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- May 17, 2008 |
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"Thiazolidinediones to Preserve B-Cell Function and Prevent Type 2 Diabetes"Prof. Thomas A. Buchanan (biography)
English - 2003-08-28 - 39 minutes
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Summary :
Recorded during the 18th IDF Meeting, Paris: Type 2 diabetes is not just a disease of hyperglycemia but indeed one of progressive beta cell failure. This beta cell failure begins long before the diagnosis of diabetes, and this presentation will deal with how to intervene in such a way to preserve beta cell function and preclude the development of diabetes.
Fat accumulation in the body leads to varying degrees of insulin resistance depending on how the adipose tissue talks to liver and muscle, either by fatty acids blocking insulin signaling directly, or by adipokine signaling. Insulin resistance then leads to either chronic hyperinsulinemia without beta cell failure, or beta cell failure with hyperglycemia depending on how robust the beta cells are.
The TRIPOD (Troglitazone in the Prevention of Diabetes) Study showed that protection from diabetes required increased insulin sensitivity and was greatest in women who had the largest reduction in insulin requirements (“ß-cell rest”). Also, intervening at the stage of OGGT diabetes rather than before was associated with an irreversible loss of beta cell function: women while developing diabetes on placebo lost about 35% of their beta cell function, which was stabilized but not restored with troglitazone treatment commencing upon diagnosis of diabetes.
The PIPOD (Pioglitazone in the Prevention of Diabetes) Study is ongoing with women who finished the TRIPOD Study. The first year’s data from this study show a similar protective effect against diabetes as was seen in TRIPOD. As well, treatment of insulin resistance with TZDs may have different effects depending on the stage of diabetes evolution at which the treatment is given: early intervention in patients without diabetes resulted in lowered insulin levels whereas later intervention resulted in lowered insulin and glucose levels, suggesting a loss of beta cell autoregulation with disease progression.
In terms of clinical strategy it is therefore recommended to identify high-risk patients with IFG (impaired fasting glucose) or IGT (impaired glucose tolerance) and treat them with diet and exercise to stabilize rising blood sugars. Should that approach fail, pharmacological intervention should be considered with the aim of unloading beta cells and achieving an HbA1c of 5-6%.
Learning objectives :
The participant will review the results of the TRIPOD (Troglitazone in the Prevention of Diabetes) Study and learn about first year’s results of the PIPOD (Pioglitazone in the Prevention of Diabetes) Study being conducted with women who finished from TRIPOD:
TRIPOD Summary:
•Troglitazone reduced the incidence of diabetes by 55% in high-risk Hispanic women.
•Protection from diabetes:
orequired an increase in insulin sensitivity
owas greatest in women who had the largest reduction in insulin requirements (“ß-cell rest”)
•Women who were protected during the trial:
oremained protected 8 months later
ohad stable ß-cell function over a 54-month period
PIPOD Year 1 Summary:
•The low incidence of diabetes and the beta cell rest observed at 1 year in women who entered PIPOD without diabetes suggests a protective effect similar to TRIPOD
•Treatment of insulin resistance with TZDs may have different effects at different stages in the evolution of diabetes:
oEarly intervention in patients without diabetes resulted in lowered insulin levels with a minimal effect on glucose
oLater intervention resulted in lowered glucose and insulin concentrations
This suggests a loss of beta cell autoregulation with disease progression.
Bibliographic references :
Bergman RN, Phillips LS, Cobelli C. Physiologic evaluation of factors controlling glucose tolerance in man: measurement of insulin sensitivity and beta-cell glucose sensitivity from the response to intravenous glucose. J Clin Invest. 1981 Dec;68(6):1456-67.
Weyer C, Bogardus C, Mott DM, Pratley RE. The natural history of insulin secretory dysfunction and insulin resistance in the pathogenesis of type 2 diabetes mellitus. J Clin Invest. 1999 Sep;104(6):787-94.
Homko C, Sivan E, Chen X, Reece EA, Boden G. Insulin secretion during and after pregnancy in patients with gestational diabetes mellitus. J Clin Endocrinol Metab. 2001 Feb;86(2):568-73.
Buchanan TA, Xiang AH, Peters RK, Kjos SL, Marroquin A, Goico J, Ochoa C, Tan S, Berkowitz K, Hodis HN, Azen SP. Preservation of pancreatic beta-cell function and prevention of type 2 diabetes by pharmacological treatment of insulin resistance in high-risk hispanic women. Diabetes. 2002 Sep;51(9):2796-803.
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