Katsuki, Yasuhiro Sumida, Esteban C. Gabazza, Shuichi Murashima, Kohei Morioka, Noriko Maruyama, Nagako Kitagawa, Takashi Tanaka, Yasuko Hori, Kaname Nakatani, Yutaka Yano and Yukihiko Adachi. Oxidative Stress Is Associated with Adiposity and Insulin Resistance in Men The Journal of Clinical Endocrinology & Metabolism 2003; Vol. 88, No. 10 4673-4676.
Ram Weiss et al. Prediabetes in obese youth: a syndrome of impaired glucose tolerance, severe insulin resistance, and altered myocellular and abdominal fat partitioning Lancet 2003; 362(9388):951-957
C. Weyer, J. E. Foley, C. Bogardus, P.A. Tataranni, R.E. Pratley. Enlarged subcutaneous abdominal adipocyte size, but not obesity itself, predicts Type II diabetes independent of insulin resistance Diabetologia 2000; 43(12):1498-1506.
Haiyan Xu, Glenn T. Barnes, Qing Yang, Guo Tan, Daseng Yang, Chieh J. Chou, Jason Sole, Andrew Nichols, Jeffrey S. Ross, Louis A. Tartaglia and Hong Chen. Chronic inflammation in fat plays a crucial role in the development of obesity-related insulin resistance J. Clin. Invest. 112:1821-1830 (2003).
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"Insulin Sensitivity in the Adiponectin Transgenic Mouse"Dr. Terry Combs (biography)
English - 2004-05-14 - 22 minutes
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Summary :
Adiponectin is expressed in adipose tissue, and plasma levels are positively and negatively correlated with insulin sensitivity and BMI, respectively. In this presentation Dr. Combs provides additional information gleaned fom mouse studies on the mechanism of action of this hormone.
Clinical trials have demonstrated that adiponectin is upregulated in tandem with improvement of...
Learning objectives :
After viewing the presentation the participant will be able to describe the effects of adiponectin on:
- insulin inhibition of endogenous glucose production
- enzymes in the gluconeogenic pathway: AMP-kinase activity, G6Pase and PEPCK expression
Bibliographic references :
Terry P. Combs, Utpal B. Pajvani, Anders H. Berg, Ying Lin, Linda A. Jelicks, Mathieu Laplante, Andrea R. Nawrocki, Michael W. Rajala, Albert. F. Parlow, Laurelle Cheeseboro, Yang-Yang Ding, Robert G. Russell, Dirk Lindemann, Adam Hartley, Glynn R. C. Baker, Silvana Obici, Yves Deshaies, Marian Ludgate, Luciano Rossetti and Philipp E. Scherer A Transgenic Mouse with a Deletion in the Collagenous Domain of Adiponectin Displays Elevated Circulating Adiponectin and Improved Insulin Sensitivity Endocrinology 2004; 145(1):367-383
Terry P. Combs, John A. Wagner, Joel Berger, Tom Doebber, Wen-Jun Wang, Bei B. Zhang, Michael Tanen, Anders H Berg, Stephen O’Rahilly, David B. Savage, Krishna Chatterjee, Stuart Weiss, Patrick J. Larson, Keith M. Gottesdiener, Barry J. Gertz, Maureen J. Charron, Philipp E. Scherer and David E. Moller. Induction of Adipocyte Complement-Related Protein of 30 Kilodaltons by PPAR Agonists: A Potential Mechanism of Insulin Sensitization Endocrinology 2004; 143(3):998-1007
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"A PPAR gamma Mutation and the Lipodystrophic Phenotype - A window into the Metabolic Syndrome ?"Dr. Thomas Ransom (biography)
English - 2004-05-14 - 22 minutes
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Summary :
The metabolic syndrome is increasingly being recognized as a threat to the health of Canadian society. Dr. Thomas Ransom discusses in this talk the extreme forms of the metabolic syndrome – the lipodystrophy syndromes.
Features common to all lipodystrophy syndromes are presented and the differences between the syndromes are examined. Dr. Ransom makes the case for studying...
