The murine GLUT4 gene was disrupted using homologous recombination in embryonic stem cells. Mice homozygous for the gene disruption (GLUT4 null) exhibit decreased longevity, growth retardation, cardiac hypertrophy, reduced adipose tissue stores and insulin resistance. Surprisingly, GLUT4 null mice are not overtly diabetic as evidenced by their normal fasting and fed glucose levels. In vitro studies have revealed a glucose transport activity in soleus muscle that is activated in response to GLUT4 ablation. This transport activity is not associated with upregulation of any of the known facilitative glucose transporters. Genetic complementation of GLUT4 null mice with a muscle specific GLUT4 transgene restored whole body insulin sensitivity but did not replete adipose tissue mass. In vivo and in vitro studies to characterize the compensatory responses to GLUT4 ablation are ongoing.
|Original language||English (US)|
|Journal||Biochemical Society transactions|
|Publication status||Published - Jan 1 1997|
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