Zamorano P L, Mahesh V B, De Sevilla L M, Chorich L P, Bhat G K, Brann D W
Department of Physiology and Endocrinology, Medical College of Georgia, Augusta 30912-3000, USA.
Neuroendocrinology. 1997 Mar;65(3):223-8. doi: 10.1159/000127276.
The obese gene (ob) product, leptin, has recently been shown to be produced by adipocytes and to circulate in the plasma acting as a hormone to modulate appetite and metabolism. Intriguingly, the ob/ob mutant female mouse, which does not produce an active form of leptin due to a mutation of the ob gene, has been shown to be acyclic and sterile. This sterility can be reversed by treatment with recombinant leptin, but not by diet restriction--suggesting that leptin is required for normal reproductive function. The mechanism(s) whereby leptin modulates reproductive function are unknown; however, it is possible that leptin could directly regulate reproductive tissues. To determine whether endocrine and neuroendocrine tissues could be targets for leptin action, we examined whether these tissues express the leptin receptor mRNA by utilizing reverse-transcription polymerase chain reaction (RT-PCR) analysis in selected tissues from the male and female rat. The results revealed that the leptin receptor mRNA transcript is highly expressed in the ovary, uterus and testis, moderately expressed in the hypothalamus and anterior pituitary, with low to no expression in the adrenal. The RT-PCR results were confirmed by Northern analysis. Furthermore, immortalized GnRH (GT1-7 and NLT) neurons and ovarian granulosa cells were also demonstrated by RT-PCR analysis to express the leptin receptor, suggesting that GnRH neurons and steroid-producing cells of the ovary could be targets for leptin action. Immunohistochemical studies revealed dense immunolocalization of the leptin receptor in the choroid plexus, and interestingly, in the arcuate nucleus/median eminence of the female rat--a key sit in the control of feeding and reproduction. Finally, treatment of the ob/ob mouse with recombinant leptin (0.15 mg/kg/day x 2 weeks) was found to markedly upregulate side chain cleavage and 17 alpha-hydroxylase mRNA levels in the ovary, demonstrating that leptin, acting either through a direct or indirect mechanism, can regulate gene expression in reproductive tissues.
肥胖基因(ob)的产物瘦素,最近已被证明由脂肪细胞产生,并作为一种调节食欲和新陈代谢的激素在血浆中循环。有趣的是,ob/ob突变雌性小鼠由于ob基因突变而不产生活性形式的瘦素,已被证明是无发情周期且不育的。这种不育可通过重组瘦素治疗逆转,但不能通过饮食限制逆转,这表明瘦素是正常生殖功能所必需的。瘦素调节生殖功能的机制尚不清楚;然而,瘦素有可能直接调节生殖组织。为了确定内分泌和神经内分泌组织是否可能是瘦素作用的靶点,我们利用逆转录聚合酶链反应(RT-PCR)分析,检测了雄性和雌性大鼠选定组织中这些组织是否表达瘦素受体mRNA。结果显示,瘦素受体mRNA转录本在卵巢、子宫和睾丸中高度表达,在下丘脑和垂体前叶中度表达,在肾上腺中低表达或不表达。RT-PCR结果通过Northern分析得到证实。此外,RT-PCR分析还表明,永生化的促性腺激素释放激素(GnRH)神经元(GT1-7和NLT)和卵巢颗粒细胞也表达瘦素受体,这表明GnRH神经元和卵巢的类固醇生成细胞可能是瘦素作用的靶点。免疫组织化学研究显示,瘦素受体在脉络丛中有密集的免疫定位,有趣的是,在雌性大鼠的弓状核/正中隆起中也有密集的免疫定位,而弓状核/正中隆起是控制进食和生殖的关键部位。最后,发现用重组瘦素(0.15 mg/kg/天×2周)治疗ob/ob小鼠可显著上调卵巢中侧链裂解酶和17α-羟化酶mRNA水平,表明瘦素通过直接或间接机制作用,可调节生殖组织中的基因表达。