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瘦素在印度短鼻果蝠胚胎发育延迟中的作用。

Role of leptin in delayed embryonic development in the Indian short-nosed fruit bat, Cynopterus sphinx.

机构信息

Department of Zoology, Banaras Hindu University, Varanasi, UP 221 005, India.

出版信息

Gen Comp Endocrinol. 2010 Aug 1;168(1):36-45. doi: 10.1016/j.ygcen.2010.04.002. Epub 2010 Apr 22.

Abstract

An adiposity-associated rise in leptin occurs at the time of delayed embryonic development in Cynopterus sphinx. The aim of present study was to examine the mechanism by which leptin may inhibit progesterone, and therefore could be responsible for delayed development. The study showed a significant increase in circulating leptin level during the period of increased fat accumulation, which coincided with significant decrease in serum progesterone level and delayed embryonic development in C. sphinx. The study showed increased Ob-R expression in the corpus luteum and in the utero-embryonic unit during the period of delayed embryonic development. The in vitro study showed suppressive effect of leptin on progesterone synthesis. The effect of high dose of leptin on ovarian steroidogenesis was found to be mediated through decreased expression of StAR and LH-R proteins in the ovary. The treatment with leptin caused increased expression of STAT 3 and iNOS proteins in the ovary, which correlated with decreased expression of StAR protein in the ovary. The inhibitory effects of leptin on progesterone synthesis in the ovary are thus mediated through STAT 3 and iNOS-NO signaling pathways. This study further demonstrated low expression of PCNA coinciding with the increased concentration of the leptin receptor in the utero-embryonic unit and high circulating leptin level during November. In conclusion, adiposity associated increased leptin level during November-December might play role in suppressing progesterone synthesis in the corpus luteum as well as suppressing the rate of cell-proliferation in the utero-embryonic unit thereby causing delayed embryonic development in C. sphinx.

摘要

在大蹼足蝠胚胎发育延迟时期,瘦素水平会随着肥胖而升高。本研究旨在探讨瘦素抑制孕酮的机制,以及其是否可能导致胚胎发育延迟。研究表明,在脂肪积累增加期间,循环瘦素水平显著升高,同时血清孕酮水平显著下降,胚胎发育延迟。研究表明,在胚胎发育延迟期间,黄体和子宫-胚胎单位中的 Ob-R 表达增加。体外研究表明,瘦素对孕酮合成具有抑制作用。高剂量瘦素对卵巢类固醇生成的作用是通过降低卵巢中 StAR 和 LH-R 蛋白的表达来介导的。瘦素处理导致卵巢中 STAT3 和 iNOS 蛋白表达增加,与卵巢中 StAR 蛋白表达减少相关。因此,瘦素对卵巢中孕酮合成的抑制作用是通过 STAT3 和 iNOS-NO 信号通路介导的。本研究进一步表明,在 11 月,PCNA 的低表达与黄体中瘦素受体浓度的增加以及循环中瘦素水平的升高相吻合。总之,11 月至 12 月期间与肥胖相关的瘦素水平升高可能在抑制黄体中孕酮合成以及抑制子宫-胚胎单位中的细胞增殖率方面发挥作用,从而导致大蹼足蝠胚胎发育延迟。

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