Insulin receptors and insulin resistance in human pregnancy: evidence for a postreceptor defect in insulin action.
Pregnancy is accompanied, in its later stages, by physiological resistance to the action of insulin. We studied the potential contribution of altered insulin receptors to this phenomenon in 12 healthy pregnant women during their third trimester. For comparison, we studied the same women again several weeks postpartum. We also used a group of randomly chosen nonpregnant subjects as a control population. Women in this control group were studied during the luteal phase of the menstrual cycle. Plasma insulin and insulin to glucose ratios were significantly higher in the pregnant women. Insulin binding to peripheral blood monocytes was higher in pregnancy than postpartum in the majority of women, and as a group, the pregnant subjects showed significantly higher insulin binding than the nongravid subjects. This appeared to be due to a greater number of receptor sites per cell. We found no correlation between plasma insulin and insulin binding in pregnancy. We conclude that the insulin resistance of pregnancy is not attended by impaired binding of insulin to cellular receptors, at least in the monocyte. Our data suggest that the defect in insulin action lies at a site distal to the receptor.
D000328:Adult; D001786:Blood Glucose / Q000378:metabolism; D005260:Female; D005951:Glucose Tolerance Test; D006801:Humans; D007328:Insulin / Q000097:blood; D007333:Insulin Resistance; D008297:Male; D009000:Monocytes / Q000378:metabolism; D049590:Postpartum Period; D011247:Pregnancy; D011263:Pregnancy Trimester, Third; D011972:Receptor, Insulin / Q000378:metabolism*
D001786:Blood Glucose; D007328:Insulin; D011972:Receptor, Insulin