Dridi Sami, Swennen Quirine, Decuypere Eddy, Buyse Johan
Laboratory of Physiology and Immunology of Domestic Animals, KU Leuven, 3001 Heverlee, Belgium.
Brain Res. 2005 Jun 21;1047(2):214-23. doi: 10.1016/j.brainres.2005.04.034.
While there have been many studies in various species examining the mode of central leptin action on food intake, there is however a paucity of data in birds. We have, therefore, addressed this issue in broiler chickens because this strain was selected for high growth rate, hence high food intake. Continuous infusion of recombinant chicken leptin (8 microg/kg/h) during 6 h at a constant rate of 3 ml/h resulted in a significant reduction (49-57%) of food intake in 3-week-old broiler chickens (P < 0.05). The effect of leptin within the central nervous system (CNS) was mediated via selective hypothalamic neuropeptides. Leptin significantly decreased the expression of its receptor (Ob-R), neuropeptide Y (NPY), orexin (ORX), and orexin receptor (ORXR) (P < 0.05), but not that of agouti-related protein (AgRP) (anabolic/orexigenic effectors) in chicken hypothalamus. However, the catabolic/anorexigenic neuropeptides namely proopiomelanocortin (POMC) and corticotropin-releasing hormone (CRH) mRNA levels remained unchanged after leptin treatment. Despite the absence of leptin effect on AgRP (the antagonist of melanocortin receptor MCR) and POMC (the precursor of alpha-melanocyte stimulating hormone which is a potent agonist for MCR), leptin significantly decreased the expression of MCR-4/5 gene in chicken hypothalamus (P < 0.05) suggesting that leptin acts directly (as ligand) or indirectly (via other ligands) on MCRs to regulate food intake in birds. Additionally, leptin down-regulated the expression of fatty acid synthase (FAS) gene in chicken hypothalamus, indicating an additional pathway of leptin action on food intake such as described for FAS inhibitors. These findings provide new insight into the mechanism of leptin control of food intake in chickens.
虽然已经有许多针对不同物种的研究，探讨中枢性瘦素对食物摄入量的作用模式，但有关鸟类的数据却很匮乏。因此，我们选用肉鸡来研究这一问题，因为该品系鸡因生长速度快、食物摄入量高而被选育。以3 ml/h的恒定速率持续6小时输注重组鸡瘦素（8微克/千克/小时），导致3周龄肉鸡的食物摄入量显著减少（49 - 57%）（P < 0.05）。瘦素在中枢神经系统（CNS）内的作用是通过选择性下丘脑神经肽介导的。瘦素显著降低了鸡下丘脑其受体（Ob - R）、神经肽Y（NPY）、食欲素（ORX）和食欲素受体（ORXR）的表达（P < 0.05），但对刺鼠相关蛋白（AgRP）（合成代谢/促食欲效应因子）的表达没有影响。然而，分解代谢/抑食欲神经肽即阿黑皮素原（POMC）和促肾上腺皮质激素释放激素（CRH）的mRNA水平在瘦素处理后保持不变。尽管瘦素对AgRP（黑皮质素受体MCR的拮抗剂）和POMC（α - 黑素细胞刺激素的前体，α - 黑素细胞刺激素是MCR的强效激动剂）没有影响，但瘦素显著降低了鸡下丘脑MCR - 4/5基因的表达（P < 0.05），这表明瘦素直接（作为配体）或间接（通过其他配体）作用于MCRs以调节鸟类的食物摄入量。此外，瘦素下调了鸡下丘脑脂肪酸合酶（FAS）基因的表达，这表明瘦素对食物摄入量的作用存在另一条途径，就像FAS抑制剂所描述的那样。这些发现为瘦素控制鸡食物摄入量的机制提供了新的见解。
