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自噬及其与2型糖尿病的联系。

Autophagy and its link to type II diabetes mellitus.

作者信息

Yang Jai-Sing, Lu Chi-Cheng, Kuo Sheng-Chu, Hsu Yuan-Man, Tsai Shih-Chang, Chen Shih-Yin, Chen Yng-Tay, Lin Ying-Ju, Huang Yu-Chuen, Chen Chao-Jung, Lin Wei-De, Liao Wen-Lin, Lin Wei-Yong, Liu Yu-Huei, Sheu Jinn-Chyuan, Tsai Fuu-Jen

机构信息

Department of Medical Research, China Medical University Hospital, China Medical University, Taichung 404, Taiwan.

School of Pharmacy, China Medical University, Taichung 404, Taiwan.

出版信息

Biomedicine (Taipei). 2017 Jun;7(2):8. doi: 10.1051/bmdcn/2017070201. Epub 2017 Jun 14.

Abstract

Autophagy, a double-edged sword for cell survival, is the research object on 2016 Nobel Prize in Physiology or Medicine. Autophagy is a molecular mechanism for maintaining cellular physiology and promoting survival. Defects in autophagy lead to the etiology of many diseases, including diabetes mellitus (DM), cancer, neurodegeneration, infection disease and aging. DM is a metabolic and chronic disorder and has a higher prevalence in the world as well as in Taiwan. The character of diabetes mellitus is hyperglycemia resulting from defects in insulin secretion, insulin action, or both. Type 2 diabetes mellitus (T2DM) is characterized by insulin resistance and failure of producing insulin on pancreatic beta cells. In T2DM, autophagy is not only providing nutrients to maintain cellular energy during fasting, but also removes damaged organelles, lipids and miss-folded proteins. In addition, autophagy plays an important role in pancreatic beta cell dysfunction and insulin resistance. In this review, we summarize the roles of autophagy in T2DM.

摘要

自噬是细胞生存的双刃剑,也是2016年诺贝尔生理学或医学奖的研究对象。自噬是一种维持细胞生理功能和促进细胞存活的分子机制。自噬缺陷会导致许多疾病的发生,包括糖尿病(DM)、癌症、神经退行性疾病、感染性疾病和衰老。糖尿病是一种代谢性慢性疾病,在全球以及台湾地区的患病率都较高。糖尿病的特征是由于胰岛素分泌缺陷、胰岛素作用缺陷或两者兼而有之导致的高血糖。2型糖尿病(T2DM)的特征是胰岛素抵抗以及胰腺β细胞产生胰岛素的功能衰竭。在T2DM中,自噬不仅在禁食期间提供营养以维持细胞能量,还能清除受损的细胞器、脂质和错误折叠的蛋白质。此外,自噬在胰腺β细胞功能障碍和胰岛素抵抗中也起着重要作用。在这篇综述中,我们总结了自噬在T2DM中的作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8757/5479440/8b33982443ee/bmdcn-7-8-fig1.jpg

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