Insulin binding and action in adipocytes of pregnant rats: evidence that insulin resistance is caused by post-receptor binding defects.
Insulin resistance was investigated in the adipose cell of rats which were at days 16 and 20 of pregnancy. Data are presented to relate insulin binding and biological effect, which was evaluated by the ability of insulin to stimulate [1-14C]glucose oxidation. Adipocytes from pregnant rats bound more insulin than fat cells from control (non-pregnant) animals and the number of insulin receptors per adipocyte increased during pregnancy. Basal glucose oxidation rate was decreased at 16 and 20 days of pregnancy: however, the dose-response curve for insulin-stimulated glucose oxidation was significantly depressed only after 20 days of pregnancy. The concentration at which insulin increased glucose oxidation by 50% increased with the duration of pregnancy. We conclude that during pregnancy in the rat the adipocyte response to insulin was decreased, despite an increase in insulin binding. This result suggests that a major determinant of insulin resistance in rat adipocytes during pregnancy is present after the initial insulin-receptor interaction. Consequently, a post-receptor defect may be largely responsible for the insulin resistance.
D000273:Adipose Tissue / Q000166:cytology / Q000187:drug effects / Q000378:metabolism*; D000818:Animals; D004305:Dose-Response Relationship, Drug; D005260:Female; D005947:Glucose / Q000378:metabolism; D066298:In Vitro Techniques; D007328:Insulin / Q000378:metabolism* / Q000494:pharmacology; D007333:Insulin Resistance; D010084:Oxidation-Reduction; D011247:Pregnancy; D011270:Pregnancy, Animal; D051381:Rats; D011919:Rats, Inbred Strains
D007328:Insulin; D005947:Glucose