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Free access | 10.1172/JCI110674

Mechanism of Insulin-resistant Glucose Transport Activity in the Enlarged Adipose Cell of the Aged, Obese Rat: RELATIVE DEPLETION OF INTRACELLULAR GLUCOSE TRANSPORT SYSTEMS

Paul J. Hissin, James E. Foley, Lawrence J. Wardzala, Eddy Karnieli, Ian A. Simpson, Lester B. Salans, and Samuel W. Cushman

Cellular Metabolism and Obesity Section, National Institute of Arthritis, Diabetes, and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20205

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Cellular Metabolism and Obesity Section, National Institute of Arthritis, Diabetes, and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20205

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Cellular Metabolism and Obesity Section, National Institute of Arthritis, Diabetes, and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20205

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Cellular Metabolism and Obesity Section, National Institute of Arthritis, Diabetes, and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20205

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Cellular Metabolism and Obesity Section, National Institute of Arthritis, Diabetes, and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20205

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Cellular Metabolism and Obesity Section, National Institute of Arthritis, Diabetes, and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20205

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Cellular Metabolism and Obesity Section, National Institute of Arthritis, Diabetes, and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20205

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Published October 1, 1982 - More info

Published in Volume 70, Issue 4 on October 1, 1982
J Clin Invest. 1982;70(4):780–790. https://doi.org/10.1172/JCI110674.
© 1982 The American Society for Clinical Investigation
Published October 1, 1982 - Version history
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Abstract

The effects of increasing cell size on glucose transport activity and metabolism and on the concentrations of glucose transport systems in both the plasma and low density microsomal membranes in isolated adipose cells from the aging rat model of obesity have been examined. Glucose transport activity was assessed by measuring l-arabinose transport and the concentration of glucose transport systems estimated by measuring specific d-glucose-inhibitable cytochalasin B-binding. Basal glucose transport activity increases from 0.3 to 1.4 fmol/cell/min with a 10-fold increase in cell size, but remains constant per unit cellular surface area and is accompanied by a constant 5 pmol of glucose transport systems/mg of membrane protein in the plasma membrane fraction. Maximally insulin-stimulated glucose transport activity, on the other hand, remains constant at 2.3 fmol/cell per min with increasing cell size, but markedly decreases per unit cellular surface area and is accompanied by a decrease from 30 pmol of glucose transport systems/mg of plasma membrane protein to the basal level. These diminished effects of insulin on glucose transport activity and the number of glucose transport systems in the plasma membrane fraction in enlarged cells are paralleled by an 80% decrease in the basal number of glucose transport systems/mg of membrane protein in the low density microsomal membrane fraction, the source of those glucose transport systems appearing in the plasma membrane in response to insulin. The effects of cell size on the metabolism of a low concentration of [1-14C]glucose (0.56 mM) directly parallel those on glucose transport activity and the concentration of glucose transport systems in the plasma membrane fraction, and are not associated with significant alterations in the cell's sensitivity to insulin. Thus, adipose cellular enlargement is accompanied by the development of a marked “insulin resistance” at the glucose transport level, which may be the consequence of a relative depletion of glucose transport systems in the intracellular pool.

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