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Leptin receptor signaling inhibits ovarian follicle development and egg laying in chicken hens

文献类型： 外文期刊

作者： Lei, Ming M. 1 ; Wu, Si Q. 2 ; Li, Xiao W. 2 ; Wang, Cong L. 2 ; Chen, Zhe 1 ; Shi, Zhen D. 1 ;

作者机构： 1.Jiangsu Acad Agr Sci, Inst Anim Sci, Lab Anim Breeding & Reprod, Nanjing 210014, Jiangsu, Peoples R China

2.South China Agr Univ, Coll Anim Sci, Guangzhou 510642, Guangdong, Peoples R China

关键词： Chicken leptin receptor;Extra-cellular domain;Antibody;Ovarian follicule development;Gene expression;Hens

期刊名称：REPRODUCTIVE BIOLOGY AND ENDOCRINOLOGY （ 影响因子：5.211； 五年影响因子：5.017 ）

ISSN： 1477-7827

年卷期： 2014 年 12 卷

页码：

收录情况： SCI

摘要： Background: Nutrition intake during growth strongly influences ovarian follicle development and egg laying in chicken hens, yet the underlying endocrine regulatory mechanism is still poorly understood. The relevant research progress is hindered by difficulties in detection of leptin gene and its expression in the chicken. However, a functional leptin receptor (LEPR) is present in the chicken which has been implicated to play a regulatory role in ovarian follicle development and egg laying. The present study targeted LEPR by immunizing against its extracellular domain (ECD), and examined the resultant ovarian follicle development and egg-laying rate in chicken hens. Methods: Hens that have been immunized four times with chicken LEPR ECD were assessed for their egg laying rate and feed intake, numbers of ovarian follicles, gene expression profiles, serum lipid parameters, as well as STAT3 signaling pathway. Results: Administrations of cLEPR ECD antigen resulted in marked reductions in laying rate that over time eventually recovered to the levels exhibited by the Control hens. Together with the decrease in egg laying rate, cLEPR-immunized hens also exhibited significant reductions in feed intake, plasma concentrations of glucose, triglyceride, high-density lipoprotein, and low-density lipoprotein. Parallelled by reductions in feed intake, mRNA gene expression levels of AgRP, orexin, and NPY were down regulated, but of POMC, MC4R and lepR up-regulated in Immunized hen hypothalamus. cLEPR-immunization also promoted expressions of apoptotic genes such as caspase3 in theca and fas in granulosa layer, but severely depressed IGF-I expression in both theca and granulosa layers. Conclusions: Immunization against cLEPR ECD in egg-laying hens generated antibodies that mimic leptin bioactivity by enhancing leptin receptor transduction. This up-regulated apoptotic gene expression in ovarian follicles, negatively regulated the expression of genes that promote follicular development and hormone secretion, leading to follicle atresia and interruption of egg laying. The inhibition of progesterone secretion due to failure of follicle development also lowered feed intake. These results also demonstrate that immunization against cLEPR ECD may be utilized as a tool for studying bio-functions of cLEPR.

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