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[肥胖症的病理生理学与治疗]

[Physiopathology and treatment of obesity].

作者信息

Jéquier E

出版信息

Schweiz Med Wochenschr. 1983 Jun 18;113(24):870-5.

PMID:6348939
Abstract

Obesity results from an energy imbalance affecting both energy intake and output to various degrees. In some individuals hyperphagia may be the obvious cause of the imbalance, whereas in other obese patients a defective thermogenic capacity unable to adapt energy expenditure to a variable intake plays an important role. The mechanisms of this thermogenic defect are not well understood: decreased sensitivity to the thermogenic effects of the sympathetic nervous system and insulin resistance may be implicated. The thermogenic defect favours weight gain; it is likely that body weight reaches a plateau (th obese state) when the body weight gain is accompanied by a rise in basal metabolic rate which compensates the thermogenic defect. The excess in body weight becomes a compensated state which allows the whole energy intake to be expended. The principles of the protein sparing modified fast (low carbohydrate and lipid, but high protein intake) are outlined. After the end of the hypocaloric diet period the recommendations for maintaining the new body weight should stress the need to maintain a low lipid intake but allow carbohydrate intake (mainly starch). It is important to realize that the energy needs of the patient are lowered after weight loss.

摘要

肥胖是由能量失衡导致的,这种失衡在不同程度上影响能量的摄入和输出。在一些个体中,食欲亢进可能是失衡的明显原因,而在其他肥胖患者中,产热能力缺陷无法使能量消耗适应变化的摄入量则起着重要作用。这种产热缺陷的机制尚未完全了解:可能与对交感神经系统产热效应的敏感性降低和胰岛素抵抗有关。产热缺陷有利于体重增加;当体重增加伴随着基础代谢率的升高以补偿产热缺陷时,体重可能会达到一个稳定水平(肥胖状态)。体重超标成为一种代偿状态,使全部能量摄入得以消耗。概述了蛋白质节省改良禁食法(低碳水化合物和脂质,但高蛋白摄入)的原则。在低热量饮食期结束后,维持新体重的建议应强调保持低脂肪摄入的必要性,但允许碳水化合物摄入(主要是淀粉)。必须认识到,体重减轻后患者的能量需求会降低。

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