Insulin binding, glucose oxidation, and methylglucose transport in isolated adipocytes from pregnant rats near term.
To elucidate the mechanism of insulin resistance during late pregnancy, we studied [125I]iodoinsulin binding, [1-14C]glucose oxidation, and 3-O-[methyl-14C]glucose transport in adipocytes isolated from pregnant rats on day 19 or 20 of gestation. Neither the affinity or number of insulin receptors on pregnant rat adipocytes differed from those on age-matched nonpregnant female rats. Insulin-stimulated glucose oxidation was reduced in the pregnant rat adipocytes. The maximum velocity of insulin-stimulated methylglucose transport was also significantly reduced in the pregnant rat adipocytes. These results suggest that insulin resistance in isolated adipocytes from pregnant rats near term is caused by some postreceptor changes, one of which is a reduction in the number and/or mobility of insulin-stimulated hexose transporters.
D019325:3-O-Methylglucose; D000273:Adipose Tissue / Q000166:cytology / Q000378:metabolism*; D000818:Animals; D001692:Biological Transport; D002469:Cell Separation; D005260:Female; D005947:Glucose / Q000378:metabolism*; D007328:Insulin / Q000378:metabolism*; D007743:Labor, Obstetric; D008757:Methylglucosides / Q000378:metabolism*; D008759:Methylglycosides / Q000378:metabolism*; D010084:Oxidation-Reduction; D011247:Pregnancy; D051381:Rats; D011919:Rats, Inbred Strains
D007328:Insulin; D008757:Methylglucosides; D008759:Methylglycosides; D019325:3-O-Methylglucose; D005947:Glucose