设定点理论(英语:Set point theory (body weight))于1953年首次推出,假设每个身体都有一个预先设定的体重,并具有调节机制来补偿。这一理论很快被采用并用于解释在开发有效和持续的减肥程序方面的失败。于2019年对人类多种体重变化干预措施(包括节食、锻炼和暴饮暴食)进行的系统评价发现,所有这些程序都存在系统性“能量错误”,即卡路里的无补偿损失或增加。这表明身体不能精确地补偿能量和卡路里摄入的误差,这与设定点理论的假设相反,并可能解释体重减轻和体重增加(如肥胖)。这项审查是针对短期研究进行的,因此从长远来看,不能排除设定点理论的可能,因为目前缺乏这个时间框架的证据。[11][12]
^ 2.02.1Malenka RC, Nestler EJ, Hyman SE. Sydor A, Brown RY , 编. Molecular Neuropharmacology: A Foundation for Clinical Neuroscience 2nd. New York: McGraw-Hill Medical. 2009: 179, 262–263. ISBN 9780071481274. Orexin neurons are regulated by peripheral mediators that carry information about energy balance, including glucose, leptin, and ghrelin. ... Accordingly, orexin plays a role in the regulation of energy homeostasis, reward, and perhaps more generally in emotion. ... The regulation of energy balance involves the exquisite coordination of food intake and energy expenditure. Experiments in the 1940s and 1950s showed that lesions of the lateral hypothalamus (LH) reduced food intake; hence, the normal role of this brain area is to stimulate feeding and decrease energy utilization. In contrast, lesions of the medial hypothalamus, especially the ventromedial nucleus (VMH) but also the PVN and dorsomedial hypothalamic nucleus (DMH), increased food intake; hence, the normal role of these regions is to suppress feeding and increase energy utilization. Yet discovery of the complex networks of neuropeptides and other neurotransmitters acting within the hypothalamus and other brain regions to regulate food intake and energy expenditure began in earnest in 1994 with the cloning of the leptin (ob, for obesity) gene. Indeed, there is now explosive interest in basic feeding mechanisms given the epidemic proportions of obesity in our society, and the increased toll of the eating disorders, anorexia nervosa and bulimia. Unfortunately, despite dramatic advances in the basic neurobiology of feeding, our understanding of the etiology of these conditions and our ability to intervene clinically remain limited.
^ 3.03.1Morton GJ, Meek TH, Schwartz MW. Neurobiology of food intake in health and disease. Nat. Rev. Neurosci. 2014, 15 (6): 367–378. PMC 4076116. PMID 24840801. doi:10.1038/nrn3745. However, in normal individuals, body weight and body fat content are typically quite stable over time2,3 owing to a biological process termed ‘energy homeostasis’ that matches energy intake to expenditure over long periods of time. The energy homeostasis system comprises neurons in the mediobasal hypothalamus and other brain areas4 that are a part of a neurocircuit that regulates food intake in response to input from humoral signals that circulate at concentrations proportionate to body fat content4-6. ... An emerging concept in the neurobiology of food intake is that neurocircuits exist that are normally inhibited, but when activated in response to emergent or stressful stimuli they can override the homeostatic control of energy balance. Understanding how these circuits interact with the energy homeostasis system is fundamental to understanding the control of food intake and may bear on the pathogenesis of disorders at both ends of the body weight spectrum.
^Levitsky, DA; Sewall, A; Zhong, Y; Barre, L; Shoen, S; Agaronnik, N; LeClair, JL; Zhuo, W; Pacanowski, C. Quantifying the imprecision of energy intake of humans to compensate for imposed energetic errors: A challenge to the physiological control of human food intake.. Appetite. 1 February 2019, 133: 337–343. PMID 30476522. S2CID 53712116. doi:10.1016/j.appet.2018.11.017.