The effects of high-fat/low-carbohydrate feeding on glucose transport activity and on the concentrations of glucose transport systems in the plasma and low-density microsomal membranes in isolated rat adipose cells have been examined. Glucose transport activity was assessed by measuring 3-O-methylglucose transport and the concentration of glucose transport systems estimated by measuring specific D-glucose-inhibitable cytochalasin B-binding. Basal glucose transport activity is not significantly influenced by high-fat/low-carbohydrate relative to low-fat/high-carbohydrate feeding and is accompanied by a constant 10 pmol of glucose transport systems/mg of membrane protein in the plasma membrane fraction. In contrast, maximally insulin-stimulated glucose transport activity decreases from 4.72 to 2.29 fmol/cell/min and is accompanied by a decrease from 44 to 26 pmol of glucose transport systems/mg of plasma membrane protein. These diminished effects of insulin on glucose transport activity and the concentration of glucose transport systems in the plasma membrane fraction are paralleled by a 48% 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. Thus, the “insulin-resistant” glucose transport of the adipose cell with high-fat/low-carbohydrate feeding may be the consequence of a depletion of glucose transport systems in the intracellular pool.
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July 01 1982
A Possible Mechanism of Insulin Resistance in the Rat Adipose Cell with High-Fat/Low-Carbohydrate Feeding: Depletion of Intracellular Glucose Transport Systems
Paul J Hissin;
Paul J Hissin
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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Eddy Karnieli;
Eddy Karnieli
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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Ian A Simpson;
Ian A Simpson
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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Lester B Salans;
Lester B Salans
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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Samuel W Cushman
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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Address reprint requests to Samuel W. Cushman at the above address.
1
A preliminary report of this work was presented at the 41st Annual Meeting of the American Diabetes Association, Cincinnati, Ohio, June 1981.
Citation
Paul J Hissin, Eddy Karnieli, Ian A Simpson, Lester B Salans, Samuel W Cushman; A Possible Mechanism of Insulin Resistance in the Rat Adipose Cell with High-Fat/Low-Carbohydrate Feeding: Depletion of Intracellular Glucose Transport Systems. Diabetes 1 July 1982; 31 (7): 589–592. https://doi.org/10.2337/diab.31.7.589
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