Bray G A
Section of Diabetes and Clinical Nutrition, University of Southern California, Los Angeles.
Am J Clin Nutr. 1989 Nov;50(5):891-902. doi: 10.1093/ajcn/50.5.891.
The elements of a feedback system for regulating body fat stores consists of an afferent limb providing feedback signals to the central controller in the brain, which integrates information from the sensory and autonomic nervous systems with signals from the internal milieu and modulates ingestive behavior and thermogenic components of the adrenergic nervous system. The search for defective mechanisms that produce obesity has utilized animals with genetic, hypothalamic, and dietary types of obesity. In all three cases, obesity is associated with an absolute or relative decrease in the activity of the sympathetic nervous system. Experimental situations associated with reduced activity of the sympathetic nervous system are generally accompanied by increased food intake and vice versa. Hypothalamic obesity results from damage to the ventromedial hypothalamus, which disrupts modulation of the autonomic nervous system by nutrient and hormonal signals. Recessively inherited obesity may result from failure to modulate the steroid-receptor complex interaction with the promoter region of the genome. Impaired acetylation of melanocyte-stimulating hormone (MSH) may be involved in the development of obesity in the obese yellow mouse. In all cases adrenalectomy arrests the progression or reverses the obesity. These findings further strengthen the autonomic and endocrine hypothesis for obesity.
调节体内脂肪储存的反馈系统的组成要素包括一个传入分支，它向大脑中的中央控制器提供反馈信号，该中央控制器将来自感觉神经系统和自主神经系统的信息与来自内环境的信号整合起来，并调节摄食行为和肾上腺素能神经系统的产热成分。对导致肥胖的缺陷机制的研究利用了患有遗传性、下丘脑性和饮食性肥胖的动物。在所有这三种情况下，肥胖都与交感神经系统活动的绝对或相对降低有关。与交感神经系统活动降低相关的实验情况通常伴随着食物摄入量的增加，反之亦然。下丘脑性肥胖是由腹内侧下丘脑受损引起的，这会破坏营养和激素信号对自主神经系统的调节。隐性遗传肥胖可能是由于未能调节类固醇受体复合物与基因组启动子区域的相互作用。黑素细胞刺激激素（MSH）乙酰化受损可能与肥胖黄小鼠肥胖的发生有关。在所有情况下，肾上腺切除术都会阻止肥胖的进展或使其逆转。这些发现进一步强化了肥胖的自主神经和内分泌假说。
