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GLUT4 heterozygous knockout mice develop muscle insulin resistance and diabetes.

Abstract：

:GLUT4, the insulin-responsive glucose transporter, plays an important role in postprandial glucose disposal. Altered GLUT4 activity is suggested to be one of the factors responsible for decreased glucose uptake in muscle and adipose tissue in obesity and diabetes. To assess the effect of GLUT4 expression on whole-body glucose homeostasis, we disrupted the murine GLUT4 gene by homologous recombination. Male mice heterozygous for the mutation (GLUT4 +/-) exhibited a decrease in GLUT4 expression in adipose tissue and skeletal muscle. This decrease in GLUT4 expression did not result in obesity but led to increased serum glucose and insulin, reduced muscle glucose uptake, hypertension, and diabetic histopathologies in the heart and liver similar to those of humans with non-insulin-dependent diabetes mellitus (NIDDM). The male GLUT4 +/- mice represent a good model for studying the development of NIDDM without the complications associated with obesity.

journal_name

Nat Med

journal_title

Nature medicine

authors

Stenbit AE,Tsao TS,Li J,Burcelin R,Geenen DL,Factor SM,Houseknecht K,Katz EB,Charron MJ

doi

10.1038/nm1097-1096

subject

Has Abstract

pub_date

1997-10-01 00:00:00

pages

1096-101

issue

10

eissn

1078-8956

issn

1546-170X

journal_volume

3

pub_type

杂志文章

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