LRH-1 heterozygous knockout mice are prone to mild obesity

Taisuke Hattori, Katsumi Iizuka, Yukio Horikawa, Jun Takeda

Research output: Contribution to journalArticlepeer-review

10 Citations (Scopus)


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.

Original languageEnglish
Pages (from-to)471-480
Number of pages10
Journalendocrine journal
Issue number5
Publication statusPublished - 2014
Externally publishedYes

All Science Journal Classification (ASJC) codes

  • Endocrinology, Diabetes and Metabolism
  • Endocrinology


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