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体重减轻和酮症对餐后胆囊收缩素和游离脂肪酸浓度的影响。

Effect of weight loss and ketosis on postprandial cholecystokinin and free fatty acid concentrations.

作者信息

Chearskul Supornpim, Delbridge Elizabeth, Shulkes Arthur, Proietto Joseph, Kriketos Adamandia

机构信息

Department of Physiology, Faculty of Medicine Siriraj Hospital, Mahidol University, Bangkok, Thailand.

出版信息

Am J Clin Nutr. 2008 May;87(5):1238-46. doi: 10.1093/ajcn/87.5.1238.

DOI:10.1093/ajcn/87.5.1238
PMID:18469245
Abstract

BACKGROUND

Weight regain after weight loss may not be due primarily to voluntary return to social habits but may be explained by changes in peripheral hormonal signals activating hunger and encouraging feeding behavior.

OBJECTIVE

The objective of this study was to investigate physiologic adaptations to weight loss that may encourage weight regain.

DESIGN

The study had a within-subject repeated-measure design [12 healthy, obese men, 33-64 y, body mass index (in kg/m(2)) 30-46] and was a clinical intervention investigation of circulating metabolites and hunger-satiety responses before and after weight loss. Measures included anthropometry (bioelectrical impedance, body weight, and waist circumference), concentrations of circulating hormones and metabolites [ketone bodies, free fatty acids (FFAs), insulin, leptin, glucose, and cholecystokinin (CCK)], and measures of hunger and satiety at baseline, 8 wk after weight loss with a very-low-energy diet, and 1 wk after weight maintenance.

RESULTS

Weight loss led to a reduction in postprandial CCK secretion (P = 0.016). However, when subjects were ketotic (elevated circulating beta-hydroxybutyrate concentrations), CCK secretion was sustained at concentrations before weight loss. After weight loss, there were reduced postprandial FFA concentrations (P = 0.0005). The presence of ketosis sustained FFA to concentrations before weight loss (P = 0.60).

CONCLUSION

Rapid weight loss of approximately 10% of initial body weight results in a reduction in postprandial CCK and FFA concentrations.

摘要

背景

体重减轻后的体重反弹可能并非主要归因于恢复社交习惯,而可能是由激活饥饿感并促进进食行为的外周激素信号变化所解释。

目的

本研究的目的是调查可能促使体重反弹的体重减轻后的生理适应性。

设计

该研究采用受试者内重复测量设计[12名健康肥胖男性,年龄33 - 64岁,体重指数(kg/m²)为30 - 46],是一项关于体重减轻前后循环代谢物及饥饿 - 饱腹感反应的临床干预研究。测量指标包括人体测量学指标(生物电阻抗、体重和腰围)、循环激素和代谢物浓度[酮体、游离脂肪酸(FFA)、胰岛素、瘦素、葡萄糖和胆囊收缩素(CCK)],以及基线、采用极低能量饮食减重8周后和维持体重1周后的饥饿感和饱腹感测量。

结果

体重减轻导致餐后CCK分泌减少(P = 0.016)。然而,当受试者处于酮症状态(循环β - 羟基丁酸浓度升高)时,CCK分泌维持在体重减轻前的浓度水平。体重减轻后,餐后FFA浓度降低(P = 0.0005)。酮症状态的存在使FFA浓度维持在体重减轻前的水平(P = 0.60)。

结论

初始体重快速减轻约10%会导致餐后CCK和FFA浓度降低。

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