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Objectives: Ghrelin, an endogenous growth hormone secretagogue, is a known accelerator of feeding behavior and suppresses pulsatile secretion of luteinizing hormone (LH) in ovariectomized rats. However, the mechanisms underlying this action remain unclear. We examined the effects of naloxone (NAL), a specific opioid antagonist, on the suppression of pulsatile LH secretion by ghrelin to determine whether β-endorphin (β-END) is involved in this suppressive effect. Methods: Ghrelin was administered intracerebroventricularly, and NAL was injected intravenously in ovariectomized rats; then, serum LH concentrations were measured by radioimmunoassay in blood samples drawn every 6 min for 2 h to analyze pulsatile secretion. Results: Administration of ghrelin significantly reduced mean LH concentration and pulse frequency. Coadministration of NAL with ghrelin significantly restored mean LH concentration and pulse frequency. Conclusion: Suppressive effect of intracerebroventricular injection of ghrelin on pulsatile LH secretion was mediated by β-END, suggesting that hypothalamic ghrelin suppressed pulsatile gonadotropin-releasing hormone secretion via β-END in female rats.

Pregnancy and lactation induce dynamic changes in maternal bone and calcium metabolism. A novel cytokine termed osteoprotegerin (OPG)/osteoclastogenesisinhibitory factor (OCIF) was recently isolated; this cytokine inhibits osteoclast maturation. To define the effects of pregnancy and lactation on circulating OPG/OCIF in mothers, we studied the changes in the levels of OPG/ OCIF as well as those of calcium-regulating hormones and biochemical markers of bone turnover in the maternal circulation during pregnancy (at 8-11 weeks, at 22-30 weeks, at 35-36 weeks and immediately before delivery) and lactation (at 4 days and at 1 month postpartum).Serum intact parathyroid hormone levels did not change and were almost within the normal range in this period. In contrast, serum 1,25-dihydroxyvitamin D levels increased with gestational age and were above the normal range during pregnancy. After delivery, they fell rapidly and significantly (P<0·01) to the normal range. The levels of serum bone-specific alkaline phosphatase, one of the markers of bone formation, increased with gestational age.After delivery, these levels were further increased at 1 month postpartum. The levels at 1 month postpartum were significantly higher than those at 8-11 and 22-30 weeks of pregnancy (P<0·01 and P<0·05 respectively). The levels of serum C-terminal telopeptides of type I collagen, one of the markers of bone resorption, did not change during pregnancy. After delivery, they rapidly and significantly (P<0·01) rose at 4 days postpartum, and had then fallen by 1 month postpartum. Circulating OPG/ OCIF levels gradually increased with gestational age and significantly (P<0·01) increased immediately before delivery to 1·40 0·53 ng/ml (means S.D.) compared with those in the non-pregnant, non-lactating controls (0·58 0·11 ng/ml). After delivery, they fell rapidly to 0·87 0·27 ng/ml at 4 days postpartum and had fallen further by 1 month postpartum.These results suggest that the fall in OPG/OCIF levels may be partially connected with the marked acceleration of bone resorption after delivery.

Background: Leptin, which is the product of the obese gene, is believed to play important roles in pubertal development and reproductive function in females. In a study using adult male rats, it was found that leptin stimulated secretion of gonadotropin from the pituitary in a dose-related manner. However, there has been no such study in female rats. Objective: To investigate the effects of leptin on the production of LH and FSH from the pituitary in female rats, using primary cultured pituitary cells. Methods: In this study, we determined body weight, serum leptin concentration and serum estradiol (E 2 ) concentration in female Wistar rats at 3, 5, 6, 7, 9 and 11 weeks of age, and cultured pituitary cells from 6-week-old female Wistar rats with leptin (0±10 27 mol/l) and GnRH (0 or 10 28 mol/l). Then basal and GnRH-stimulated extra-and intracellular LH and FSH were assayed by RIA. Results: Serum leptin concentration increased with increases in body weight and E 2 concentration. The pubertal serum leptin concentration was about 10 210 mol/l. At a lower or moderate concentration, leptin produced dose-related increases in both basal and GnRH-stimulated extraand intracellular LH and FSH in pituitary cells. At a concentration of 10 210 mol/l, leptin significantly P , 0X05 stimulated both basal and GnRH-stimulated extra-and intracellular LH and FSH. However, at greater concentrations, these effects diminished. Conclusions: These results indicated that leptin induced pituitary cells to produce and secrete both LH and FSH, with or without GnRH. The concentration of leptin that induced the greatest production of gonadotropins by pituitary cells was 10 210 mol/l, which was the same as the physiological pubertal concentration. Leptin may be involved in the onset of puberty. It is also conceivable that leptin may be a cause of ovulatory failure, not only in weight loss but also in weight gain.