Learning objectives :
After viewing this presentation, participants will be able to discuss:
• The NCEP and WHO definitions of the metabolic syndrome.
• The value of studying monogenetic forms of lipodystrophy.
• The different lipodystrophy syndromes.
• The molecular basis for the development of lipodystrophy syndromes.
Bibliographic references :
Hegele RA, Cao H, Frankowski C, Mathews ST, Leff T. PPARG F388L, a transactivation-deficient mutant, in familial partial lipodystrophy. Diabetes. 2002 Dec;51(12):3586-90.
Garg A. Acquired and inherited lipodystrophies. N Engl J Med. 2004 Mar 18;350(12):1220-34.
Savage DB, Tan GD, Acerini CL, Jebb SA, Agostini M, Gurnell M, Williams RL, Umpleby AM, Thomas EL, Bell JD, Dixon AK, Dunne F, Boiani R, Cinti S, Vidal-Puig A, Karpe F, Chatterjee VK, O'Rahilly S. Human metabolic syndrome resulting from dominant-negative mutations in the nuclear receptor peroxisome proliferator-activated receptor-gamma. Diabetes. 2003 Apr;52(4):910-7.
Agarwal AK, Garg A. A novel heterozygous mutation in peroxisome proliferator-activated receptor-gamma gene in a patient with familial partial lipodystrophy. J Clin Endocrinol Metab. 2002 Jan;87(1):408-11.
Gurnell M. PPARgamma and metabolism: insights from the study of human genetic variants. Clin Endocrinol (Oxf). 2003 Sep;59(3):267-77.
Other References of Interest
Hegele RA. Monogenic forms of insulin resistance: apertures that expose the common metabolic syndrome. Trends Endocrinol Metab. 2003 Oct;14(8):371-7.
Hegele RA. Phenomics, lipodystrophy, and the metabolic syndrome. Trends Cardiovasc Med. 2004 May;14(4):133-7.
Hegele RA, Leff T. Unbuckling lipodystrophy from insulin resistance and hypertension. J Clin Invest. 2004 Jul;114(2):163-5.
Agarwal AK, Garg A. Congenital generalized lipodystrophy: significance of triglyceride biosynthetic pathways. Trends Endocrinol Metab. 2003 Jul;14(5):214-21.
Agarwal AK, Simha V, Oral EA, Moran SA, Gorden P, O'Rahilly S, Zaidi Z, Gurakan F, Arslanian SA, Klar A, Ricker A, White NH, Bindl L, Herbst K, Kennel K, Patel SB, Al-Gazali L, Garg A. Phenotypic and genetic heterogeneity in congenital generalized lipodystrophy. J Clin Endocrinol Metab. 2003 Oct;88(10):4840-7.
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"New Insights in Diabetic Retinopathy"Dr. Filiberto Altomare (biography)
English - 2003-10-31 - 40 minutes
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Summary :
The underlying pathogenesis of diabetic retinopathy has long been thought of as being primarily vascular in nature, but there is growing evidence that there are not only vascular but neuronal changes (1, 2) involved.
A better understanding of the molecular biology of the ocular angiogenesis pathway has led to the development of new therapeutic targets. For example, inhibition of ...
Learning objectives :
The participant will get a new understanding of the pathogenesis of diabetic retinopathy and learn about advances in its treatment.
Conclusion:
- Diabetic retinopathy is a disease that includes neurodegenerative as well as vascular pathologies. Therefore, vision loss can be attributed to neuronal dysfunction and vascular abnormalities.
- Great acheivements in the understanding of the molecular biology of angiogenesis have occurred. This has permitted the identification of novel targets in the management of diabetic retinopathy.
- A number of clinical trials are underway, the outcome of which will initiate a new era whereby diabetic retinopathy is managed pharmacologically, rather than with laser photocoagulation.
