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- May 17, 2008 |
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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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"Based on these mechanisms, are beta-cells a therapeutic target for slowing or possibly preventing disease progression?"Dr. Julio Rosenstock (biography)
English - 2004-06-04 - 17 minutes
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Summary :
The UKPDS showed that conventional monotherapy does not affect the progressive decline in beta cell function. Different factors drive this process, such as hyperglycemia, lipotoxicity (elevated free fatty acids and triglycerides) and protein glycation. Autopsy studies have demonstrated that diabetic patients also have a reduced beta cell volume. This in turn is a result of increased beta cell apoptosis.
Studies suggest that thiazolidinediones may preserve beta cell function, and the ADOPT (A Diabetes Outcome Progression Trial) Study is currently underway to compare rosiglitazone, glyburide and metformin monotherapy. The primary endpoint of the study is time to monotherapy failure, and secondary endpoints include beta cell function, insulin sensitivity and markers of macrovascular disease risk.
Copyright © 2004 E-MedHosting.com Inc.
Learning objectives :
After viewing these slides the participant will be able to discuss:
- Factors driving the progressive decline in beta cell function in type 2 diabetes
- Pharmacologic options which may preserve beta cell function
Bibliographic references :
Thomas A. Buchanan, Anny H. Xiang, Ruth K. Peters, Siri L. Kjos, Aura Marroquin, Jose Goico, Cesar Ochoa, Sylvia Tan, Kathleen Berkowitz, Howard N. Hodis, and Stanley P. Azen. Preservation of Pancreatic ß-Cell Function and Prevention of Type 2 Diabetes by Pharmacological Treatment of Insulin Resistance in High-Risk Hispanic Women
Diabetes 2002;51:2796-2803.
Alexandra E. Butler, Juliette Janson, Susan Bonner-Weir, Robert Ritzel, Robert A. Rizza, and Peter C. Butler. ß-Cell Deficit and Increased ß-Cell Apoptosis in Humans With Type 2 Diabetes Diabetes 2003;52:102-110.
Diane T. Finegood, M. Dawn McArthur, David Kojwang, Marion J. Thomas, Brian G. Topp, Thomas Leonard, and Robin E. Buckingham.ß-Cell Mass Dynamics in Zucker Diabetic Fatty Rats Rosiglitazone Prevents the Rise in Net Cell Death Diabetes 2001;50:1021-1029.
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.
Giancarlo Viberti, MD, Steven E. Kahn, MB, CHB, Douglas A. Greene, MD, William H. Herman, MD, Bernard Zinman, MD, Rury R. Holman, MD, Steven M. Haffner, MD, Daniel Levy, MD, John M. Lachin, SCD, Rhona A. Berry, BSC, Mark A. Heise, PHD, Nigel P. Jones, MA and Martin I. Freed, MD.A Diabetes Outcome Progression Trial (ADOPT)An international multicenter study of the comparative efficacy of rosiglitazone, glyburide, and metformin in recently diagnosed type 2 diabetes Diabetes Care 2002;25:1737-1743.
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