Wellman P J
Department of Psychology, Texas A&M University, College Station, Texas 77843-4235, USA.
Nutrition. 2000 Oct;16(10):837-42. doi: 10.1016/s0899-9007(00)00415-9.
The focus of the present review is to reconsider the role of endogenous norepinephrine (NE) in brain, specifically within the hypothalamic paraventricular nucleus (PVN), with regard to its potential role in eliciting eating or satiety. The PVN is innervated by NE fibers and is a site at which infusion of exogenous NE elicits eating at low doses. Two subtypes of alpha-adrenergic receptors within the PVN exert antagonistic actions on eating in the rat: activation of PVN alpha(2)-adrenoceptors increases eating, whereas activation of PVN alpha(1)-adrenoceptors suppresses eating. Pharmacologic manipulations that elevate NE can increase or decrease food intake, depending on the site and type of NE manipulation. Certain antiobesity drugs may act to reduce eating via release of NE and subsequent activation of alpha(1)-adrenoceptors. The PVN exhibits a reliable rhythm in the secretion of endogenous NE over the dark-and-light cycle, and this rhythm may interact with changes in numbers of PVN alpha(1)- and alpha(2)-adrenoceptors to modulate eating during the dark-and-light cycle. Push-and-pull and microdialysis studies indicate that NE secretion is strongly associated with eating, particularly at the start of the dark phase. The present review considers potential interactions of NE with substances such as leptin and neuropeptide Y that alter eating.
本综述的重点是重新审视内源性去甲肾上腺素（NE）在大脑中的作用，特别是在下丘脑室旁核（PVN）内，探讨其在引发进食或饱腹感方面的潜在作用。PVN由NE纤维支配，是一个低剂量注入外源性NE会引发进食的部位。PVN内的两种α-肾上腺素能受体亚型对大鼠的进食发挥拮抗作用：激活PVNα₂-肾上腺素能受体会增加进食，而激活PVNα₁-肾上腺素能受体则会抑制进食。提高NE水平的药理学操作可增加或减少食物摄入量，这取决于NE操作的部位和类型。某些抗肥胖药物可能通过释放NE并随后激活α₁-肾上腺素能受体来减少进食。PVN在内源性NE的分泌上呈现出可靠的昼夜节律，这种节律可能与PVNα₁-和α₂-肾上腺素能受体数量的变化相互作用，从而在昼夜周期中调节进食。推挽式和微透析研究表明，NE分泌与进食密切相关，尤其是在黑暗期开始时。本综述考虑了NE与诸如瘦素和神经肽Y等改变进食的物质之间的潜在相互作用。
