Insulin binding and hexose transport in rat adipocytes. Relation to cell size

Diabetologia. 1980 Sep;19(3):234-41. doi: 10.1007/BF00275275.


Insulin binding, initial velocity of [14C]methylglucose transport, uptake of [14C]deoxyglucose and conversion of [U-14C]glucose to CO2, glyceride-glycerol and fatty acids were measured at 37 degrees C in adipocytes from rats of different weights (135-450 g) and therefore with different mean cell volumes (53-389 pl). Insulin binding per cell increased with increasing cell size and binding was 2.3 times higher in the largest cells than in the smallest cells with tracer alone. The difference was largely accounted for by an increase in the apparent affinity. Influx of methylglucose per cell increased with increasing cell size in the absence of insulin and remained constant as a function of cell size in its presence. The effect of insulin ranged from 11 fold in small cells to 3.5 fold in large cells. The rat of conversion of [U-14C]glucose to CO2 and lipids was about half of the rate of methylglucose transport under all conditions. In contrast, the uptake of deoxyglucose in insulin-stimulated cells decreased markedly with increasing cell size. Increasing cell size caused a small decrease in sensitivity which could be explained by a smaller amont of insulin bound per unit surface area. The results show that increasing cell size/animal weight causes changes in insulin binding which may explain changes in sensitivity. In addition, the hexose transport system is modified in a way which is not explained by changes in insulin binding. Finally, changes in deoxyglucose uptake with cell size do not parallel changes in methylglucose transport.

MeSH terms

  • Adipose Tissue / drug effects
  • Adipose Tissue / metabolism*
  • Animals
  • Biological Transport, Active
  • Cell Count
  • Deoxyglucose / metabolism
  • Glucose / metabolism
  • Hexoses / metabolism*
  • Insulin / metabolism*
  • Insulin / pharmacology
  • Kinetics
  • Male
  • Methylglucosides / metabolism
  • Rats
  • Receptor, Insulin / metabolism*


  • Hexoses
  • Insulin
  • Methylglucosides
  • Deoxyglucose
  • Receptor, Insulin
  • Glucose