pubmed.ncbi.nlm.nih.gov

PED/PEA-15 gene controls glucose transport and is overexpressed in type 2 diabetes mellitus - PubMed

  • ️Thu Jan 01 1998

PED/PEA-15 gene controls glucose transport and is overexpressed in type 2 diabetes mellitus

G Condorelli et al. EMBO J. 1998.

Abstract

We have used differential display to identify genes whose expression is altered in type 2 diabetes thus contributing to its pathogenesis. One mRNA is overexpressed in fibroblasts from type 2 diabetics compared with non-diabetic individuals, as well as in skeletal muscle and adipose tissues, two major sites of insulin resistance in type 2 diabetes. The levels of the protein encoded by this mRNA are also elevated in type 2 diabetic tissues; thus, we named it PED for phosphoprotein enriched in diabetes. PED cloning shows that it encodes a 15 kDa phosphoprotein identical to the protein kinase C (PKC) substrate PEA-15. The PED gene maps on human chromosome 1q21-22. Transfection of PED/PEA-15 in differentiating L6 skeletal muscle cells increases the content of Glut1 transporters on the plasma membrane and inhibits insulin-stimulated glucose transport and cell-surface recruitment of Glut4, the major insulin-sensitive glucose transporter. These effects of PED overexpression are reversed by blocking PKC activity. Overexpression of the PED/PEA-15 gene may contribute to insulin resistance in glucose uptake in type 2 diabetes.

PubMed Disclaimer

Similar articles

Cited by

References

    1. Anal Biochem. 1987 Apr;162(1):156-9 - PubMed
    1. Diabetologia. 1997 Sep;40(9):991-1003 - PubMed
    1. J Biol Chem. 1991 Jun 5;266(16):10122-30 - PubMed
    1. Recent Prog Horm Res. 1991;47:349-87; discussion 387-8 - PubMed
    1. Sci Am. 1992 Jan;266(1):86-91 - PubMed

Publication types

MeSH terms

Substances