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Donath, M Y; Ehses, J A; Maedler, K; Schumann, D M; Ellingsgaard, H; Eppler, E; Reinecke, M (2005). Mechanisms of beta-cell death in type 2 diabetes. Diabetes, 54(Suppl 2):S108-S113.

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Abstract

A decrease in the number of functional insulin-producing beta-cells contributes to the pathophysiology of type 2 diabetes. Opinions diverge regarding the relative contribution of a decrease in beta-cell mass versus an intrinsic defect in the secretory machinery. Here we review the evidence that glucose, dyslipidemia, cytokines, leptin, autoimmunity, and some sulfonylureas may contribute to the maladaptation of beta-cells. With respect to these causal factors, we focus on Fas, the ATP-sensitive K+ channel, insulin receptor substrate 2, oxidative stress, nuclear factor-kappaB, endoplasmic reticulum stress, and mitochondrial dysfunction as their respective mechanisms of action. Interestingly, most of these factors are involved in inflammatory processes in addition to playing a role in both the regulation of beta-cell secretory function and cell turnover. Thus, the mechanisms regulating beta-cell proliferation, apoptosis, and function are inseparable processes.

Item Type:Journal Article, refereed, further contribution
Communities & Collections:04 Faculty of Medicine > Institute of Anatomy
DDC:570 Life sciences; biology
610 Medicine & health
Language:English
Date:December 2005
Deposited On:23 Mar 2010 10:24
Last Modified:28 Nov 2013 02:22
Publisher:American Diabetes Association
ISSN:0012-1797
Free access at:PubMed ID. An embargo period may apply.
Publisher DOI:10.2337/diabetes.54.suppl_2.S108
PubMed ID:16306327
Citations:Web of Science®. Times Cited: 145
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