Bibliographic references :
1. Scott TM, Foote J, Peat B, Galway G. “Vascular and neural changes in the rat optic nerve following induction of diabetes with streptozotocin.” J Anat. 1986 Feb;144:145-52.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2961719&dopt=Abstract
2. Barber AJ, Lieth E, Khin SA, Antonetti DA, Buchanan AG, Gardner TW. “Neural apoptosis in the retina during experimental and human diabetes. Early onset and effect of insulin.” J Clin Invest. 1998 Aug 15;102(4):783-91.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9710447&dopt=Abstract
3. Ozaki H, Seo MS, Ozaki K, Yamada H, Yamada E, Okamoto N, Hofmann F, Wood JM, Campochiaro PA. “Blockade of vascular endothelial cell growth factor receptor signaling is sufficient to completely prevent retinal neovascularization.” Am J Pathol. 2000 Feb;156(2):697-707.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10666398&dopt=Abstract
4. Gilbert RE, Kelly DJ, Cox AJ, Wilkinson-Berka JL, Rumble JR, Osicka T, Panagiotopoulos S, Lee V, Hendrich EC, Jerums G, Cooper ME. “Angiotensin converting enzyme inhibition reduces retinal overexpression of vascular endothelial growth factor and hyperpermeability in experimental diabetes.” Diabetologia. 2000 Nov;43(11):1360-7.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11126403&dopt=Abstract
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"The Wheres and Whats of Body Fat Distribution"Prof. Steven Kahn (biography)
English - 2003-07-14 - 37 minutes
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Summary :
We have been focusing a lot lately on the roles of adipocytokines, although the distribution of body fat also plays an important part in insulin resistance. We now know that there are lean as well as obese insulin resistant patients, and about 47% of the variance in insulin sensitivity among healthy (non-diabetic) subjects can be explained by intra-abdominal fat area (Cnop M et al. Diabetes 51:...
Learning objectives :
The participant will learn about the importance of body fat distribution in insulin resistance, and receive new information about the adipokines leptin and adiponectin in relation to body fat distribution:
- There are lean as well as obese insulin resistant patients, and about 47% of the variance in insulin sensitivity among healthy (non-diabetic) subjects can be explained by intra-abdominal fat area (Cnop M et al. Diabetes 51: 1005-15; 2002).
- Central adiposity contributes to an atherogenic lipid profile (Nieves DJ et al. Diabetes 52: 172-79; 2003).
- Leptin levels increase with increasing subcutaneous fat and this phenomenon is more pronounced in women (Cnop M et al. Diabetes 51: 1005-15; 2002).
- Adiponectin levels, which are associated with insulin sensitivity, decrease with increasing intra-abdominal fat, increase with age and are higher in women than in men; also adiponectin and leptin levels are not related (Cnop M et al. Diabetologia. 46: 459-69; 2003).
- Adiponectin levels are inversely related to triglyceride levels, and tightly correlated with HDL cholesterol levels (Cnop M et al. Diabetologia. 46: 459-69; 2003).
Bibliographic references :
Cnop M, Havel PJ, Utzschneider KM, Carr DB, Sinha MK, Boyko EJ, Retzlaff BM, Knopp RH, Brunzell JD, Kahn SE. Relationship of adiponectin to body fat distribution, insulin sensitivity and plasma lipoproteins: evidence for independent roles of age and sex. Diabetologia. 2003 Apr;46(4):459-69.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi
Nieves DJ, Cnop M, Retzlaff B, Walden CE, Brunzell JD, Knopp RH, Kahn SE. The atherogenic lipoprotein profile associated with obesity and insulin resistance is largely attributable to intra-abdominal fat. Diabetes. 2003 Jan;52(1):172-9.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi
Cnop M, Landchild MJ, Vidal J, Havel PJ, Knowles NG, Carr DR, Wang F, Hull RL, Boyko EJ, Retzlaff BM, Walden CE, Knopp RH, Kahn SE. The concurrent accumulation of intra-abdominal and subcutaneous fat explains the association between insulin resistance and plasma leptin concentrations : distinct metabolic effects of two fat compartments. Diabetes. 2002 Apr;51(4):1005-15.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi
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"Nuclear Receptor Diseases Mechanisms"Dr. Mitchell Lazar (biography)
English - 2002-10-28 - 47 minutes
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Summary :
Nuclear receptors are important mediators of disease in general. In this talk Dr Lazar focuses on two mechanistic aspects, showing how these receptors may be targeted for disease. Nuclear hormone receptors are transcription factors that are found in the nucleus of cells, and bind to ligands. Classical members of the nuclear receptor family are thyroid hormone, the steroid hormones, and vitamins A...
