LEPTIN ENHANCES PITUITARY GONADAL AXIS AFTER FOOD RESTRICTION IN MALE MONKEYS

瘦素是脂肪细胞的激素产物，其在 调节体重和新陈代谢。 在啮齿动物中， 脂肪调节物质作为代谢信号， 生殖轴，可以扭转食物的抑制作用 限制青春期年龄和促性腺激素分泌。 许多 人类临床研究已经报道了瘦素与 水平和代谢（和体重）的变化，但瘦素的作用，如果 在灵长类生殖轴上的任何位置都是未知的。 使用食品 我们的同事J.卡梅隆博士已经展示了限制性协议， 抑制恒河猴脉冲促黄体生成激素（LH），我们 设计了一项研究来确定瘦素是否可以逆转这种情况 食物限制性LH抑制。 我们让雄性猴子禁食（只喝水） (4-6 kg），猕猴，持续44小时（h），在此期间， 动物接受瘦素（134 g/kg BW/h，iv）或盐水。 每晚 使用小鼠间质细胞生物测定LH的模式 每20天采集一次血液样本， 分钟，两个12小时的时间段（发病前和发病后32-44小时）。 第一个18小时的快速）和每小时的快速。 在4只猴子中， 用生理盐水处理，LH脉冲完全被抑制 在禁食期间。 相反，4只接受瘦素治疗的猴子中有3只表现出 在禁食的最后8小时内出现明显的LH脉冲。 此外，意味着 在同一时期，瘦素治疗组的LH水平较高， 动物中比在媒介物处理的对照中。 血的模式 两组雄性个体的睾酮（T）显示， 与LH的趋势相似，尽管T的8小时平均水平 瘦素组和赋形剂组之间无差异（P > 0.05）。 我们在华盛顿大学的合作者正在确认 通过定位细胞， 含有瘦素受体mRNA。 结果表明，在灵长类动物中， 在啮齿类动物中，瘦素是生殖轴的代谢信号 并且含有神经肽Y和/或阿黑皮素原的细胞 可能是瘦素在大脑中作用的介质。 今后的努力将 重点是完成和公布调查结果，因为研究报告 可以为理解 饮食失调和某些生殖问题。

Leptin is a hormonal product of adipocytes that has a role in the regulation of body weight and metabolism. In rodents, this fat-regulating substance acts as a metabolic signal to the reproductive axis and can reverse the inhibitory effects of food restriction on pubertal age and gonadotropin secretion. Numerous clinical studies in humans have reported correlations between leptin levels and metabolic (and weight) changes, but the role of leptin, if any, on the primate reproductive axis is unknown. Using a food restriction protocol that our colleague Dr. J. Cameron had shown to inhibit pulsatile luteinizing hormone (LH) in rhesus monkeys, we designed a study to determine if leptin could reverse this food-restricted LH inhibition. We fasted (water only) male monkeys (4-6 kg), Macaca mulatta, for 44 hours (h), during which time the animals received either leptin (134 g/kg BW/h, iv) or saline. Nightly patterns of LH were bioassayed using the mouse interstitial cell testosterone assay in blood samples that were collected every 20 minutes for two 12 h periods (before and 32-44 h after onset of the fast) and hourly for the first 18 h of the fast. In 4 of 4 monkeys treated with saline, there was complete suppression of LH pulses during fasting. Conversely, 3 of 4 leptin-treated monkeys showed distinct pulses of LH during the last 8 h of the fast. Moreover, mean LH levels during the same period were higher in the leptin-treated animals than in the vehicle-treated controls. Patterns of blood testosterone (T) in the individual males of the two groups showed similar trends to those of LH, although the 8-h mean levels of T between the leptin- and vehicle-groups were not different (P > 0.05). Our collaborators at the University of Washington are identifying possible neural targets for leptin's action by locating cells that contain leptin receptor mRNA. The results suggest that in primates, as in rodents, leptin is a metabolic signal to the reproductive axis and that neuropeptide Y and/or proopiomelanocortin containing cells may be mediators of leptin's action in the brain. Future efforts will focus on completion and publication of the findings, since the studies may provide a foundation for understanding relationships between eating disorders and certain reproductive problems.