Concentrations of luteinizing hormone (LH) were measured in plasma samples obtained from rat fetuses after injecting them with synthetic gonadotrophin-releasing hormone (GnRH) in utero. On days 17½, 18½ or 19½ post-conception (p.c), fetuses in one uterine horn were injected subcutaneously with 100 ng GnRH in 2 μl of saline. Fetuses in the other uterine horn were injected with saline (four litters at each gestational age). Plasma samples were collected beginning 30 min after injection of GnRH. The concentration of LH in 20 μl of fetal plasma was measured by a microvolume radioimmunoassay. On day 17½ p.c, LH was detectable only in plasma samples of GnRH-injected fetuses. In l8½- and 19½-day-old fetuses LH reached detectable levels (>6 ng/ml) in most saline-injected fetuses. In 18½- and 19½-day-old fetuses of both sexes, plasma LH titers of GnRH-injected fetuses were significantly higher than in saline-injected littermates. On day 19½ GnRH-treated females had higher levels of plasma LH than similarly treated males. Thus fetal rat pituitaries were shown to have the capacity to release LH in vivo in response to circulating GnRH as early as 17½ days p.c.

Withdrawal of exogenous insulin for 24 h in ovariectomized, streptozotocin-diabetic rats significantly impairs estradiol uptake in whole homogenate fractions of hypothalamus-preoptic area and pituitary gland. Significant reductions in cell nuclear fractions from the same tissues are seen after 36 h of insulin deprivation. Subsequent reinstatement of insulin treatment does not yield full recovery of estradiol uptake after 24 h of insulin replacement. Fat content of the diet has no effect on brain or pituitary estradiol uptake in diabetic animals deprived of insulin for 36 h. Circulating levels of triglycerides, ketones, glucose, glycerol and free fatty acids were found to predict uptake levels to a significant extent, but no single metabolite is reliably predictive across tissues. These data demonstrate that insulin-dependent changes in brain and pituitary uptake of estradiol in rats are slow to develop, and they support the hypothesis that at least some of the reproductive dysfunctions observed in diabetic rats may be the result of impaired cell nuclear estradiol binding in hypothalamus and pituitary.

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