Woods Stephen C, Benoit Stephen C, Clegg Deborah J, Seeley Randy J
Department of Psychiatry, University of Cincinnati, 2170 East Galbraith Road, Cincinnati, OH 45237, USA.
Best Pract Res Clin Endocrinol Metab. 2004 Dec;18(4):497-515. doi: 10.1016/j.beem.2004.08.004.
The increased incidence of obesity makes it imperative to understand the regulation of food intake and body weight. We review the signals that interact with the brain to control energy homeostasis, i.e. energy intake and expenditure. Three broad categories can be distinguished. Signals generated in the gastrointestinal tract during meals ('satiety' signals, e.g. cholecystokinin) elicit satiation and contribute to stopping the meal. The potency of these acutely acting signals must be increased if they are to be used therapeutically. Hormonal signals whose secretion is proportional to body fat (adiposity signals, leptin and insulin) robustly reduce food intake and body weight by directly stimulating receptors locally in the brain. Therapeutic applications will have to find ways to circumvent the systemic actions of these hormones, targeting only the brain. Satiety and adiposity signals interact with neuronal circuits in the brain that utilize myriad neurotransmitters to cause net catabolic or anabolic responses. Considerable effort is being directed towards finding ways to intervene in specific circuits to help accomplish weight loss.
肥胖发病率的上升使得了解食物摄入和体重的调节变得势在必行。我们综述了与大脑相互作用以控制能量平衡（即能量摄入和消耗）的信号。可区分出三大类。进餐期间在胃肠道产生的信号（“饱腹感”信号，如胆囊收缩素）引发饱腹感并有助于停止进餐。如果要将这些急性作用的信号用于治疗，就必须增强其效力。其分泌与体脂成比例的激素信号（肥胖信号、瘦素和胰岛素）通过直接刺激大脑局部的受体，有力地减少食物摄入和体重。治疗应用必须找到方法来规避这些激素的全身作用，仅针对大脑。饱腹感和肥胖信号与大脑中的神经回路相互作用，这些神经回路利用无数神经递质引起净分解代谢或合成代谢反应。人们正在投入大量精力寻找干预特定回路以帮助实现体重减轻的方法。
