These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: IRS-3 mediates insulin-induced glucose uptake in differentiated IRS-2(-/-) brown adipocytes.
    Author: Escribano O, Arribas M, Valverde AM, Benito M.
    Journal: Mol Cell Endocrinol; 2007 Mar 30; 268(1-2):1-9. PubMed ID: 17316975.
    Abstract:
    IRS-2 mediates insulin-induced glucose uptake in brown preadipocytes. Upon differentiation, basal IRS-3 expression increased concurrently with an enhancement in the IRS-3-associated phosphatidylinositol (PI) 3-kinase activity in the Triton-insoluble fraction in wild-type and IRS-2-deficient brown adipocytes stimulated with insulin. Moreover, insulin induced protein kinase B (Akt) and protein kinase C (PKC) zeta phosphorylation in both kinds of cells. More importantly, insulin induced glucose uptake in differentiated IRS-2-deficient brown adipocytes in a wortmannin-dependent manner. However, while insulin induced Akt phosphorylation occurred mainly in the cytosolic fraction, PKC zeta activation was constrained to the Triton-insoluble fraction. The reduction of IRS-3 expression by siRNA inhibited insulin-induced glucose uptake and also PKC zeta activation in differentiated IRS-2(-/-) brown adipocytes. In addition, inhibition of PKC zeta totally blunted insulin-induced glucose uptake in those cells. Our results provide evidences suggesting that IRS-3/PI 3-kinase/PKC zeta signaling is the main responsible for the insulin-induced glucose uptake observed upon differentiation of brown adipocytes lacking IRS-2.
    [Abstract] [Full Text] [Related] [New Search]