期刊
CELL METABOLISM
卷 27, 期 2, 页码 314-331出版社
CELL PRESS
DOI: 10.1016/j.cmet.2017.11.004
关键词
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资金
- German Research Foundation (DFG)
- European Research Council (ERC)
- JDRF
- EFSD/Lilly Fellowship Programme
- European Foundation for the Study of Diabetes [Lilly FS 2017_3] Funding Source: researchfish
The mechanistic target of rapamycin complex 1 (mTORC1) is a central regulator of metabolic and nutrient cues that integrates environmental inputs into downstream signaling pathways to control cellular metabolism, growth, and survival. While numerous in vitro and in vivo studies reported the positive functions of mTORC1 in the regulation of beta cell survival and proliferation under physiological conditions, more recent work demonstrates the opposite in the long term; this is exemplified by the constitutive inappropriate hyper-activation of mTORC1 in diabetic islets or beta cells under conditions of increased beta cell stress and metabolic demands. These recent findings uncover mTORC1's importance as an emerging significant player in the development and progression of beta cell failure in type 2 diabetes and suggest that mTORC1 may act as a double edge sword in the regulation of beta cell mass and function in response to metabolic stress such as nutrient overload and insulin resistance.
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