Beta-adrenergic activity preserves GLUT4 protein in glycolytic fibers in fasting

Muscle Nerve. 2009 Nov;40(5):847-54. doi: 10.1002/mus.21359.

Abstract

Glucose transporter 4 (GLUT4) expression in adipose tissue decreases during fasting. In skeletal muscle, we hypothesized that GLUT4 expression might be maintained in a beta-adrenergic-dependent way to ensure energy disposal for contractile function. Herein we investigate beta-blockade or beta-stimulation effects on GLUT4 expression in oxidative (soleus) and glycolytic [extensor digitorum longus (EDL)] muscles of fasted rats. Fasting increased GLUT4 mRNA in soleus (24%) and EDL (40%), but the protein content increased only in soleus (30%). beta1-beta2-, and beta1-beta2-beta3-blockade decreased (20-30%) GLUT4 mRNA content in both muscles, although GLUT4 protein decreased only in EDL. When mRNA and GLUT4 protein regulations were discrepant, changes in the mRNA poly(A) tail length were detected, indicating a posttranscriptional modulation of gene expression. These results show that beta-adrenergic activity regulates GLUT4 gene expression in skeletal muscle during fasting, highlighting its participation in preservation of GLUT4 protein in glycolytic muscle.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adrenergic beta-Agonists / pharmacology
  • Adrenergic beta-Antagonists / pharmacology
  • Animals
  • Fasting / metabolism*
  • Gene Expression*
  • Glucose Transporter Type 4 / biosynthesis*
  • Glycolysis / drug effects
  • Glycolysis / physiology*
  • Male
  • Muscle Fibers, Skeletal / drug effects
  • Muscle Fibers, Skeletal / metabolism*
  • RNA, Messenger / biosynthesis
  • Rats
  • Rats, Wistar
  • Receptors, Adrenergic, beta / metabolism*

Substances

  • Adrenergic beta-Agonists
  • Adrenergic beta-Antagonists
  • Glucose Transporter Type 4
  • RNA, Messenger
  • Receptors, Adrenergic, beta
  • Slc2a4 protein, rat