Molecular mechanisms of insulin resistance in diabetes.
Molecular mechanisms of insulin resistance in diabetes.
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DOI：
10.1007/978-1-4614-5441-0_19
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发表时间：
2012
影响因子：
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通讯作者：
K. Soumaya
中科院分区：
文献类型：
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作者：
K. Soumaya
胰岛素信号通路受损的分子组分已经出现，人们对了解环境和遗传易感性如何结合联合收割机导致这一基本通路的缺陷从而导致胰岛素抵抗越来越感兴趣。当胰岛素抵抗与葡萄糖刺激的胰岛素分泌中的β细胞缺陷结合时，可导致葡萄糖耐量受损、高血糖症或2型糖尿病。最常见的潜在原因是肥胖，尽管正常体重个体中的原发性胰岛素抵抗也是可能的。脂肪组织释放的游离脂肪酸导致胰岛素抵抗，同时也作为一个相关的内分泌器官产生调节胰岛素信号的介质（脂肪因子）。本章讨论了促进胰岛素抵抗的核心因素，这些因素与胰岛素信号通路受损和脂肪细胞功能障碍有关。详细了解这些基本的病理生理学机制对于开发治疗糖尿病的新治疗策略至关重要。
Molecular components of impaired insulin signaling pathway have emerged with growing interest to understand how the environment and genetic susceptibility combine to cause defects in this fundamental pathway that lead to insulin resistance. When insulin resistance is combined with β-cell defects in glucose-stimulated insulin secretion, impaired glucose tolerance, hyperglycemia, or Type 2 diabetes can result. The most common underlying cause is obesity, although primary insulin resistance in normal-weight individuals is also possible. The adipose tissue releases free fatty acids that contribute to insulin resistance and also acts as a relevant endocrine organ producing mediators (adipokines) that can modulate insulin signalling.This chapter deals with the core elements promoting insulin resistance, associated with impaired insulin signalling pathway and adipocyte dysfunction. A detailed understanding of these basic pathophy siological mechanisms is critical for the development of novel therapeutic strategies to treat diabetes.