Learning objectives :
Nuclear recptors are ligand-activated transcription factors, and their mechanisms of action can be understood to develop ways to treat some diseases, for example type 2 diabetes.
The drugs called thiazolidinediones (TZDs) act as ligands to the PPARγ nuclear recptors, thereby downregulating the insulin resistance molecule resistin, and upregulating adiponectin which increases insulin action. These produce clinically antidiabetic effects, thus making TZDs a treatment option for type 2 diabetes.
TZDs also promote fat uptake and storage, and have recently been found to affect the enzyme glycerol kinase in this process.
Bibliographic references :
Thiazolidinedione activation of peroxisome proliferator-activated receptor gamma can enhance mitochondrial potential and promote cell survival.
Wang YL, Frauwirth KA, Rangwala SM, Lazar MA, Thompson CB.
Abramson Family Cancer Research Institute, Department of Cancer Biology, University of Pennsylvania, Philadelphia, Pennsylvania 19104-6160, USA.
Thiazolidinediones (TZDs) are widely used for treatment of type 2 diabetes mellitus. Peroxisome proliferator-activated receptor gamma (PPAR gamma) is the molecular target of TZDs and is believed to mediate the apoptotic effects of this class of drugs in a variety of cell types, including B and T lymphocytes. The finding that TZDs induce lymphocyte death has raised concerns regarding whether TZDs might further impair immune functions in diabetics. To address this issue, we investigated the roles of PPAR gamma and TZDs in lymphocyte survival. PPAR gamma was up-regulated upon T cell activation. As previously reported, PPAR gamma agonists induced T cell death in a dose-dependent manner. However, the concentrations of TZD needed to cause T cell death were above those needed to induce PPAR gamma-dependent transcription. Surprisingly, at concentrations that induce optimal transcriptional activation, TZD activation of PPAR gamma protected cells from apoptosis following growth factor withdrawal. The survival-enhancing effects depended on both the presence and activation of PPAR gamma. Measurements of mitochondrial potential revealed that PPAR gamma activation enhanced the ability of cells to maintain their mitochondrial potential. These data indicate that activation of PPAR gamma with TZDs can promote cell survival and suggest that PPAR gamma activation may potentially augment the immune responses of diabetic patients.
J Biol Chem 2002 Aug 30;277(35):31781-8
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"Beta Cell Failure in type 2 Diabetes: A Paradigm Revisited"Dr. Minna Woo (biography)
English - 2002-01-19 - 20 minutes
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Summary :
Pathology of type 2 diabetes is a combination of insulin resistance and defective beta-cells. Overview of the impact of b cells in this pathology and a conclusion that demonstrates that a change in the cellular function and mass of beta-cells are both involved in the development of type 2 diabetes.
Learning objectives :
Upon completion of this presentation, participants should be able to understand the:
1.Importance of b cell failure in the development and progression of Type 2 DM.
2.Potential causes of b cell failure.
3.Mechanisms of b cell failure.
Bibliographic references :
Executionary pathway for apoptosis: lessons from mutant mice.
Woo M, Hakem R, Mak TW.
Amgen Institute and Ontario Cancer Institute, Department of Immunology, University of Toronto, Canada. mwoo@oci.utoronto.ca
Apoptosis or programmed cell death (PCD) is an evolutionarily conserved cellular process that is essential for normal development and homeostasis of multicellular organisms. Defects in the apoptosis signaling result in many diseases including autoimmune diseases and cancer. The apoptosis signaling pathway was first described genetically in the nematode Caenorhabditis elegans which serves as a framework for the more complex apoptotic pathways that exist in mammals. In this review, we will discuss the apoptotic pathways that are emerging in mammals as elucidated by studies of gene-targeted mutant mice.
Cell Res 2000 Dec;10(4):267-78
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