GnRH secretion is inhibited by adiponectin through activation of AMP-activated protein kinase and extracellular signal-r
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ORIGINAL ARTICLE
GnRH secretion is inhibited by adiponectin through activation of AMP-activated protein kinase and extracellular signal-regulated kinase Xiao-Bing Cheng • Jun-Ping Wen • Jun Yang Ying Yang • Guang Ning • Xiao-Ying Li
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Received: 16 February 2010 / Accepted: 2 July 2010 / Published online: 5 November 2010 Ó Springer Science+Business Media, LLC 2010
Abstract Adipokines produced from adipose tissues participate in regulation of reproduction, energy homeostasis, food intake, and neuroendocrine function in the hypothalamus. We have previously reported that adiponectin significantly reduced GnRH secretion from GT1-7 hypothalamic GnRH neuron cells. In this study, we further investigated the inhibition of GnRH secretion by adiponectin in vivo and found that extracellular signal-regulated kinase (ERK) was inhibited and AMPK activated. Furthermore, we found that activated AMPK by adiponectin reduced ERK phosphorylation, which possibly impaired GnRH secretion in GT1-7 cells. Keywords
Adiponectin GnRH AMPK MAPK
X.-B. Cheng J.-P. Wen J. Yang Y. Yang G. Ning X.-Y. Li (&) Shanghai Clinical Center for Endocrine and Metabolic Diseases, Shanghai Institute of Endocrinology and Metabolism, Key Laboratory of Endocrine and Metabolic Diseases of Chinese Health Ministry, and the Endocrine and Metabolic Division, E-Institutes of Shanghai Universities, Rui-Jin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China e-mail: [email protected] G. Ning Laboratory of Endocrinology and Metabolism, Institute of Health Sciences, Shanghai Institutes for Biological Sciences (SIBS), Chinese Academy of Sciences (CAS), Shanghai, China Present Address: J.-P. Wen Department of Endocrinology, Fujian Provincial Hospital, Fujian Medical University, Fuzhou, China X.-Y. Li Department of Endocrinology and Metabolism, Rui-Jin Hospital, Shanghai Jiao-Tong University School of Medicine, 197, Rui-Jin 2nd Road, Shanghai 200025, China
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Introduction Obesity is associated with a diverse set of metabolic disorders and reproductive disorders which poorly understood. Adipose tissues participate in regulation of feeding, thermogenesis, and reproduction through adipokines [1]. Leptin deficient (ob/ob) mice show obese and infertile. It is also noted that serum adiponectin levels are reduced in obesity. However, it is rarely investigated whether adiponectin participates in the regulation of reproduction. Adiponectin (also known as Acrp30) is specifically secreted from adipose tissues into the circulation [2]. It participates in the regulation of food intake [3], and glucose and lipid homeostasis [4]. Adiponectin consists of an N-terminal collagenous domain and a C-terminal globular domain [5]. Adiponectins circulate in the blood in distinctly stable forms including trimers, low-molecularweight hexamers and high-molecular-weight multimeric complexes [5]. Recently, two adiponectin receptors, adiponectin receptor 1 (AdipR1) and adiponectin receptor 2 (AdipR2) that contain seven-transmembrane domains, were identif
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