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- December 1, 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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"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 secretory demand. In individuals who are at increased risk of developing type 2 diabetes, this adaptive response is inadequate and results in deteriorating glucose tolerance. In fact, even within the normal range of fasting glucose, beta-cell function declines as plasma glucose increases. There has been a resurgence of interest in changes in beta-cell morphology in type 2 diabetes. It is clear that the number of beta-cells is decreased in the disease, and this is in part due to the deposition of islet amyloid. In addition to reductions in beta-cell mass, functional changes in secretory function also occur independently. For example, in humans acute elevations in free fatty acids are associated with decreased beta-cell function.Thus, the reduced insulin release observed in type 2 diabetes and in high-risk states is clearly multifactorial, and is related to both genetics and environmental changes. With a better understanding of the critical role of the beta-cell in the pathogenesis of type 2 diabetes comes the opportunity for the development of more directed and successful approaches to treating and possibly preventing the disease.
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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