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<blockquote data-quote="kokhongw" data-source="post: 1796260" data-attributes="member: 277199"><p>Other than sulfonylureas, there are many other contributory factors for beta cells death...</p><p><span style="font-size: 22px"><strong>Mechanisms of β-Cell Death in Type 2 Diabetes</strong></span></p><p><a href="http://diabetes.diabetesjournals.org/content/54/suppl_2/S108" target="_blank">http://diabetes.diabetesjournals.org/content/54/suppl_2/S108</a></p><p><span style="font-size: 18px"><strong>Abstract</strong></span></p><p>A decrease in the number of functional insulin-producing β-cells contributes to the pathophysiology of type 2 diabetes. Opinions diverge regarding the relative contribution of a decrease in β-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 β-cells. With respect to these causal factors, we focus on Fas, the ATP-sensitive K+ channel, insulin receptor substrate 2, oxidative stress, nuclear factor-κB, 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 β-cell secretory function and cell turnover. Thus, the mechanisms regulating β-cell proliferation, apoptosis, and function are inseparable processes.</p></blockquote><p></p>
[QUOTE="kokhongw, post: 1796260, member: 277199"] Other than sulfonylureas, there are many other contributory factors for beta cells death... [SIZE=6][B]Mechanisms of β-Cell Death in Type 2 Diabetes[/B][/SIZE] [URL]http://diabetes.diabetesjournals.org/content/54/suppl_2/S108[/URL] [SIZE=5][B]Abstract[/B][/SIZE] A decrease in the number of functional insulin-producing β-cells contributes to the pathophysiology of type 2 diabetes. Opinions diverge regarding the relative contribution of a decrease in β-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 β-cells. With respect to these causal factors, we focus on Fas, the ATP-sensitive K+ channel, insulin receptor substrate 2, oxidative stress, nuclear factor-κB, 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 β-cell secretory function and cell turnover. Thus, the mechanisms regulating β-cell proliferation, apoptosis, and function are inseparable processes. [/QUOTE]
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