细胞器应激在糖尿病和肥胖症中的作用:对治疗的启示

Yi-Cheng Chang, S. Hee, M. Hsieh, Y. Jeng, L. Chuang
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引用次数: 20

摘要

近几十年来,2型糖尿病的流行是一个巨大的全球健康威胁。这种流行病的主要原因是营养过剩和全世界肥胖流行率的增加。相比之下,限制热量摄入和减轻体重可以大大预防2型糖尿病,这表明营养过剩在糖尿病的发展中起着核心作用。近年来,营养过剩、细胞器应激和代谢性疾病发展之间的分子联系得到了广泛的研究。具体来说,过多的营养会触发内质网应激,增加线粒体活性氧的产生,导致应激信号通路激活、炎症反应、脂肪生成和胰腺β细胞死亡。自噬是清除肝脏脂质、减轻胰腺β细胞应激和白色脂肪细胞分化所必需的。在临床前模型中,活性氧清除剂、化学伴侣和自噬激活剂在治疗胰岛素抵抗和糖尿病方面已显示出良好的效果。人们热切期待临床试验的进一步结果。
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The Role of Organelle Stresses in Diabetes Mellitus and Obesity: Implication for Treatment
The type 2 diabetes pandemic in recent decades is a huge global health threat. This pandemic is primarily attributed to the surplus of nutrients and the increased prevalence of obesity worldwide. In contrast, calorie restriction and weight reduction can drastically prevent type 2 diabetes, indicating a central role of nutrient excess in the development of diabetes. Recently, the molecular links between excessive nutrients, organelle stress, and development of metabolic disease have been extensively studied. Specifically, excessive nutrients trigger endoplasmic reticulum stress and increase the production of mitochondrial reactive oxygen species, leading to activation of stress signaling pathway, inflammatory response, lipogenesis, and pancreatic beta-cell death. Autophagy is required for clearance of hepatic lipid clearance, alleviation of pancreatic beta-cell stress, and white adipocyte differentiation. ROS scavengers, chemical chaperones, and autophagy activators have demonstrated promising effects for the treatment of insulin resistance and diabetes in preclinical models. Further results from clinical trials are eagerly awaited.
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