Disruption of feeding behavior in CRH receptor I‐deficient mice is dependent on glucocorticoids
Disruption of feeding behavior in CRH receptor I‐deficient mice is dependent on glucocorticoids
复制标题
CRH 受体 I 缺陷小鼠摄食行为的破坏依赖于糖皮质激素
作者：
M. Müller;M. Keck;S. Zimmermann;F. Holsboer;W. Wurst
研究发现促肾上腺皮质激素释放激素（CRH）可以显着抑制食物摄入并减轻体重。然而，这些作用是否是通过 CRH 受体 I (CRHRI) 或 CRH 受体 2 (CRHR2) 或两种受体亚型介导仍有待澄清。因此，我们研究了 CRHRI 缺陷小鼠 (CRHRI-KO) 是否表现出体重和进食行为异常。 CRHRI-KO 和野生型小鼠的食物摄入总量没有差异。然而，食物摄入的昼夜节律分布受到显着破坏：CRHRI 突变体在光照期间消耗明显更多的食物（p <0.01）。通过口服 21-硫酸皮质酮（5 mg/l 添加到水基流质饮食中）可以完全恢复正常的昼夜模式。因此，我们得出结论，在 CRHRI-KO 小鼠中，摄食行为的破坏可能与糖皮质激素缺乏有关，但 CRHRI 不太可能在摄食行为的基础调节中发挥关键作用。
Corticotropin-releasing hormone (CRH) has been found to markedly suppress food intake and reduce body weight. However, it still remains to be clarified whether those effects are mediated via either the CRH receptor I (CRHRI) or the CRH receptor 2 (CRHR2), or both receptor subtypes. Therefore, we investigated whether CRHRI-deficient mice (CRHRI-KO) show abnormalities in body weight and feeding behavior. CRHRI-KO and wildtype mice showed no difference in the total amount of food intake. However, there was a significant disruption in the circadian distribution of food intake: CRHRI mutants consumed significantly more food during the light period (p <0.01). The normal diurnal pattern could be completely restored by oral administration of corticosterone 21-sulfate (5 mg/l added to the water-based liquid diet). We therefore conclude that in CRHRI-KO mice, the disruption of feeding behavior might be causally related to glucocorticoid deficiency, but that the CRHRI is not likely to play a critical role in the basal regulation of ingestive behavior.