EstrogenおよびProgesterone投与ラットにおけるInsulin抵抗性に関する検討:Euglycemic Glucose Clamp法を用いて

概要

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To clarify the mechanism of insulin resistance in pregnancy, we have used the eu-glycemic glucose clamp technique in estradiol (E) treatment (n =6), progesterone (P) treatment (n=28), and Control (n =29) female rats. E (10μg/day) and P (10mg/day) were injected subcutaneously into female rats for 14 days, to increase E and P concentrations to pregnant levels. Glucose production and glucose utilization were measured by using [3-3F] -glucose. The results were as follows, 1) Glucose production was almost suppressed at hyperinsu-linemia (11,000μU/ml) both Control and P treatment rats. Then at hyperinsulinemia, glucose utilization rate was almost equal to glucose infusion rate. 2) In P treatment rats glucose utilization was significantly lower (p<0.05) than in Control rats at hyperinsulinemia (11,000 μU/ml). 3) In P treatment rats glucose infusion rate was significantly lower than in Control rats at plasma insulin concentrations of 1,000μU/ml (p<0.02), and 11,000μU/ml (p<0.01), and lower than in E treatment rats at plasma insulin concentrations of 11,000μU/ml (p< 0.05). 4) In a dose-response curve for the effects of four different concentrations of insulin on glucose infusion rate, the insulin resistance induced by progesterone is characterized by a decreased responsiveness to insulin. The results suggest that progesterone may play an important role in inducing insulin resistance in pregnancy.
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