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- March 10, 2010 |
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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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"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 binding of the nuclear receptor PPARγ which is highly expressed in adipose tissue, results in the activation of distinct pathways leading to insulin sensitisation and anti-inflammatory effects.
PPARγ is expressed in different cell types in adipose tissue depots, such as pre-adipocytes, small insulin-responsive adipocytes and large insulin-resistant adipocytes, and the function of the receptor in these cells is dependent on the cell type. Prolonged thiazolidinedione activation of PPARγ in adipose tissue depots leads to an increase in the number of small insulin-responsive adipocytes (1).
Insulin resistant adipocytes secrete multiple signaling molecules involved in insulin resistance as well as inflammation including free fatty acids, and adiponectin - low levels of which are associated with insulin resistance. Thiazolidinedione activation of PPARγ results in a suppression of free fatty acid release and stimulation of adiponectin release from adipose tissue depots. The reduced availability of circulating free fatty acids to skeletal muscle and liver is of particular importance in the drug's mechanism to improve insulin sensitivity in these tissues (1).
Copyright © 2006 E-MedHosting.com Inc.
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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