GSK3 involvement in amylin signaling in isolated rat soleus muscle.

Journal Article

Amylin can evoke insulin resistance by antagonizing insulin in a non-competitive manner. Here, we investigated the glycogenolytic effect of amylin in isolated skeletal muscle and compared it to the effects of a calcitonin gene-related peptide (CGRP). Amylin alone had no statistically significant effect on glucose transport. However, amylin decreased insulin-stimulated glucose transport by about 30%. The involvement of cAMP could not be detected at the concentrations shown to promote glycogenolysis. Previously, it has been shown that increased glycogen synthase kinase 3 (GSK3) activity plays a role in insulin resistance. Here, the ratio of GSK3 alpha:beta isoforms in rat soleus was found to be 1.2:1. We found that amylin increased GSK3alpha activity, which in turn led to increased phosphorylation of glycogen synthase and decreased glycogen synthesis de novo.

Full Text

Duke Authors

Cited Authors

  • Abaffy, T; Cooper, GJS

Published Date

  • December 2004

Published In

Volume / Issue

  • 25 / 12

Start / End Page

  • 2119 - 2125

PubMed ID

  • 15572200

Electronic International Standard Serial Number (EISSN)

  • 1873-5169

International Standard Serial Number (ISSN)

  • 0196-9781

Digital Object Identifier (DOI)

  • 10.1016/j.peptides.2004.08.016

Language

  • eng