Fasting-Induced Changes in Pulsatile Luteinizing Hormone (LH) Secretion in Male Rats. The Role of Testosterone and the Hypothalamic Paraventricular Nucleus.

Abstract

Abstract.We have previously shown that 48-h fasting profoundly suppresses pulsatile LH secretion in female rats in the presence of estrogen, and that the paraventricular nucleus (PVN) is an estrogen action site mediating this inhibition. The present study determined whether fasting suppresses pulsatile LH secretion in male rats in a testosterone-dependent manner, and whether the PVN is involved in the fasting-induced changes in pulsatile LH release. Mean LH concentrations and baseline levels of LH pulses were significantly reduced by 48-h fasting in castrated males implanted with various length (6, 12, and 24 mm) of subcutaneous testosterone implants. LH pulse frequency was significantly lower in fasted rats with a 24-mm testosterone implant compared with unfasted controls. On the contrary, mean LH levels and the amplitude and baseline of LH pulses were significantly increased by fasting in castrated rats without testosterone treatment. PVN lesions partially blocked the inhibitory effect of fasting on LH release in the testosterone-implanted rat model. In addition, local implantation of testosterone or estradiol into the PVN reversed fasting-induced increase in both mean LH levels and the pulse amplitude in castrated males, but did not cause a further suppression of these pulse parameters. These results suggest that testosterone is required to suppress LH pulses during fasting in the male rat. The PVN may mediate, at least partly, the fasting-induced inhibition of LH secretion, and is not the single steroid feedback site mediating the fasting-induced suppression of LH secretion in the male.

Effect of Fasting on c-Fos Expression in the Hypothalamic Nuclei and Nucleus of the Solitary Tract in Male Rats: Time Course Study and the Role of Testosterone.

“…These data suggest that c-Fos expression was induced by a fasting signal after 6 h of fasting (at 1900 h, when the lights went out) and not by a circadian signal. These data also suggest that the fasting signal begins to stimulate neuronal activity in discrete regions, such as the PVN, NTS, SON and AMYG, at a defined time from the start of fasting, activating neural pathways involved in fasting-related events, such as suppression of LH release as shown in our recent study [8]. The absence of the increase in the FLI at later fasting times is consistent with earlier reports showing that 15-, 22-, 24-, 27-and 48-h food deprivation in intact male rats did not significantly induce FLI in the PVN and NTS [10][11][12].…”

“…Aseptically, rats (n=36) were bilaterally castrated under ether anesthesia and half of them were subcutaneously implanted with Silastic tubing (i.d., 2.6 mm; o.d., 4.9 mm; 12 mm in length, Dow Corning, Midland, MI, USA) containing crystalline testosterone (Sigma Chemical Co., St. Louis, MO, USA). We have previously shown that rats subjected to this testosterone treatment had plasma testosterone concentrations of 4.39 ± 0.09 ng/ml (mean ± SEM, n=4) [8].…”

“…Intracerebroventricular (icv) administration of CRH antagonist removes the inhibitory effect of 48-h fasting on LH secretion [17]. Recently, we have shown that PVN lesions partially restored the fasting-induced inhibition of LH release in testosterone-treated castrates suggesting that the PVN, at least in part, mediates fasting-induced LH suppression [8]. Thus, it seems likely that activation of CRH neurons in the PVN induces the fasting-induced suppression of LH release observed in testosterone-treated castrates.…”

“…We have previously reported that 48-h fasting suppresses pulsatile luteinizing hormone (LH) secretion in female rats in an estrogen-dependent manner [6,7]. Using the same fasting conditions in male rats, 48-h fasting inhibits LH release in a testosterone-dependent manner [8]. These studies suggest that the cascade of events culminating in suppression of LH secretion during fasting depends upon the steroidal status in both genders.…”

Minor involvement of somatic growth in the onset of puberty of Hatano high- and low-avoidance rats

“…Since the amount of milk secretion by LAA dams is smaller than that of HAA dams and probably smaller than that of SD dams, LAA pups under their biological dams might be maintained in a slightly poor nutritional condition and this could affect neurosecretory activity. In contrast to female LAAs, fostering did not affect the timing of puberty in male LAAs, although it was reported that the nutritional disruption affected pulsatile LH release in male rats (Badger et al 1985, Tsukamura et al 2000. Causes of the different effects of the fostering on the timing of puberty in male and female LAAs might be explained by a difference in the duration of the period from weaning to the occurrence of puberty; however, the present results demonstrate a sex difference in the effects of the fostering on the timing of puberty.…”