Use of GLUT-4 null mice to study skeletal muscle glucose uptake.
Authors Charron MJ, Gorovits N, Laidlaw JS, Ranalletta M, Katz EB
Submitted By Erwin Bottinger on 2/23/2009
Status Published
Journal Clinical and experimental pharmacology & physiology
Year 2005
Date Published 4/1/2005
Volume : Pages 32(4) : 308 - 313
PubMed Reference 15810997
Abstract 1. The present review focuses on the effects of varying levels of GLUT-4, the
insulin-sensitive glucose transporter, on insulin sensitivity and whole body
glucose homeostasis. 2. Three mouse models are discussed including myosin light
chain (MLC)-GLUT-4 mice which overexpress GLUT-4 specifically in skeletal
muscle, GLUT-4 null mice which express no GLUT-4 and the MLC-GLUT-4 null mice
which express GLUT-4 only in skeletal muscle. Overexpressing GLUT-4 specifically
in the skeletal muscle results in increased insulin sensitivity in the
MLC-GLUT-4 mice. In contrast, the GLUT-4 null mice exhibit insulin intolerance
accompanied by abnormalities in glucose and lipid metabolism. Restoring GLUT-4
expression in skeletal muscle in the MLC-GLUT-4 null mice results in normal
glucose metabolism but continued abnormal lipid metabolism. 3. The results of
experiments using these mouse models demonstrates that modifying the expression
of GLUT-4 profoundly affects whole body insulin action and consequently glucose
and lipid metabolism.

Complications









Genes
SymbolDescription
Slc2a4solute carrier family 2 (facilitated glucose transporter), member 4