We found a match
Your institution may have access to this item. Find your institution then sign in to continue.
- Title
A possible mechanism of insulin resistance in the rat adipose cell with high-fat/low-carbohydrate feeding. Depletion of intracellular glucose transport systems.
- Authors
Hissin, Paul J.; Karnieli, Eddy; Simpson, Ian A.; Salans, Lester B.; Cushman, Samuel W.; Hissin, P J; Karnieli, E; Simpson, I A; Salans, L B; Cushman, S W
- Abstract
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.
- Publication
Diabetes, 1982, Vol 31, Issue 7, p589
- ISSN
0012-1797
- Publication type
journal article
- DOI
10.2337/diab.31.7.589