Insulin receptors and placental proteins in normal and gestational-diabetic pregnancies.

We studied 125I-insulin binding to monocytes and plasma levels of two trophoblastic proteins from 38 pregnant patients with varying degrees of carbohydrate intolerance, including 10 pregnant controls (PC), 17 Class A diabetics (A), 6 Class B diabetics - prior to insulin therapy (B-noRx) and 5 different Class B diabetics studied 1-6 weeks following initiation of insulin therapy (B-Rx). All studies were performed in the second half of pregnancy. In comparison to six age- and weight-matched nonpregnant controls (NPC), insulin binding to monocytes was somewhat higher in both PC and A. B.noRx patients had significantly lower tracer binding than did PC (0.71 +/- 0.3 vs 2.6 +/- 0.6%/10(7) cells, p less than 0.01). Insulin treatment of Class B patients restored insulin tracer binding levels to above normal. Levels of human placental lactogen (HPL) were significantly elevated in B-noRx patients compared to PC and A and were lowered to levels comparable to normal in insulin-treated B patients. A highly significant inverse relationship existed between HPL levels and the tracer binding of insulin for all patients studied (r = -0.52, p less than 0.005). Elevations of pregnancy-specific beta 1 glycoprotein were observed in patients with mild carbohydrate intolerance (A) as well as Bno-Rx, but were comparable to normal in those B-patients receiving insulin therapy. There were no significant differences of insulin binding or receptor number in the patient groups in the postpartum state. This further supports the hypothesis that placental factors may be responsible for the insulin binding defects seen in gestational diabetes.