Receptor binding and effects of insulin and NSILA-S on glucose transport and metabolism in adipocytes from hypophysectomized rats.
Isolated fat cells from normal and hypophysectomized rats have been compared with respect to: 1) binding of insulin and NSILA-S, and 2) effects of these two hormones on glucose transport and metabolism. Although both insulin and NSILA levels were decreased in the serum of hypophysectomized rats, insulin binding was decreased to about 63% of normal, whereas NSILA-S binding remained unchanged. Basal lipogenesis was similar in adipocytes of normal and hypophysectomized rats, but was not stimulated by either insulin or NSILA-S. Similarly, neither of the two hormones stimulated the net gas exchange of "intact" fat pads from hypophysectomized rats. In striking contrast to these findings, 3-O-methylglucose transport in unstimulated fat cells of hypophysectomized rats proceeded at a maximal  rate which was not further enhanced by insulin or NSILA-S. These results suggest that the lack of one or several hormones of the pituitary causes one or several enzyme deficiencies responsible for the limited rate of lipogenesis, which otherwise would proceed at a very rapid rate because of unrestrained glucose transport.
D000273:Adipose Tissue / Q000378:metabolism*; D000818:Animals; D001667:Binding, Competitive; D001693:Biological Transport, Active; D005947:Glucose / Q000494:pharmacology*; D007016:Hypophysectomy; D066298:In Vitro Techniques; D007328:Insulin / Q000378:metabolism*; D008297:Male; D008757:Methylglucosides / Q000378:metabolism; D051381:Rats; D011972:Receptor, Insulin / Q000378:metabolism*; D013002:Somatomedins / Q000378:metabolism*
D005947:Glucose; D007328:Insulin; D008757:Methylglucosides; D011972:Receptor, Insulin; D013002:Somatomedins