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Autophagy and its link to type II diabetes mellitus
Author(s) -
JaiSing Yang,
ChiCheng Lu,
Sheng-Chu Kuo,
YuanMan Hsu,
Shih Chang Tsai,
Shih-Yin Chen,
YngTay Chen,
Ying-Ju Lin,
Yu-Chuen Huang,
ChaoJung Chen,
Wei-De Lin,
Wenlin Liao,
WeiYong Lin,
Yu-Huei Liu,
Jinn-Chyuan Sheu,
FuuJen Tsai
Publication year - 2017
Publication title -
biomedicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.498
H-Index - 26
eISSN - 2211-8039
pISSN - 2211-8020
DOI - 10.1051/bmdcn/2017070201
Subject(s) - autophagy , insulin resistance , diabetes mellitus , type 2 diabetes mellitus , insulin , medicine , mitophagy , neurodegeneration , type 2 diabetes , disease , endocrinology , beta cell , biology , bioinformatics , biochemistry , apoptosis , islet
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.

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