Ishizuka B, Quigley M E, Yen S S
J Clin Endocrinol Metab. 1983 Dec;57(6):1111-6. doi: 10.1210/jcem-57-6-1111.
The synchrony of PRL and cortisol release with feeding is now well established. To delineate further the neuroendocrine mechanisms involved, meal-related pituitary and adrenal cortical activities were investigated in seven normal men in a series of experiments conducted in random sequence at 1-week intervals. Ingestion of a standardized mixed meal elicited a consistent acute release of PRL and cortisol at noon (1200 h), but not at breakfast (0800 h). No measurable changes in other pituitary hormones were observed. The relative magnitudes of PRL and cortisol release in response to lunch were not significantly influenced by a preceding breakfast. These responses appear unrelated to the cephalic or oral phases of food ingestion. However, the composition of the meals was found to be important. Whereas carbohydrate meals had no discernible effects, high protein meals induced a large increase in both PRL and cortisol; high fat meals caused selective release of PRL. Ingestion of L-tyrosine and L-tryptophan induced remarkable increments in serum concentrations of both PRL and cortisol, suggesting that these essential amino acids may be active components of the high protein meal. Choline had no effect. Meal-mediated PRL and cortisol release was unaffected by prior receptor blockade of the opioidergic and cholinergic systems with naloxone and atropine, respectively. These observations indicate that the protein component of the meal was responsible for the midday surges of PRL and cortisol and that the cephalic-vagal pathway was not required in food-entrained pituitary hormone release. Further, our data suggest that the neurotransmitter substrates in the protein meal may serve to link the gut and brain by modifying central catecholamine and serotonin biosynthesis, and thereby influence the hypothalamic factors controlling pituitary PRL and ACTH secretion. The possibility that gastrointestinal hormones may also influence the hypothalamic-pituitary system remains to be explored.
泌乳素(PRL)和皮质醇释放与进食的同步性现已得到充分证实。为了进一步阐明其中涉及的神经内分泌机制,在一系列实验中,以随机顺序、每隔1周对7名正常男性的与进餐相关的垂体和肾上腺皮质活动进行了研究。摄入标准化混合餐会在中午(12:00)引起PRL和皮质醇持续的急性释放,但在早餐时(08:00)不会。未观察到其他垂体激素有可测量的变化。午餐时PRL和皮质醇释放的相对幅度不受之前早餐的显著影响。这些反应似乎与食物摄入的头期或口腔期无关。然而,发现餐食的成分很重要。碳水化合物餐没有明显影响,高蛋白餐会使PRL和皮质醇都大幅增加;高脂肪餐会导致PRL的选择性释放。摄入L-酪氨酸和L-色氨酸会使PRL和皮质醇的血清浓度显著升高,这表明这些必需氨基酸可能是高蛋白餐的活性成分。胆碱没有作用。分别用纳洛酮和阿托品对阿片能和胆碱能系统进行预先的受体阻断,并不影响进餐介导的PRL和皮质醇释放。这些观察结果表明,餐食中的蛋白质成分是导致中午PRL和皮质醇激增的原因,并且在食物诱导的垂体激素释放中不需要头-迷走神经通路。此外,我们的数据表明,蛋白质餐中的神经递质底物可能通过改变中枢儿茶酚胺和5-羟色胺的生物合成来连接肠道和大脑,从而影响控制垂体PRL和促肾上腺皮质激素(ACTH)分泌的下丘脑因子。胃肠激素也可能影响下丘脑-垂体系统,这一可能性仍有待探索。