| First Author | Hattori T | Year | 2014 |
| Journal | Endocr J | Volume | 61 |
| Issue | 5 | Pages | 471-80 |
| PubMed ID | 24531913 | Mgi Jnum | J:318200 |
| Mgi Id | MGI:6858732 | Doi | 10.1507/endocrj.ej14-0017 |
| Citation | Hattori T, et al. (2014) LRH-1 heterozygous knockout mice are prone to mild obesity. Endocr J 61(5):471-80 |
| abstractText | 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. |
