title: Insulin receptors in circulating erythrocytes and monocytes from women on oral contraceptives or pregnant women near term.
abstract: Altered carbohydrate metabolism occurs in women during pregnancy and in those using oral contraceptives (OC). Insulin binding to circulating erythrocytes and monocytes was studied in 77 nonobese, healthy women volunteers; they were divided into 4 groups: 1) late pregnant (n = 19),2) OC users taking 50 microgram estrogen daily (OC-50; n = 19),3) OC users taking 35 microgram estrogen daily (OC-35; n = 18), and 4) a control group (n = 21). All nonpregnant volunteers were in the luteal phase (days 18-21) of the menstrual cycle. Oral glucose tolerance tests were normal in all groups. Fasting plasma insulin was higher (P < 0.001) in the pregnant group, and plasma insulin responses to the oral glucose tolerance test were higher (P < 0.05) in the pregnant, OC-35, and OC-50 groups compared to that in the control group. The percentage of specific binding of [125I]insulin to 1.2 x 10(7) monocytes/ml (and 4.4 x 10(9) erythrocytes/ml) was similar in all groups (mean +/- SE): pregnant, 6.85 +/- 0.48% (6.85 +/- 0.59%); OC-35, (6.85 +/- 0.40%); OC-50, 6.95 +/- 0.55% (6.73 +/- 0.59%); and control 6.66 +/- 0.64% (7.17 +/- 0.44%). No correlation was found between insulin binding to erythrocytes and monocytes. Average affinity profiles and binding sites per cell (70/erythrocyte and 50,000/monocyte, respesctively) were similar in all groups. Since insulin binding to monocytes in decreased during the secretory phase of the menstrual cycle, one could extrapolate from our data that pregnant women will have lower insulin binding compared to nonpregnant women in the proliferative phase of the cycle; such a report has appeared recently (Beck-Nielsen et al., J Clin Endocrinol Metab 49: 810, 1979). Differences in plasma levels of estrogen and progesterone between the secretory and proliferative phases of the cycle are much smaller than between the nonpregnant state and late pregnancy. Therefore, it remains to be seen whether these steroid hormones would cause, by the same mechanism, a decrease in insulin binding (and insulin resistance) during late pregnancy and in the secretory phase of the cycle.
mesh_terms: D000328:Adult; D003276:Contraceptives, Oral / Q000494:pharmacology*; D003278:Contraceptives, Oral, Hormonal / Q000494:pharmacology*; D004912:Erythrocytes / Q000378:metabolism*; D004967:Estrogens / Q000494:pharmacology*; D005260:Female; D005951:Glucose Tolerance Test; D006801:Humans; D007328:Insulin / Q000097:blood; D007700:Kinetics; D009000:Monocytes / Q000378:metabolism*; D011247:Pregnancy; D011263:Pregnancy Trimester, Third; D011972:Receptor, Insulin / Q000187:drug effects / Q000378:metabolism*
chemical_list: D003276:Contraceptives, Oral; D003278:Contraceptives, Oral, Hormonal; D004967:Estrogens; D007328:Insulin; D011972:Receptor, Insulin