Department of Veterinary Physiology, Faculty of Agriculture, University of Miyazaki, Miyazaki, 889-2192, Japan.
Amino Acids. 2012 Apr;42(4):1397-404. doi: 10.1007/s00726-011-0836-z. Epub 2011 Feb 4.
The ingestion of a valine (Val)-deficient diet results in a significant reduction of food intake and body weight within 24 h, and this phenomenon continues throughout the period over which such a diet is supplied. Both microarray and real-time PCR analyses revealed that the expression of somatostatin mRNA was increased in the hypothalamus in anorectic mice that received a Val-deficient diet. On the other hand, when somatostatin was administered intracerebroventricularly to intact animals that were fed a control diet, their 24-h food intake decreased significantly. In addition, Val-deficient but not pair-fed mice or those fasted for 24 h showed a less than 0.5-fold decrease in the hypothalamic mRNA expression levels of Crym, Foxg1, Itpka and two unknown EST clone genes and a more than twofold increase in those of Slc6a3, Bdh1, Ptgr2 and one unknown EST clone gene. These results suggest that hypothalamic somatostatin and genes responsive to Val deficiency may be involved in the central mechanism of anorexia induced by a Val-deficient diet.
摄入缬氨酸(Val)缺乏的饮食会在 24 小时内导致食物摄入量和体重明显减少,这种现象会持续到提供这种饮食的整个期间。微阵列和实时 PCR 分析显示,接受 Val 缺乏饮食的厌食症小鼠下丘脑的生长抑素 mRNA 表达增加。另一方面,当将生长抑素脑室内给予喂食对照饮食的完整动物时,它们的 24 小时食物摄入量显著减少。此外,Val 缺乏但不是配对喂养的小鼠或禁食 24 小时的小鼠,其下丘脑 Crym、Foxg1、Itpka 和两个未知 EST 克隆基因的 mRNA 表达水平下降不到 0.5 倍,而 Slc6a3、Bdh1、Ptgr2 和一个未知 EST 克隆基因的 mRNA 表达水平增加超过两倍。这些结果表明,下丘脑生长抑素和对 Val 缺乏有反应的基因可能参与由 Val 缺乏饮食引起的厌食症的中枢机制。