Rictor/mTORC2 is essential for maintaining a balance between beta-cell proliferation and cell size.

ABSTRACT:

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)

SUBMITTER: Gu Y 

PROVIDER: S-EPMC3046843 | biostudies-literature | 2011 Mar

REPOSITORIES: biostudies-literature