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Glucoseingestion causes GLUT4 translocation in human skeletal muscle
Research Division, Brigham and Women's Hospital, New England Deaconess Hospital, Boston MA, United States; Metabolism Section, Joslin Diabetes Center, One Joslin Place, Boston MA, United States.
Research Division, Brigham and Women's Hospital, New England Deaconess Hospital, Boston MA, United States.
Research Division, Brigham and Women's Hospital, New England Deaconess Hospital, Boston MA, United States.
Division of Endocrinology, Department of Medicine, University of Vermont, Burlington VT, United States.
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1996 (English)In: Diabetes, ISSN 0012-1797, E-ISSN 1939-327X, Vol. 45, no 8, p. 1051-1056Article in journal (Refereed) Published
Abstract [en]

In humans, ingestion of carbohydrates causes an increase in blood glucose concentration, pancreatic insulin release, and increased glucose disposal into skeletal muscle. The underlying molecular mechanism for the increase in glucose disposal in human skeletal muscle after carbohydrate ingestion is not known. We determined whether glucoseingestion increases glucose uptake in human skeletal muscle by increasing the number of glucose transporter proteins at the cell surface and/or by increasing the activity of the glucose transporter proteins in the plasma membrane. Under local anesthesia, approximately 1 g of vastus lateralis muscle was obtained from six healthy subjects before and 60 min after ingestion of a 75-g glucose load. Plasma membranes were isolated from the skeletal muscle and used to measure GLUT4 and GLUT1 content and glucosetransport in plasma membrane vesicles. Glucose ingestion increased the plasma membrane content of GLUT4 per gram muscle (3,524 +/- 729 vs. 4,473 +/- 952 arbitrary units for basal and 60 min, respectively; P < 0.005). Transporter-mediated glucosetransport into plasma membrane vesicles was also significantly increased (130 +/- 11 vs. 224 +/- 38 pmol.mg-1.s-1; P < 0.017), whereas the calculated ratio of glucose transport to GLUT4, an indication of transporter functional activity, was not significantly increased 60 min after glucose ingestion (2.3 +/- 0.4 vs. 3.0 +/- 0.5 pmol.GLUT4 arbitrary units-1.s-1; P < 0.17). These results demonstrate that oral ingestion of glucose increases the rate of glucose transport across the plasma membrane and causes GLUT4 translocation in human skeletal muscle. These findings suggest that under physiological conditions the translocation of GLUT4 is an important mechanism for the stimulation of glucose uptake in human skeletal muscle.

Place, publisher, year, edition, pages
American Diabetes Association , 1996. Vol. 45, no 8, p. 1051-1056
National Category
Endocrinology and Diabetes Physiology
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URN: urn:nbn:se:oru:diva-63868DOI: 10.2337/diabetes.45.8.1051PubMedID: 8690151Scopus ID: 2-s2.0-0029740564OAI: oai:DiVA.org:oru-63868DiVA, id: diva2:1171009
Note

Funding agencies:

NIAMS NIH HHS AR-42238

NIDDK NIH HHS DK-46188

Available from: 2018-01-05 Created: 2018-01-05 Last updated: 2018-02-06Bibliographically approved

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Ljungqvist, Olle

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