Seeley R J, Matson C A, Chavez M, Woods S C, Dallman M F, Schwartz M W
Department of Psychology, University of Washington, Seattle 98195-1525, USA.
Am J Physiol. 1996 Sep;271(3 Pt 2):R819-23. doi: 10.1152/ajpregu.1996.271.3.R819.
The suppression of food intake after a period of forced overfeeding is potent and long lasting, yet little is known of the underlying mechanisms for this regulatory response. Rats were overfed via a surgically implanted gastrostomy tube. During overfeeding, plasma insulin and corticotropin-releasing hormone (CRH) mRNA in the paraventricular nucleus of the hypothalamus were elevated compared with controls and with overfed rats allowed 3 days to recover from the overfeeding regimen such that body weight returned to the level of controls. In contrast, rats that were not overfed but were pair-fed to the low spontaneous food intake of previously overfed rats lost weight and had significantly reduced plasma insulin and elevated mRNA for neuropeptide Y (NPY) in the arcuate nucleus of the hypothalamus. The results indicate that overfeeding produces an activation of hypothalamic CRH system that may contribute to the hypophagia that accompanies involuntary overfeeding. Furthermore, the hypothalamic NPY response to food restriction is not tied to low food intake per se, but rather to negative energy balance.
经过一段时间的强制过度喂养后，食物摄入量的抑制作用强烈且持久，但对于这种调节反应的潜在机制却知之甚少。通过手术植入胃造口管对大鼠进行过度喂养。在过度喂养期间，与对照组以及从过度喂养方案中恢复3天以使体重恢复到对照组水平的过度喂养大鼠相比，下丘脑室旁核中的血浆胰岛素和促肾上腺皮质激素释放激素（CRH）mRNA水平升高。相比之下，未进行过度喂养但与先前过度喂养大鼠的低自发食物摄入量进行配对喂养的大鼠体重减轻，血浆胰岛素显著降低，而下丘脑弓状核中神经肽Y（NPY）的mRNA水平升高。结果表明，过度喂养会激活下丘脑CRH系统，这可能导致非自愿过度喂养时伴随的食欲减退。此外，下丘脑NPY对食物限制的反应并非与低食物摄入量本身相关，而是与负能量平衡有关。
