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PMID: 7814644 Published · ppublish English Journal Article Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, P.H.S.

Overexpression of Glut4 protein in muscle increases basal and insulin-stimulated whole body glucose disposal in conscious mice.

The Journal of clinical investigation ·Vol. 95 ·No. 1 ·1995-01-00 ·Pages 429-32

Ren JM, Marshall BA, Mueckler MM, McCaleb M, Amatruda JM, Shulman GI

Abstract

The effect of increased Glut4 protein expression in muscle and fat on the whole body glucose metabolism has been evaluated by the euglycemic hyperinsulinemic clamp technique in conscious mice. Fed and fasting plasma glucose concentrations were 172 +/- 7 and 78 +/- 7 mg/dl, respectively, in transgenic mice, and were significantly lower than that of nontransgenic littermates (208 +/- 5 mg/dl in fed; 102 +/- 5 mg/dl in fasting state). Plasma lactate concentrations were higher in transgenic mice, (6.5 +/- 0.7 mM in the fed and 5.8 +/- 1.0 mM in fasting state) compared with that of non-transgenic littermates (4.7 +/- 0.3 mM in the fed and 4.2 +/- 0.5 mM in fasting state). In the fed state, the rate of whole body glucose disposal was 70% higher in transgenic mice in the basal state, 81 and 54% higher during submaximal and maximal insulin stimulation. In the fasting state, insulin-stimulated whole body glucose disposal was also higher in the transgenic mice. Hepatic glucose production after an overnight fast was 24.8 +/- 0.7 mg/kg per min in transgenic mice, and 25.4 +/- 2.7 mg/kg per min in nontransgenic mice. Our data demonstrate that overexpression of Glut4 protein in muscle increases basal as well as insulin-stimulated whole body glucose disposal. These results suggest that skeletal muscle glucose transport is rate-limiting for whole body glucose disposal and that the Glut4 protein is a potential target for pharmacological or genetic manipulation for treatment of patients with non-insulin-dependent diabetes mellitus.

MeSH Terms
Animals Blood Glucose/metabolism Consciousness Eating Fasting Glucose Transporter Type 4 Male Mice Mice, Transgenic Monosaccharide Transport Proteins/biosynthesis,genetics,metabolism Muscle Proteins Muscles/metabolism Splanchnic Circulation
Chemicals
Blood Glucose Glucose Transporter Type 4 Monosaccharide Transport Proteins Muscle Proteins Slc2a4 protein, mouse
Authors & Affiliations
6 authors, click to expand affiliations / ORCID
Ren J M
Institute for Metabolic Disorders, Miles Inc., West Haven, Connecticut 06516.
Marshall B A
Mueckler M M
McCaleb M
Amatruda J M
Shulman G I
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Article Info
Journal
The Journal of clinical investigation
Abbr.
J Clin Invest
ISSN
0021-9738
Published
1995-01-00
Pages
429-32
Language
English
Region
United States
NLM ID
7802877
PMCID
PMC295454
Subset
IM
Grants
NIDDK NIH HHS · R01 DK040936 · United States
NIDDK NIH HHS · DK-38495 · United States
NIDDK NIH HHS · DK-40936 · United States
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