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The regulation of gonadotropin secretion was studied in anorexia nervosa, in voluntarily starving healthy subjects, and in the starved rat. In all cases, a hypothalamic disturbance is observed, resulting in an impaired ability to secrete gonadotropin-releasing hormone (GnRH) from the median eminence. This effect is weight-dependent in man and animals. The central neurofransmitters noradrenaline, dopamine, dynorphin, and prostaglandin E2 are involved in the regulation of GnRH release. A decreased activity of the catecholaminersic system and an increased activity of the endorphinergic system may be responsible for the impaired GnRH release. [ABSTRACT FROM AUTHOR]

The effect of starvation was studied in male Wistar rats. After only 2 days of food deprivation, LH concentrations in serum are greatly suppressed, while a significant increase in plasma corticosterone occurs after 5 days' starvation. The noradrenaline and dopamine turnover in the basal hypothalamus is decreased after 2 days. The catecholamine turnover is also reduced in the preoptic area, and in the median eminence. Injection of the catecholamine precursor L-dopa (100 mg/kg) can prevent the increase of plasma corticosterone, but not the decrease of LH. The alpha-agonist clonidine (150 micrograms/kg), but neither the beta-agonist salbutamol (0.5 mg/kg), nor the dopamine agonist apomorphine (1.0 mg/kg) can prevent the starvation induced corticosterone increase. The decrease of plasma LH is not influenced by the dopamine or noradrenaline agonists. From these data, it appears that a decreased activity of noradrenergic neurons may be responsible for the corticosterone increase in the plasma of starved rats.

The incretory testicular function was tested in 21 patient with varicocele aged 19 to 39 years. In one group baseline testosterone was measured, while a second group received a single injection of 5000 IU HCG. Testosterone was studied in peripheral plasma in the spermatic vein and in testicular tissue. Baseline values after stimulation were not different from those of normal controls. Testosterone in the spermatic vein rose, and in testicular tissue was greatly increased after HCG. The data provide further evidence that Leydig cell function is normal in patients with varicocele. In varicocele spermatogenesis is not impaired by low intratesticular testosterone concentrations.

The average capillary blood flow in the testes was found to be 181 microliter/min/g testis tissue (n = 19) in rats starved for 5 days and 273 microliter/min/g (n = 18, p less than 0.01) in the control group. Plasma testosterone was significantly decreased in the starved animals (1.00 +/- 0.06 ng/ml vs 5.43 +/- 0.63 ng/ml). When starved and control rats were stimulated with human chorion gonadotropin, testosterone values in plasma were greatly increased in both groups. The capillary blood flow was not altered. The date indicate that human chorion gonadotropin can stimulate testosterone production in the starved rat without influencing the reduced capillary blood flow.

The suppressing effect of dihydrotestosterone (DHT) on LH secretion in freshly castrated starved and control rats was studied by implanting DHT releasing silastic capsules of various sizes. Lower plasma levels of DHT are needed to suppress the castration induced LH increase in the starved animals. Intravenous injection of tritiated testosterone (18 muCi/100 g b.wt) revealed a significantly longer half-life (12.4 vs 8.9; P less than 0.05) in the starved rat. The ratio [3H]-DHT/[3H]-T in plasma at various times after injection was not significantly different in starved and control animals. The results indicate that the increased sensitivity of the T-LH feedback report earlier [1] cannot be explained by a greater conversion T-DHT in the starved male rat.