Effects of insulin and NSILA on adipocytes of normal and diabetic rats: receptor binding, glucose transport and glucose metabolism.
Isolated fat cells from normal and streptozotocin-diabetic rats were compared with respect to metabolic indices (glucose-uptake, 3-0-methyl-glucose efflux) with and without stimulation by insulin and nonsuppressible insulin-like activity (NSI-LA). In addition, binding studies were carried out with these two hormones. Basal 14C-glucose oxidation and incorporation into lipids was decreased in diabetic cells and their response to insulin and NSILA was greatly reduced. Basal efflux of 3-0-methylglucose from diabetic cells was somewhat faster than from normal cells. The response to insulin and NSILA was less than in normal cells and it was delayed. The apparent number of insulin binding sites as well as their affinity for insulin was increased in diabetic cells. In contrast, the apparent number of binding sites for NSILA was decreased in diabetic cells and their affinity for NSILA was increased. In normal cells insulin enhanced binding of 125I-NSILA more markedly than in diabetic cells. These findings show that the rate-limiting step of impaired glucose metabolism (oxidation and lipogenesis) in diabetic fat cells is beyond the interaction of the hormone with the receptor. They suggest that the apparent number of hormone receptors (insulin, NSILA) on the cell membrane is regulated individually for each binding site.
D000273:Adipose Tissue / Q000378:metabolism*; D000818:Animals; D003920:Diabetes Mellitus / Q000139:chemically induced / Q000378:metabolism*; D005947:Glucose / Q000378:metabolism*; D007328:Insulin / Q000494:pharmacology*; D008297:Male; D008757:Methylglucosides / Q000378:metabolism; D051381:Rats; D011972:Receptor, Insulin / Q000378:metabolism; D013311:Streptozocin; D013002:Somatomedins / Q000494:pharmacology*
D005947:Glucose; D007328:Insulin; D008757:Methylglucosides; D011972:Receptor, Insulin; D013311:Streptozocin; D013002:Somatomedins