Beta-cell failure in the pathogenesis of type 2 diabetes mellitus.
Beta-cell failure in the pathogenesis of type 2 diabetes mellitus.
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DOI：
10.1007/s11892-004-0019-3
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发表时间：
2004-06-01
影响因子：
4.2
通讯作者：
Horton, Edward S
中科院分区：
文献类型：
--
作者：
Steppel, Jeanne H;Horton, Edward S
2型糖尿病是在胰岛素抵抗恶化的情况下胰腺β细胞功能进行性损害的结果。对高危人群的研究表明，在糖尿病进展过程中，β细胞功能下降，失去胰岛素分泌的第一阶段，导致餐后肝脏葡萄糖生成抑制不足。此外，胰岛素分泌的振荡与葡萄糖的正常偶联变得不匹配。有几种机制被认为是导致β细胞功能受损的原因，包括葡萄糖毒性和脂肪毒性，并可能导致β细胞损失。分子科学的进步已经阐明了几种细胞因子和转录因子可能与β细胞质量的损失有关。在过去的15年里，临床试验为可能延缓或预防糖尿病进展的潜在疗法带来了希望。改变生活方式和药物治疗仍然是最有希望的干预措施。
Type 2 diabetes is the result of a progressive impairment of pancreatic beta-cell function in the setting of worsening insulin resistance. Studies in high-risk populations have demonstrated that during progression to diabetes, beta cells have declining function and lose the first phase of insulin secretion, resulting in less than adequate suppression of hepatic glucose production following meals. In addition, oscillations of insulin secretion become unmatched from their normal coupling with glucose. Several mechanisms are thought to be responsible for impaired beta-cell function, including glucose toxicity and lipotoxicity, and potentially contribute to beta-cell loss. Advances in molecular science have elucidated several cytokines and transcription factors possibly implicated in the loss of beta-cell mass. In the past 15 years, clinical trials have given hope for potential therapies that may either delay or prevent the progression to diabetes. Lifestyle modification and pharmaceutical treatment remain the most promising interventions.