Mechanisms for the central and peripheral regulation of food and water intake in the neonatal chick

瘦素在调节大鼠和小鼠的食物摄入和代谢中起重要作用。然而，中央给药瘦素并没有改变雏鸡的食物摄入量。低水平的去甲肾上腺素刺激了雏鸡的摄食行为，并随着去甲肾上腺素的进一步产生而降低。中枢GLP-1抑制食物摄入和诱导睡眠行为。中枢吗啡也能诱导睡眠行为，从而抑制食物摄入。研究了GLP-1与吗啡在大脑中的关系，但未发现相互作用。GLP-1抑制水分摄入和食物摄入。提示n端组氨酸在GLP-1的作用中起关键作用。中枢胃泌素作为脑肠肽抑制作物的食物摄入和食物通道。CCK具有与胃泌素相似的氨基酸序列，可以抑制食物摄入，并且在大分子中效果比在小分子中效果更强。中枢组胺、a-MSH和bombesin强烈抑制食物摄入。在哺乳动物中，食欲素、MCH、丙氨酸和胃动素已被认为是一种促食因子。然而，这些肽并没有增加雏鸡的摄食量。外周给药红霉素，具有类似胃动素的作用，对喂养没有任何影响。脑内一氧化氮合成的抑制抑制了NPY和去甲肾上腺素的促氧作用。阿片肽抑制精氨酸缩宫素的释放。高渗状态下精氨酸缩宫素的合成和释放同时减少。

Leptin plays an important role in regulation of food intake and metabolism in rats and mice. However, central administration of leptin did not alter food intake of chicks. Feeding behavior was stimulated by low levels of norepinephrine and decreased by further production of norepinephrine in chicks. Central GLP-1 suppressed food intake and induced sleeping behavior. Sleeping behavior was also induced by central morphine and consequently food intake was suppressed. Relationships between GLP-1 and morphine in the brain were studied, but no interaction was detected. GLP-1 inhibited water intake as well as food intake. It was suggested that N-terminal histidine had a key role for the action of GLP-1. Central gastrin as a brain-gut peptide inhibited both food intake and food passage from the crop. CCK, having a similar amino acid sequence for gastrin, suppressed food intake and the effect was stronger in a large size molecule than in a small one. Central histamine, a-MSH and bombesin strongly inhibited food intake. In mammalian species, orexin, MCH, galanin and motilin have been recognized as an orexigenic factors. However, these peptides did not enhance food intake of chicks. Peripheral administration of erythromycin, having an action like motilin, did not show any effects for feeding. Orexigenic actions of both NPY and norepinephrine were depressed by the inhibition of nitric oxide synthesis in the brain. Release of arginine vasotocin inhibited by opioid peptide. Synthesis and release of arginine vasotocin was simultaneously decreased under a hypertonic condition.