Heinrichs S C, Richard D
Department of Psychology, Boston College, Chestnut Hill, MA, 02467, USA.
Neuropeptides. 1999 Oct;33(5):350-9. doi: 10.1054/npep.1999.0047.
Participation of the hypothalamo-pituitary-adrenocortical axis, and its primary brain trigger, corticotropin-releasing factor (CRF) in the control of ingestive behavior can be inferred from data suggesting that CRF and its homologue urocortin act in brain to limit appetite following administration in rodents. Moreover, levels of endogenous CRF, CRF(1)and CRF(2)receptors and CRF-binding protein, which sequesters CRF and urocortin, are altered by changes in nutritional status brought about by food restriction/repletion. Mediation of the anorexic effects of CRF and urocortin appear not to privilege CRF(1)receptors, unlike the anxiogenic effects of CRF which are primarily a consequence of CRF(1)receptor activation. Such fear-like consequences of CRF system activation constitute a non-specific mechanism whereby the emergence of behaviors incompatible with food intake may appear to suppress appetite without affecting hunger per se. However, enhanced appetite following administration of CRF receptor antagonists and the involvement of CRF systems in sexual appetite and drug-seeking behavior all suggest a role for CRF in ingestive behavior. In particular, available evidence suggests that physiologically relevant suppression of appetite may accompany CRF system activation occurring as a consequence of stressor exposure induced by nutrient imbalance, for example, or under conditions of excessive intake or consumption of unfamiliar foodstuffs.
下丘脑 - 垂体 - 肾上腺皮质轴及其主要脑触发因子促肾上腺皮质激素释放因子（CRF）参与摄食行为的调控，这可从以下数据推断得出：在啮齿动物中给药后，CRF及其同源物尿皮质素在脑内发挥作用以限制食欲。此外，内源性CRF、CRF(1)和CRF(2)受体以及隔离CRF和尿皮质素的CRF结合蛋白的水平，会因食物限制/补充所导致的营养状况变化而改变。与CRF的致焦虑作用主要是CRF(1)受体激活的结果不同，CRF和尿皮质素的厌食作用似乎并不优先作用于CRF(1)受体。CRF系统激活所产生的这种类似恐惧的后果构成了一种非特异性机制，由此与食物摄入不相容的行为的出现可能看似抑制了食欲而不影响饥饿本身。然而，给予CRF受体拮抗剂后食欲增强以及CRF系统参与性食欲和觅药行为，均表明CRF在摄食行为中发挥作用。特别是，现有证据表明，例如由于营养失衡引起的应激源暴露，或在过量摄入或食用不熟悉食物的情况下，CRF系统激活可能会伴随生理性的食欲抑制。
