Role of the Mammalian Target of Rapamycin (mTOR) Complexes in Pancreatic β-Cell Mass Regulation

被引:17
|
作者
Bartolome, Alberto [1 ,2 ,3 ]
Guillen, Carlos [1 ,2 ,3 ]
机构
[1] Univ Complutense, Fac Farm, Dept Bioquim & Biol Mol 2, E-28040 Madrid, Spain
[2] Ctr Invest Biomed Red Diabet & Enfermedades Metab, Barcelona, Spain
[3] Hosp Clin San Carlos Madrid IdISSC, Inst Invest Sanitaria, Madrid, Spain
来源
PANCREATIC BETA CELL | 2014年 / 95卷
关键词
ACTIVATED PROTEIN-KINASE; INSULIN-RECEPTOR SUBSTRATE-2; TUBEROUS SCLEROSIS COMPLEX-2; GLYCOGEN-SYNTHASE KINASE-3; SUPPRESSOR GENE-PRODUCT; MICE LACKING; PHOSPHATIDYLINOSITOL; 3-KINASE; SIGNAL-TRANSDUCTION; TSC1-TSC2; COMPLEX; UP-REGULATION;
D O I
10.1016/B978-0-12-800174-5.00017-X
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Exquisite regulation of insulin secretion by pancreatic beta-cells is essential to maintain metabolic homeostasis. beta-Cell mass must be accordingly adapted to metabolic needs and can be largely modified under different situations. The mammalian target of rapamycin (mTOR) complexes has been consistently identified as key modulators of beta-cell mass. mTOR can be found into two different complexes, mTORC1 and mTORC2. Under systemic insulin resistance, mTORC1/mTORC2 signaling in beta-cells is needed to increase beta-cell mass and insulin secretion. However, type 2 diabetes arises when these compensatory mechanisms fail, being the role of mTOR complexes still obscure in beta-cell failure. In this chapter, we introduce the protein composition and regulation of mTOR complexes and their role in pancreatic (beta-cells. Furthermore, we describe their main signaling effectors through the review of numerous animal models, which indicate the essential role of mTORC1/mTORC2 in pancreatic beta-cell mass regulation.
引用
收藏
页码:425 / 469
页数:45
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