Discrepancy between glucose transport and transporters in human femoral adipocytes

Abstract

Obesity is known to be associated with insulin resistance in human and rat adipocytes. However, it is not known what are the perturbations in insulin action that contribute to disproportional femoral obesity. Thus femoral subcutaneous adipose tissue was obtained from lean women with various degrees of disproportional obesity, by liposuction. 3-O-methylglucose (3-O-methyl-D-glucopyranose) transport was measured in intact cells, and glucose transporter levels in plasma and low-density microsomal membranes were assessed using the cytochalasin B binding assay. A sixfold cellular enlargement was associated with increase in both basal and insulin-stimulated glucose transport activity in the intact cell, and a 300-600% increase in insulin stimulating effect per se. However, when glucose transporter levels were assessed, this cellular enlargement was accompanied by a 40-70% transporter depletion (in largest cells compared with smallest ones) in both subcellular fractions examined, from either basal or insulin-stimulated cells. This discrepancy, between increasing cellular glucose transport rates and relative depletion of transporter levels, suggests that these cells are not insulin resistant, as could be expected from their large size. A role for other factor(s), additional to glucose transporter levels, in the regulation of cellular glucose uptake rate is thus suggested.