Woods S C, Seeley R J
Department of Psychiatry, University of Cincinnati Medical Center, Cincinnati, Ohio 45267, USA.
Nutrition. 2000 Oct;16(10):894-902. doi: 10.1016/s0899-9007(00)00454-8.
Recent technologic innovations have enabled probing the workings of individual cells and even molecules. As a result, our knowledge of the biological controls over eating and the regulation of body adiposity is increasing at a rapid pace. We review the evidence that food intake is controlled by separate but interacting groups of molecular signals. One group, termed satiety signals, are proportional to what is being consumed and help to determine meal size. Cholecystokinin is the best known of these, and its premeal administration causes a dose-dependent reduction of meal size. In and of itself, however, cholecystokinin (and other satiety signals) has little impact on body-fat stores. The second group, termed adiposity signals, circulate in proportion to body adiposity and enter the brain, where they interact with satiety signals in the brainstem and hypothalamus. Insulin and leptin are the best known of these adiposity signals, and the administration of either into the brain causes a dose-dependent reduction of both food intake and body weight. Within the brain, parallel but opposing pathways originating in the hypothalamic arcuate nuclei integrate adiposity signals with satiety signals. Those with a net anabolic effect increase food intake and reduce energy expenditure and are represented (among many such signals) by neuropeptide Y; those with a net catabolic effect decrease food intake and energy expenditure and are represented by brain melanocortins. This complex regulatory mechanism allows individuals to adapt their feeding schedule to idiosyncratic environmental constraints, eating whenever it is desirable or possible. Body-weight regulation occurs as adiposity signals alter the efficacy of meal-generated satiety signals.
最近的技术创新使得探究单个细胞甚至分子的运作成为可能。因此，我们对饮食的生物控制和身体肥胖调节的了解正在迅速增加。我们回顾了证据，即食物摄入量由不同但相互作用的分子信号组控制。一组称为饱腹感信号，与所摄入的食物量成正比，并有助于确定每餐的食量。胆囊收缩素是其中最著名的一种，餐前给予胆囊收缩素会导致食量呈剂量依赖性减少。然而，就其本身而言，胆囊收缩素（以及其他饱腹感信号）对身体脂肪储存几乎没有影响。第二组称为肥胖信号，其循环与身体肥胖程度成正比，并进入大脑，在那里它们与脑干和下丘脑的饱腹感信号相互作用。胰岛素和瘦素是这些肥胖信号中最著名的，将它们中的任何一种注入大脑都会导致食物摄入量和体重呈剂量依赖性减少。在大脑中，起源于下丘脑弓状核的平行但相反的途径将肥胖信号与饱腹感信号整合在一起。那些具有净合成代谢作用的信号会增加食物摄入量并减少能量消耗，神经肽Y（在许多此类信号中）代表了这些信号；那些具有净分解代谢作用的信号会减少食物摄入量和能量消耗，脑黑皮质素代表了这些信号。这种复杂的调节机制使个体能够根据特殊的环境限制调整进食时间表，在任何需要或可能的时候进食。体重调节是因为肥胖信号改变了由进餐产生的饱腹感信号的效力。
