Fatty Acid-Induced Lipotoxicity in Pancreatic Beta-Cells During Development of Type 2 Diabetes.
Fatty Acid-Induced Lipotoxicity in Pancreatic Beta-Cells During Development of Type 2 Diabetes.
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DOI：
10.3389/fendo.2018.00384
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发表时间：
2018
影响因子：
5.2
通讯作者：
Jun HS
中科院分区：
文献类型：
--
作者：
Oh YS;Bae GD;Baek DJ;Park EY;Jun HS
2型糖尿病是由慢性胰岛素抵抗和β细胞功能的进行性下降引起的。最佳的β细胞功能和质量对于葡萄糖稳态是必不可少的，并且β细胞损伤导致糖尿病的发展。循环脂肪酸（FAs）水平升高和脂质代谢调节紊乱与肥胖相关，并且它们是影响2型糖尿病发病率增加的主要因素。慢性游离脂肪酸（FFA）治疗可诱导胰岛素抵抗和β细胞功能障碍;因此，降低升高的血浆FFA水平可能是肥胖和2型糖尿病的重要治疗靶点。通过受体的脂质信号和细胞内机制参与FFA诱导的细胞凋亡。在本文中，我们讨论了β细胞中的脂质作用，包括对代谢途径和应激反应的影响，以帮助进一步了解脂毒性诱导的2型糖尿病的分子机制。
Type 2 diabetes is caused by chronic insulin resistance and progressive decline in beta-cell function. Optimal beta-cell function and mass is essential for glucose homeostasis and beta-cell impairment leads to the development of diabetes. Elevated levels of circulating fatty acids (FAs) and disturbances in lipid metabolism regulation are associated with obesity, and they are major factors influencing the increase in the incidence of type 2 diabetes. Chronic free FA (FFA) treatment induces insulin resistance and beta-cell dysfunction; therefore, reduction of elevated plasma FFA levels might be an important therapeutic target in obesity and type 2 diabetes. Lipid signals via receptors, and intracellular mechanisms are involved in FFA-induced apoptosis. In this paper, we discuss lipid actions in beta cells, including effects on metabolic pathways and stress responses, to help further understand the molecular mechanisms of lipotoxicity-induced type 2 diabetes.