After 5 days of starvation, the body weight of adult male Wistar rats was on the average 34% lower than that of control animals. Luteinizing hormone (LH) and testosterone in plasma were significantly decreased in the starved animals (\m=-\95%and \m=-\82%on the average).The in vivo response to hCG (10 IU per animal for 3 days) was not diminished in the starved rats. The in vivo stimulation with synthetic LRH (100, 200, 500, 1000 ng/kg body weight iv) caused an increase of LH at all doses. The response however was quantitatively decreased in starved rats. The pituitary content of the LH and the LRH content in the preoptic area and in the hypothalamus were not influenced by starvation; the LRH content, however, was greatly increased in the median eminence (33.2 \m=+-\11.7 versus 15.5 \m=+-\ 7.1 ng per mg protein). The feedback was studied by castrating the animals and implanting silastic tubes of various sizes which released testosterone. The plasma levels of testosterone were proportional to the length of the capsules used. LH levels increased greatly (> 90 ng/ml) when testosterone levels were lower than 1.80 ng/ml in the control rats. The straved rats tolerated testosterone levels as low as 1.00 ng/ml plasma before LH was elevated. The LRH content in the median eminence increased in starved and control animals when plasma levels of testosterone dropped below 1.80 ng/ml. These data indicate that the increased sensitivity of the testosterone-LH feedback may be caused by an impaired release of LRH from the median eminence. We have recently observed (Pirke et al. 1979a) that the 24-hour sleep-wake pattern of plasma LH is disturbed in patients with anorexia nervosa. This impairment of LH secretion is strongly dependent on weight deficit. Similar observations were made bv Beumont et al. (1976), who found a weight dependence in the LRH test and by Frisch (1979), who observed a critical weight threshold below which patients recovering from anorexia nervosa did not resume cyclic ovarian function. It thus appears that the dysfunction of the hypothalamicpituitary-gonadal system in patients with anorexia is a consequence of weight loss. This assumption is further supported by the observation of Vigersky et al. (1977) that simple weight loss due to dieting brings about similar endocrine dysfunctions as ob¬ served in anorexia nervosa. In order to obtain an understanding of the hypothalamic dysfunction brought about by starvation, we have studied the rat as an animal model. This species appears to be an adequate model, since LH and gonadal hor¬ mone secretion are depressed in the starved rat Male Wistar rats weighing 200 to 220 g were obtained from the Central Institute for Laboratory Animals, Hannover, Germany. Six rats were housed in a cage under 8 h dark, 16 h light schedule. Altrumin rat food and water were available ad libitum for the control rats, while starved rats only got water. Unless otherwise stated, the rats were sacrificed by decapitation between 8.00 and 11.00 immediately after removal from their cages. Tru...

Zusammenfassung Testosteron im peripheren Plasma, der Vena spermatica und im Hodengewebe ohne und nach HCG‐Stimulation bei Patienten mit Varikozele. Bei 21 Patienten im Alter von 19 bis 39 Jahren wurde die inkretorische Hodenfunktion untersucht. Bei einer Gruppe wurde Testosteron im Plasma ohne vorherige Stimulation gemessen, während die zweite Gruppe eine einmalige Injektion von 5000 IU HCG erhielt. Testosteron wurde zugleich in der Vena spermatica und im testikulären Gewebe untersucht. Im Plasma waren die Werte ohne und nach Stimulation nicht verschieden von denen einer gleichaltrigen Kontrollgruppe. In der Vena spermatica und im Testesgewebe stiegen die Testosteron‐Konzentrationen nach HCG‐Stimulation sehr stark an. Die hier vorgelegten Daten sind weitere Hinweise darauf, daß die Leydig Zell‐Funktion bei Patienten mit Varikozele normal ist und daß die Spermatogenese nicht durch ein Absinken der testikulären Testosteronkonzentration beeinträchtigt ist.

No abstract

Abstract. 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 α-agonist clonidine (150 μg/kg), but neither the β-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.