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Research Article Free access | 10.1172/JCI113622

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

G L Dohm, E B Tapscott, W J Pories, D J Dabbs, E G Flickinger, D Meelheim, T Fushiki, S M Atkinson, C W Elton, and J F Caro

Department of Biochemistry, School of Medicine, East Carolina University, Greenville, North Carolina 27858.

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Department of Biochemistry, School of Medicine, East Carolina University, Greenville, North Carolina 27858.

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Department of Biochemistry, School of Medicine, East Carolina University, Greenville, North Carolina 27858.

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Department of Biochemistry, School of Medicine, East Carolina University, Greenville, North Carolina 27858.

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Department of Biochemistry, School of Medicine, East Carolina University, Greenville, North Carolina 27858.

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Department of Biochemistry, School of Medicine, East Carolina University, Greenville, North Carolina 27858.

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Department of Biochemistry, School of Medicine, East Carolina University, Greenville, North Carolina 27858.

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Department of Biochemistry, School of Medicine, East Carolina University, Greenville, North Carolina 27858.

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Department of Biochemistry, School of Medicine, East Carolina University, Greenville, North Carolina 27858.

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Department of Biochemistry, School of Medicine, East Carolina University, Greenville, North Carolina 27858.

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First published August 1, 1988 - More info

Published in Volume 82, Issue 2 (August 1, 1988)
J Clin Invest. 1988;82(2):486–494. doi:10.1172/JCI113622.
Copyright © 1988, The American Society for Clinical Investigation.

Published August 1, 1988
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-O-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-O-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-O-methylglucose transport was lower in muscle of obese than nonobese subjects. Morbidly 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.

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