In vivo effects of dexamethasone and sucrose on glucose transport (GLUT-4) protein tissue distribution

• Published in: The American journal of physiology Vol. 271; no. 4 Pt 1; p. E643
• Main Authors: Coderre, L, Vallega, G A, Pilch, P F, Chipkin, S R
• Format: Journal Article
• Language: English
• Published: United States 01.10.1996
• Subjects: Adipose Tissue - metabolism; Animals; Blotting, Western; Body Weight - drug effects; Dexamethasone - pharmacology; Glucose - metabolism; Glucose Transporter Type 4; Hyperglycemia - metabolism; Hyperinsulinism - metabolism; Insulin Resistance; Male; Monosaccharide Transport Proteins - metabolism; Muscle Proteins; Muscle, Skeletal - metabolism; Myocardium - metabolism; Rats; Rats, Sprague-Dawley; Sucrose - pharmacology; Tissue Distribution
• ISSN: 0002-9513
• DOI: 10.1152/ajpendo.1996.271.4.e643

Tissue-specific changes in GLUT-4 were compared in the following three different rat models by inducing varying degrees of hyperinsulinemia with or without hyperglycemia and hypertriglyceridemia: 1) sucrose feeding (Suc), 2) subcutaneous dexamethasone administration (Dex), and 3) a combination of both treatments (Dex/Suc). Suc raised circulatory insulin and triglyceride levels without affecting plasma glucose, whereas both Dex and Dex/Suc induced significant hyperinsulinemia, hyperglycemia, and hypertriglyceridemia. In adipocytes and skeletal muscle, Suc feeding was not associated with any change in total cellular GLUT-4 levels. However, Suc induced a sevenfold increase in fat cell plasma membrane GLUT-4 levels in the basal state and inhibited GLUT-4 translocation in response to insulin. Administration of Dex or Dex/Suc diminished GLUT-4 expression in fat cells, increased it in skeletal muscle, but did not induce any change in heart. Similar to Suc feeding, Dex and Dex/Suc also increased the amount of GLUT-4 detected at the plasma membrane of adipocytes in the basal state and inhibited GLUT-4 translocation in response to insulin. These results emphasize the specific regulation of GLUT-4 in insulin-sensitive tissues.