Plasma glucagon was examined after overnight fast and in response to 100 gm. oral glucose in sixteen subjects with normal carbohydrate metabolism and in ten gestational diabetics during week 30 to 40 of pregnancy and again five to eight weeks postpartum. In comparison to nulliparous, nongravid subjects, plasma glucagon after overnight fast was not significantly changed antepartum. However, on a pair-matched basis, small but significant and as yet unexplained reductions in plasma glucagon were evident during the postpartum period. Thus, hyperglucagonemia cannot be implicated in the accelerated starvation that is already manifest after overnight fast in late pregnancy, and altered basal glucagon does not constitute one of the diabetogenic factors of gestation. Following glucose administration, plasma glucagon in normal subjects subjects fell to a greater degree antepartum than postpartum. The paired observations suggest that this heightened suppressibility of circulating glucagon may be linked to the more prolonged hyperglycemia and hyperinsulinemia that occur during normal oral glucose tolerance in late pregnancy. In the gestational diabetics, oral glucose also elicited suppression of plasma glucagon antepartum, whereas suppressibility was not seen postpartum. Therefore, overt diabetogenesis in vulnerable subjects during pregnancy cannot be ascribed to lack of alpha cell suppressibility by glucose. Conversely, the exaggerated hyperinsulinemia and hyperglycemia in response to oral glucose during late pregnancy in gestational diabetics may obscure an intrinsically diminished sensitivity of their alpha cells to glucose.

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