Insulin responsiveness in skeletal muscle is determined by glucose transporter (Glut4) protein level.

ECU Author/Contributor (non-ECU co-authors, if there are any, appear on document)

G. Lynis Dohm (Creator)

Charles W. Elton (Creator)

Jacob E. Friedman (Creator)

Marialice Kern (Creator)

Phillip H. Pekala (Creator)

Jacqueline M. Stephens (Creator)

Edward B. Tapscott (Creator)

James A. Wells (Creator)

Institution

East Carolina University (ECU )

Web Site: http://www.ecu.edu/lib/

Abstract: Glucose transport in skeletal muscle is mediated by two distinct transporter isoforms designated muscle/adipose glucose transporter (Glut4) and erythrocyte/HepG2/brain glucose transporter (Glutl) which differ in both abundance and membrane distribution. The present study was designed to investigate whether differences in insulin responsiveness of red and white muscle might be due to differential expression of the glucose transporter isoforms. Glucose transport as well as Glutl and Glut4 protein and mRNA levels were determined in red and white portions of the quadriceps and gastrocnemius muscles of male Sprague-Dawley rats (body wt. approx. 250 g). Maximal glucose transport (in response to 100 nM-insulin) in the perfused hindlimb was 3.6 times greater in red than in white muscle. Red muscle contained approx. 5 times more total Glut4 protein and 2 times more Glut4 mRNA than white muscle but there were no differences in the Glutl protein or mRNA levels between the fibre types. Our data indicate that differences in responsiveness of glucose transport in specific skeletal muscle fibre types may be dependent upon the amount of Glut4 protein. Because this protein plays such an integral part in glucose transport in skeletal muscle any impairment in its expression may play a role in insulin resistance. Originally published Biochemical Journal Vol. 270 No. 2 Sep 1990

Additional Information

Publication

Other

Biochemical Journal. 270:2(September 1990) p. 397-400.

Language: English

Date: 2011

Keywords

Skeletal muscle, Glut4, Glut1, Insulin resistance

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