LRH-1 heterozygous knockout mice are prone to mild obesity

Endocrine Journal

Katsumi Iizuka¹  Yukio Horikawa¹  Taisuke Hattori¹  Jun Takeda¹ 

[1] Department of Diabetes and Endocrinology, Graduate School of Medicine, Gifu University, Gifu 501-1194, Japan

关键词: Liver receptor homologue-1;    Obesity;    CYP7A1;    CYP8B1;    Small heterodimer partner;   

DOI  :  10.1507/endocrj.EJ14-0017

学科分类：内分泌与代谢学

来源: Japan Endocrine Society

【 摘 要 】

References(26)Cited-By(2)Obesity is a global health problem that increases the risk of several common diseases.Liver receptor homologue-1 (LRH-1) has an important role in steroid hormone metabolism, which influences body weight.Whether LRH-1 gene deletion causes obesity is yet to be clarified.In this study using LRH-1 heterozygous knockout (LRH-1+/-) mice, we investigated the role of LRH-1 on body weight gain and glucose and lipid metabolism.LRH-1+/- mice showed mild but significant body weight gains compared with wild-type littermate mice after being fed a high-fat diet.We performed glucose tolerance tests and insulin tolerance tests and did not find any significant differences between wild-type and LRH-1+/- mice.To clarify how LRH-1 gene deletion affects body weight gain, we measured food intake, oxygen consumption, respiratory quotient, spontaneous activity and rectal temperature, and found no significant differences between wild-type and LRH-1+/- mice fed a normal diet and a high-fat diet.The results suggest that heterozygous gene deletion of LRH-1 causes body weight gains without any apparent worsening of glucose and lipid metabolism.Identifying the effects of LRH-1 on body weight will aid in understanding the pathogenesis of obesity.

【 授权许可】

Unknown