Tissue-specific alterations in G protein expression in genetic versus diet-induced models of non-insulin-dependent diabetes mellitus in the mouse.

Journal Article

Various tissues were obtained from the well-characterized genetic model (C57BL/6J-ob/ob) of non-insulin-dependent diabetes mellitus (NIDDM) and from a diet-induced model of NIDDM produced in the same genetic background (C57BL/6J). The objectives were to determine whether the previously observed changes in guanine nucleotide-binding regulatory protein (G protein) expression in adipose tissue from ob/ob mice were mirrored by concomitant changes in other tissues, and whether NIDDM of a different etiology would share similar alterations in G protein expression. Plasma membranes from adipocytes, brain, heart, liver, and testes were probed with alpha-subunit-specific antisera, and the level of G protein expression in each model was compared with that in its lean littermate control. Adipose, heart, and liver cell membranes from ob/ob mice contained significantly less alpha-subunit of stimulatory G protein (Gs alpha) than those from their lean littermates. As compared with the lean littermates, heart alpha-subunit-2 of inhibitory G protein (Gi alpha-2), liver Gi alpha-3, and adipocyte G1 alpha-1 and Gi alpha-3 were also reduced in ob/ob mice. In contrast, Gi alpha-2 and Go alpha were increased over lean-control levels in brain tissue from ob/ob mice, whereas Gs alpha was unchanged. G protein expression in the testes did not differ between lean and ob/ob mice. In the diet-induced model of NIDDM, Gs alpha expression in the liver was twofold greater in obese/diabetic mice as compared with lean controls. However, G protein expression in all other tissues examined did not differ between obese/diabetic animals and lean littermates.(ABSTRACT TRUNCATED AT 250 WORDS)

Full Text

Duke Authors

Cited Authors

  • Gettys, TW; Ramkumar, V; Surwit, RS; Taylor, IL

Published Date

  • June 1995

Published In

Volume / Issue

  • 44 / 6

Start / End Page

  • 771 - 778

PubMed ID

  • 7783662

International Standard Serial Number (ISSN)

  • 0026-0495

Language

  • eng

Conference Location

  • United States