Insulin-deficient states are associated with an impaired function of the hypothalamic-pituitary-gonadal axis, but the mechanisms underlying hypothalamic alterations in experimental diabetes are still unknown. We investigated the effect of glucose concentrations, in the presence and absence of insulin, on LHRH release from perifused hypothalamic fragments from female adult ovariectomized rats. Glucose and insulin were added to the perifusion medium (Earle’s, pH 7.4, gassed with 95% O₂/5% CO₂, flow rate 50 µl/min). When glucose was absent (in the presence of insulin 10 mU/1), LHRH release was reduced, peak levels being <5 pg/100 µl. The addition of glucose (100 and 300 mg/dl), in the absence of insulin, resulted in peak LHRH levels fluctuating around 35 pg/100 µl (p < 0.05 vs. glucose 0 mg/dl). When glucose (100 or 300 mg/dl) and insulin (10 mU/1) were combined, an eightfold increase in peak LHRH values was observed, and peak levels reached 300 pg/ 100 µl (p < 0.05 vs. glucose 100 and 300 mg/dl alone). In conclusion, LHRH release by perifused hypothalamic fragments is dramatically increased by low concentrations of insulin; this occurs only when glucose is available. Acutely elevated glucose levels (from 100 to 300 mg/dl) do not affect LHRH release.

Thus, treatment of pregnant rats with L-NAME, has an important effect on systolic blood pressure and on the physiology of reproduction, mainly in the third stage of pregnancy.

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