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 Presentation

"Cellular mechanisms of insulin resistance: Implications for type 2 diabetes and obesity"

Dr. Gerald Shulman (biography)
English - 2002-04-26 - 55 minutes
(53 slides)

Summary :
Insulin resistance is a major factor in the pathogenesis of type 2 diabetes ,and recent studies have demonstrated a strong relationship between increased plasma fatty acid concentrations and many insulin-resistant states, including obesity and type 2 diabetes mellitus. In a cross-sectional study of young normal-weight offspring of type 2 diabetic patients, we found an inverse relationship between fasting plasma fatty acid concentrations and insulin sensitivity, consistent with the hypothesis that altered fatty acid metabolism may play a contributing role in causing the insulin resistance in patients with type 2 diabetes. Furthermore, recent studies measuring intramuscular triglyceride content by muscle biopsy or intramyocellular triglyceride content by 1H NMR have shown an even stronger relationship between accumulation between intramyocellular triglyceride and insulin resistance. This presentation will focus on recent studies using both 13C and 31P NMR techniques to examine the pathogenesis of insulin resistance in patients with type 2 diabetes mellitus. The specific biochemical questions that will be addressed are: 1) Is the defect in muscle glycogen synthesis observed in patients with type 2 diabetes due to a block in glucose transport, hexokinase or glycogen synthase activity? 2) Is this defect primary or secondary in nature? 3) What is the mechanism of free fatty acid-induced insulin resistance? These questions will be explored in both human and novel transgenic mouse models.

Learning objectives :
This presentation focuses on recent studies using both 13C and 31P NMR techniques to examine the pathogenesis of insulin resistance in patients with type 2 diabetes mellitus. The specific biochemical questions addressed are:
1) Is the defect in muscle glycogen synthesis observed in patients with type 2 diabetes due to a block in glucose transport, hexokinase or glycogen synthase activity?
2) Is this defect primary or secondary in nature?
3) What is the mechanism of free fatty acid-induced insulin resistance?
These questions are explored in both human and novel transgenic mouse models.


Bibliographic references :
Effect of Weight Loss on Insulin Sensitivity and Intramuscular Long-Chain Fatty Acyl-CoAs in Morbidly Obese Subjects.

Houmard JA, Tanner CJ, Yu C, Cunningham PG, Pories WJ, MacDonald KG, Shulman GI.

Departments of Exercise and Sport Science, Surgery, and the Human Performance Laboratory and Diabetes/Obesity Center, East Carolina University, Greenville, North Carolina. Howard Hughes Medical Institute and the Departments of Internal Medicine and Cellular and Molecular Physiology, Yale University School of Medicine, New Haven, Connecticut.

Increases in intramyocellular long-chain fatty acyl-CoAs (LCACoA) have been implicated in the pathogenesis of insulin resistance in skeletal muscle. To test this hypothesis, we measured muscle (vastus lateralis) LCACoA content and insulin action in morbidly obese patients (n = 11) before and after weight loss (gastric bypass surgery). The intervention produced significant weight loss (142.3 +/- 6.8 vs. 79.6 +/- 4.1 kg for before versus after surgery, respectively). Fasting insulin decreased by approximately 84% (23.3 +/- 3.8 vs. 3.8 +/- 0.5 mU/ml), and insulin sensitivity, as determined by minimal model, increased by approximately 360% (1.2 +/- 0.3 vs. 4.1 +/- 0.5 min(-1). [ micro U/kg(-1)]) indicating enhanced insulin action. Muscle palmityl CoA (16:0; 0.54 +/- 0.08 vs. 0.35 +/- 0.04 nmol/g wet wt) concentration decreased by approximately 35% (P < 0.05) with weight loss, whereas stearate CoA (18:0; -17%; 0.65 +/- 0.05 vs. 0.54 +/- 0.03 nmol/g wet wt) and linoleate CoA (18:2; -30%; 2.47 +/- 0.27 vs. 1.66 +/- 0.19 nmol/g wet wt) were also reduced (P < 0.05). There were no statistically significant declines in muscle palmitoleate CoA (16:1), oleate CoA (18:1), or total LCACoA content. These data suggest that a reduction in intramuscular LCACoA content may be responsible, at least in part, for the enhanced insulin action observed with weight loss in obese individuals.

Diabetes 2002 Oct;51(10):2959-2963


   


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