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Management of Type 2 Diabetes With Thiazolidinediones Link Between beta-Cell Preservation and Durability of Response

机译:β细胞保存和响应的持久性之间的联系与噻唑烷二酮类2型糖尿病的管理。

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摘要

The clinical onset of type 2 diabetes in most patients is typically preceded by years of insulin resistance. Type 2 diabetes develops when pancreatic beta cells are unable to produce sufficient insulin to overcome the insulin resistance. Several recent trials have shown that the thiazolidinediones (TZDs) improve both insulin sensitivity and pancreatic beta-cell function. A likely mechanism for the protective effect of TZDs is improvement in lipotoxicity. The most compelling reason to use a TZD at the earliest stage of type 2 diabetes is the unique ability of these agents to rejuvenate or decelerate the decline in pancreatic /3-cell function. This article reviews both the pathophysiology of decreased beta-cell function and the evidence for rejuvenation of pancreatic beta cells with TZD therapy in both animal and human studies.
机译:在大多数患者中,2型糖尿病的临床发作通常始于多年的胰岛素抵抗。当胰岛β细胞无法产生足够的胰岛素来克服胰岛素抵抗时,就会出现2型糖尿病。最近的几项试验表明,噻唑烷二酮(TZD)可以改善胰岛素敏感性和胰腺β细胞功能。 TZDs保护作用的可能机制是改善脂毒性。在2型糖尿病的早期阶段使用TZD的最令人信服的原因是这些药物具有独特的恢复或减缓胰腺3细胞功能下降的能力。本文回顾了动物和人类研究中β细胞功能降低的病理生理学以及TZD治疗使胰腺β细胞恢复活力的证据。

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