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http://purl.uniprot.org/citations/21266327http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/21266327http://www.w3.org/2000/01/rdf-schema#comment"

Objective

We examined the role of Rictor/mammalian target of rapamycin complex 2 (mTORC2), a key component of the phosphotidylinositol-3-kinase (PI3K)/mTORC2/AKT signaling pathway, in regulating both β-cell mass and function.

Research design and methods

Mice with β-cell-specific deletions of Rictor or Pten were studied to determine the effects of deleting either or both genes on β-cell mass and glucose homeostasis.

Results

Rictor null mice exhibited mild hyperglycemia and glucose intolerance caused by a reduction in β-cell mass, β-cell proliferation, pancreatic insulin content, and glucose-stimulated insulin secretion. Islets from these mice exhibited decreased AKT-S473 phosphorylation and increased abundance of FoxO1 and p27 proteins. Conversely, Pten null (βPtenKO) mice exhibited an increase in β-cell mass caused by increased cellular proliferation and size. Although β-cell mass was normal in mice lacking both Rictor and Pten (βDKO), their β-cells were larger than those in the βPtenKO mice. Even though the β-cell proliferation rate in the βDKO mice was lower than in the βPtenKO mice, there was a 12-fold increase the phosphorylation of AKT-T308.

Conclusions

PI3K/AKT signaling through mTORC2/pAKT-S473 plays a key role in maintaining normal β-cell mass. The phosphorylation of AKT-S473, by negatively regulating that of AKT-T308, is essential for maintaining a balance between β-cell proliferation and cell size in response to proliferative stimuli."xsd:string
http://purl.uniprot.org/citations/21266327http://purl.org/dc/terms/identifier"doi:10.2337/db10-1194"xsd:string
http://purl.uniprot.org/citations/21266327http://purl.uniprot.org/core/author"Gu Y."xsd:string
http://purl.uniprot.org/citations/21266327http://purl.uniprot.org/core/author"Kumar A."xsd:string
http://purl.uniprot.org/citations/21266327http://purl.uniprot.org/core/author"Yuan W."xsd:string
http://purl.uniprot.org/citations/21266327http://purl.uniprot.org/core/author"Magnuson M.A."xsd:string
http://purl.uniprot.org/citations/21266327http://purl.uniprot.org/core/author"Lindner J."xsd:string
http://purl.uniprot.org/citations/21266327http://purl.uniprot.org/core/date"2011"xsd:gYear
http://purl.uniprot.org/citations/21266327http://purl.uniprot.org/core/name"Diabetes"xsd:string
http://purl.uniprot.org/citations/21266327http://purl.uniprot.org/core/pages"827-837"xsd:string
http://purl.uniprot.org/citations/21266327http://purl.uniprot.org/core/title"Rictor/mTORC2 is essential for maintaining a balance between beta-cell proliferation and cell size."xsd:string
http://purl.uniprot.org/citations/21266327http://purl.uniprot.org/core/volume"60"xsd:string
http://purl.uniprot.org/citations/21266327http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/21266327
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