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gprc6a null mice exhibit osteopenia, feminization and metabolic syndromegprc6a零老鼠展览骨量减少,女性化和代谢综合征
GPRC6A Null Mice Exhibit Osteopenia, Feminization and Metabolic Syndrome 1 1 1 1 1 1 2 Min Pi , Ling Chen , Min-Zhao Huang , Wenyu Zhu , Brian Ringhofer , Junming Luo , Lane Christenson , 2 3 4 4 4 4 Benyi Li , Jianghong Zhang , P. David Jackson , Pieter Faber , Kurt R. Brunden , John J. Harrington , L. Darryl Quarles1* 1The Kidney Institute, University of Kansas Medical Center, Kansas City, Kansas, United States of America, 2 Department of Molecular Integrative Physiology, University of Kansas Medical Center, Kansas City, Kansas, United States of America, 3 Center for Bone Biology, Clinical Pharmacology, Division/Medicine, Vanderbilt University, Nashville, Tennessee, United States of America, 4 Athersys, Inc., Cleveland, Ohio, United States of America Abstract Background: GPRC6A is a widely expressed orphan G-protein coupled receptor that senses extracellular amino acids, osteocalcin and divalent cations in vitro. The physiological functions of GPRC6A are unknown. Methods/Principal Findings: In this study, we created and characterized the phenotype of GPRC6A2/ 2 mice. We observed complex metabolic abnormalities in GPRC6A2/ 2 mice involving multiple organ systems that express GPRC6A, including bone, kidney, testes, and liver. GPRC6A2/ 2 mice exhibited hepatic steatosis, hyperglycemia, glucose intolerance, and insulin resistance. In addition, we observed high expression of GPRC6A in Leydig cells in the testis. Ablation of GPRC6A resulted in feminization of male GPRC6A2/ 2 mice in association with decreased lean body mass, increased
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