Nieuwenhuizen Arie G, Rutters Femke
Department of Human Biology, Maastricht University, P.O. Box 616, 6200 MD Maastricht, The Netherlands.
Physiol Behav. 2008 May 23;94(2):169-77. doi: 10.1016/j.physbeh.2007.12.011. Epub 2007 Dec 23.
Human (visceral) obesity is associated with alterations hypothalamus-pituitary-adrenal (HPA) axis functioning. It is however not completely clear whether the HPA axis is causally or co-incidentally related to (visceral) obesity. This review summarizes supporting data of an involvement of the HPA axis in the development of (visceral) obesity. First, several DNA polymorphisms related to HPA axis functioning are correlated to the development of obesity. Second, chronic elevation of circulatory glucocorticoid concentrations, as in Cushing's disease, results in increased abdominal adiposity. Third, (visceral) obesity is associated with a diminished capacity of cortisol to suppress its own secretion. HPA axis functioning might affect energy balance through affecting energy intake. Both CRH and cortisol influence physiological, central mechanisms involved in the regulation of food intake. Still, general activation of the HPA axis has shown to have inconsistent effects on food intake in humans. This inconsistency may partially be explained by gender differences, individual differences in the functioning of the HPA axis, as well as differences in attitude towards eating. In particular, women with high scores on dietary restraint are prone to stress-induced hyperphagia. Dietary restraint scores, in turn, are positively correlated to basal and dexamethasone-suppressed cortisol levels, indicating a complex dual relationship between stress, HPA axis functioning, attitude towards eating and the risk for stress-induced hyperphagia. In the Western society, with chronically high ambient levels of stress and the availability of high caloric foods, this relationship may imply a risk for the development of (visceral) obesity and the metabolic syndrome.
人类(内脏型)肥胖与下丘脑-垂体-肾上腺(HPA)轴功能改变有关。然而,HPA轴与(内脏型)肥胖是因果关系还是巧合关系尚不完全清楚。本综述总结了支持HPA轴参与(内脏型)肥胖发生发展的数据。首先,一些与HPA轴功能相关的DNA多态性与肥胖的发生发展相关。其次,如库欣病中循环糖皮质激素浓度的慢性升高会导致腹部脂肪增加。第三,(内脏型)肥胖与皮质醇抑制自身分泌的能力下降有关。HPA轴功能可能通过影响能量摄入来影响能量平衡。促肾上腺皮质激素释放激素(CRH)和皮质醇都会影响参与食物摄入调节的生理和中枢机制。然而,HPA轴的普遍激活对人类食物摄入的影响并不一致。这种不一致可能部分由性别差异、HPA轴功能的个体差异以及对饮食态度的差异来解释。特别是,饮食抑制得分高的女性容易出现应激性贪食。反过来,饮食抑制得分与基础皮质醇水平和地塞米松抑制后的皮质醇水平呈正相关,这表明压力、HPA轴功能、饮食态度和应激性贪食风险之间存在复杂的双重关系。在西方社会,由于环境压力长期居高不下且高热量食物随处可得,这种关系可能意味着(内脏型)肥胖和代谢综合征发生的风险。