Molecular Mechanisms of the Diabetogenic Effects of Arsenic: Inhibition of Insulin Signaling by Arsenite and Methylarsonous Acid | Zendy

David S. Paul | Zendy; Anne W. Harmon | Zendy; Vicenta Devesa | Zendy; David J. Thomas | Zendy; Miroslav Stýblo | Zendy

Open Access

Molecular Mechanisms of the Diabetogenic Effects of Arsenic: Inhibition of Insulin Signaling by Arsenite and Methylarsonous Acid

Author(s) -

David S. Paul,

Anne W. Harmon,

Vicenta Devesa,

David J. Thomas,

Miroslav Stýblo

Publication year - 2007

Publication title -

environmental health perspectives

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 2.257

H-Index - 282

eISSN - 1552-9924

pISSN - 0091-6765

DOI - 10.1289/ehp.9867

Subject(s) - protein kinase b , phosphorylation , pten , pi3k/akt/mtor pathway , phosphatidylinositol , signal transduction , proto oncogene proteins c akt , kinase , tensin , microbiology and biotechnology , phosphatase , biology , chemistry , protein phosphatase 2 , biochemistry , endocrinology , medicine

Increased prevalences of diabetes mellitus have been reported among individuals chronically exposed to inorganic arsenic (iAs). However, the mechanisms underlying the diabetogenic effects of iAs have not been characterized. We have previously shown that trivalent metabolites of iAs, arsenite (iAs(III)) and methylarsonous acid (MAs(III)) inhibit insulin-stimulated glucose uptake (ISGU) in 3T3-L1 adipocytes by suppressing the insulin-dependent phosphorylation of protein kinase B (PKB/Akt).

The content you want is available to Zendy users.

Already have an account? Click here to sign in.

Having issues? You can contact us here

Accelerating Research