An in vitro human muscle preparation suitable for metabolic studies. Decreased insulin stimulation of glucose transport in muscle from morbidly obese and diabetic subjects.

ECU Author/Contributor (non-ECU co-authors, if there are any, appear on document)
Samuel M. Atkinson (Creator)
Jose F. Caro (Creator)
David J. Dabbs (Creator)
G. Lynis Dohm (Creator)
Charles W. Elton (Creator)
Edward G. Flickinger (Creator)
Tohru Fushiki (Creator)
Diane Meelheim (Creator)
Walter J. Pories (Creator)
Edward B. Tapscott (Creator)
Institution
East Carolina University (ECU )
Web Site: http://www.ecu.edu/lib/

Abstract: We have developed an in vitro muscle preparation suitable for metabolic studies with human muscle tissue and have investigated the effects of obesity and non-insulin-dependent diabetes mellitus (NIDDM) on glucose transport. Transport of 3-0- methylglucose and 2-deoxyglucose was stimulated approximately twofold by insulin in muscle from normal nonobese subjects and stimulation occurred in the normal physiological range of insulin concentrations. In contrast to insulin stimulation of 3-0-methylglucose and 2-deoxyglucose transport in muscle from normal nonobese subjects tissue from morbidly obese subjects with or without NIDDM were not responsive to insulin. Maximal 3-0-methylglucose transport was lower in muscle of obese than nonobese subjects. orbidly obese patients with or without NIDDM have a severe state of insulin resistance in glucose transport. The novel in vitro human skeletal muscle preparation herein described should be useful in investigating the mechanism of this insulin resistance. Originally published Journal of Clinical investigation Vol. 82 No. 2 Aug 1988

Additional Information

Publication
Other
Journal of Clinical Investigation. 82:2(August 1988) p. 486-494.
Language: English
Date: 2011
Keywords
glucose transport, human muscle tissue, Insulin resistance, muscle preparation

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An in vitro human muscle preparation suitable for metabolic studies. Decreased insulin stimulation of glucose transport in muscle from morbidly obese and diabetic subjects.http://hdl.handle.net/10342/3261The described resource references, cites, or otherwise points to the related resource.