Document Detail


mTORC1 signaling and regulation of pancreatic β-cell mass.
MedLine Citation:
PMID:  22544327     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The capacity of β cells to expand in response to insulin resistance is a critical factor in the development of type 2 diabetes. Proliferation of β cells is a major component for these adaptive responses in animal models. The extracellular signals responsible for β-cell expansion include growth factors, such as insulin, and nutrients, such as glucose and amino acids. AKT activation is one of the important components linking growth signals to the regulation of β-cell expansion. Downstream of AKT, tuberous sclerosis complex 1 and 2 (TSC1/2) and mechanistic target of rapamycin complex 1 (mTORC1) signaling have emerged as prime candidates in this process, because they integrate signals from growth factors and nutrients. Recent studies demonstrate the importance of mTORC1 signaling in β cells. This review will discuss recent advances in the understanding of how this pathway regulates β-cell mass and present data on the role of TSC1 in modulation of β-cell mass. Herein, we also demonstrate that deletion of Tsc1 in pancreatic β cells results in improved glucose tolerance, hyperinsulinemia and expansion of β-cell mass that persists with aging.
Authors:
Manuel Blandino-Rosano; Angela Y Chen; Joshua O Scheys; Emilyn U Alejandro; Aaron P Gould; Tatyana Taranukha; Lynda Elghazi; Corentin Cras-Méneur; Ernesto Bernal-Mizrachi
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review     Date:  2012-05-15
Journal Detail:
Title:  Cell cycle (Georgetown, Tex.)     Volume:  11     ISSN:  1551-4005     ISO Abbreviation:  Cell Cycle     Publication Date:  2012 May 
Date Detail:
Created Date:  2012-06-01     Completed Date:  2012-09-24     Revised Date:  2013-09-30    
Medline Journal Info:
Nlm Unique ID:  101137841     Medline TA:  Cell Cycle     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1892-902     Citation Subset:  IM    
Affiliation:
Department of Internal Medicine; Division of Metabolism, Endocrinology and Diabetes, Brehm Center for Diabetes Research, University of Michigan Medical Center; Ann Arbor, MI, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Cell Proliferation
Homeostasis
Insulin / metabolism
Insulin-Secreting Cells / cytology,  metabolism*
Mice
Proteins / metabolism*
Proto-Oncogene Proteins c-akt / metabolism
Signal Transduction
Tumor Suppressor Proteins / genetics,  metabolism
Grant Support
ID/Acronym/Agency:
2T32DK071212-06/DK/NIDDK NIH HHS; DK-073716/DK/NIDDK NIH HHS; P60DK020572/DK/NIDDK NIH HHS; R01 DK073716/DK/NIDDK NIH HHS; R01 DK084236/DK/NIDDK NIH HHS
Chemical
Reg. No./Substance:
0/Insulin; 0/Proteins; 0/Tumor Suppressor Proteins; 0/mechanistic target of rapamycin complex 1; 0/tuberous sclerosis complex 1 protein; 4JG2LF96VF/tuberous sclerosis complex 2 protein; EC 2.7.11.1/Proto-Oncogene Proteins c-akt
Comments/Corrections

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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