GnRH secretion is inhibited by adiponectin through activation of AMP-activated protein kinase and extracellular signal-regulated kinase

• Published in: Endocrine Vol. 39; no. 1; pp. 6 - 12
• Main Authors: Cheng, Xiao-Bing, Wen, Jun-Ping, Yang, Jun, Yang, Ying, Ning, Guang, Li, Xiao-Ying
• Format: Journal Article
• Language: English
• Published: Boston Springer US 01.02.2011
• Subjects: Adiponectin - pharmacology; AMP-Activated Protein Kinases - metabolism; Animals; Cell Line; Diabetes; Endocrinology; Enzyme Activation - drug effects; Extracellular Signal-Regulated MAP Kinases - antagonists & inhibitors; Extracellular Signal-Regulated MAP Kinases - metabolism; Gonadotropin-Releasing Hormone - antagonists & inhibitors; Gonadotropin-Releasing Hormone - secretion; Humanities and Social Sciences; Hypothalamus - drug effects; Hypothalamus - enzymology; Hypothalamus - secretion; Internal Medicine; Luteinizing Hormone - secretion; Male; Medicine; Medicine & Public Health; multidisciplinary; Original Article; Phosphorylation - drug effects; Protein Kinase Inhibitors - pharmacology; Rats; Rats, Sprague-Dawley; Science; AMPK; GnRH; MAPK; Adiponectin
• ISSN: 1355-008X; 1559-0100; 1559-0100
• DOI: 10.1007/s12020-010-9375-8

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.