[Glucose oxidation and insulin receptors in isolated adipocytes from rats treated with progesterone and estradiol].
To find the cause of insulin resistance in pregnancy, the effects of estradiol (0.002 mg/day) treatment in male (n = 6) and ovariectomized (n = 8) rats, progesterone (0.05 mg/day) treatment in male (n = 9) and female (n = 6) and ovariectomized (n = 8) rats and combined estradiol and progesterone treatment in male (n = 7) and ovariectomized (n = 8) rats on (1-14C) glucose oxidation and insulin receptors in isolated fat cells were examined. All groups were treated for 5 days. Control rats were treated with the solvents. The results were as follows: 1) Decreased responsiveness to insulin on (1-14C) glucose oxidation was observed in adipocytes from male rats treated with estradiol and estradiol + progesterone, female rats treated with progesterone and ovariectomized rats treated with estradiol + progesterone. 2) There was no significant difference among the insulin bindings to adipocytes from rats treated with estradiol, progesterone and estradiol + progesterone. These results suggest that estradiol itself is potent in inducing insulin resistance in male rats, but in female rats progesterone primed with estradiol is necessary to induce insulin resistance, and that they may act at some post-receptor sites. These sex hormones may play an important role in inducing the insulin resistance in pregnancy.
D000273:Adipose Tissue / Q000378:metabolism*; D000818:Animals; D002369:Castration; D004958:Estradiol / Q000494:pharmacology*; D005260:Female; D005947:Glucose / Q000378:metabolism*; D008297:Male; D010084:Oxidation-Reduction; D011374:Progesterone / Q000494:pharmacology*; D051381:Rats; D011919:Rats, Inbred Strains; D011972:Receptor, Insulin / Q000378:metabolism*
D011374:Progesterone; D004958:Estradiol; D011972:Receptor, Insulin; D005947:Glucose