O'Connor Kristie L, Scisco Jenna L, Smith Tracey J, Young Andrew J, Montain Scott J, Price Lori Lyn, Lieberman Harris R, Karl J Philip
US Army Research Institute of Environmental Medicine, Military Nutrition Division, Natick, MA; and.
Institute for Clinical Research and Health Policy Studies, Tufts Medical Center and Tufts Clinical and Translational Science Institute, Tufts University, Boston, MA.
J Nutr. 2016 Feb;146(2):209-17. doi: 10.3945/jn.115.217976. Epub 2016 Jan 6.
Adaptive responses of appetite-mediating hormones to negative energy balance are thought to contribute to a counterregulatory response that drives weight regain, but they have not been studied while controlling for reduced diet volume.
In this secondary analysis, we aimed to determine the effects of short-term, severe energy deprivation (ED) on appetite and appetite-mediating hormone concentrations.
Twenty-one adults with a mean ± SD age of 21 ± 3 y and body mass index of 25 ± 3 kg/m(2) consumed isovolumetric diets provided over separate 48-h periods while increasing habitual energy expenditure by 1683 ± 329 kcal/d through light- and moderate-intensity exercise. Energy intake was matched to energy expenditure to maintain energy balance (EB) (-44 ± 92 kcal/d) or was <10% of energy expenditure to generate a -3696 ± 742-kcal/d energy deficit. Postprandial appetite, glucose, insulin, acyl ghrelin, peptide YY, pancreatic polypeptide (PP), and glucagon-like peptide-1 (GLP-1) responses and ad libitum energy intake were measured as secondary outcomes after both experimental periods.
Fasting insulin (-56% ± 42%) and acyl ghrelin (-60% ± 17%) concentrations decreased during ED but not during EB (condition-by-time interaction; P-interaction ≤ 0.01), whereas fasting leptin concentrations decreased more during ED compared with during EB (-47% ± 27% compared with -20% ± 27%; P-interaction = 0.05). Postprandial insulin (57% ± 63%; P < 0.001), GLP-1 (14% ± 28%; P = 0.04), and PP (54% ± 52%; P < 0.001) areas under the curve (AUCs) were higher, whereas the acyl ghrelin AUC was lower (-56% ± 13%; P < 0.001) after ED compared with after EB. After ED, self-rated appetite was greater, and ad libitum energy intake was 811 kcal/36 h (95% CI: 184, 1439 kcal/36 h) higher relative to after EB (P = 0.01).
Short-term, severe ED suppressed acyl ghrelin concentrations and increased postprandial anorexigenic hormone concentrations. These effects preceded compensatory overeating, suggesting that in adults without obesity, altered sensitivity to appetite-mediating hormones may contribute to an adaptive counterregulatory response during the initial stages of negative EB. This trial was registered at clinicaltrials.gov as NCT01603550.
食欲调节激素对负能量平衡的适应性反应被认为有助于一种反调节反应,这种反应会导致体重反弹,但在控制饮食量减少的情况下尚未对其进行研究。
在这项二次分析中,我们旨在确定短期、严重能量剥夺(ED)对食欲和食欲调节激素浓度的影响。
21名平均年龄为21±3岁、体重指数为25±3kg/m²的成年人在不同的48小时时间段内食用等体积饮食,同时通过轻度和中度强度运动使日常能量消耗增加1683±329kcal/d。能量摄入与能量消耗相匹配以维持能量平衡(EB)(-44±92kcal/d),或低于能量消耗的10%以产生-3696±742kcal/d的能量 deficit。在两个实验期后,测量餐后食欲、葡萄糖、胰岛素、酰基胃饥饿素、肽YY、胰多肽(PP)和胰高血糖素样肽-1(GLP-1)反应以及随意能量摄入作为次要结果。
在能量剥夺期间空腹胰岛素(-56%±42%)和酰基胃饥饿素(-60%±17%)浓度降低,但在能量平衡期间未降低(条件与时间交互作用;P交互作用≤0.01),而与能量平衡期间相比,能量剥夺期间空腹瘦素浓度降低更多(-47%±27%与-20%±27%相比;P交互作用=0.05)。与能量平衡后相比,能量剥夺后餐后胰岛素曲线下面积(AUC)(57%±63%;P<0.001)、GLP-1(14%±28%;P=0.04)和PP(54%±52%;P<0.001)更高,而酰基胃饥饿素AUC更低(-56%±13%;P<0.001)。能量剥夺后,自我评定的食欲更强,与能量平衡后相比,随意能量摄入高811kcal/36h(95%CI:184,1439kcal/36h)(P=0.01)。
短期、严重的能量剥夺抑制了酰基胃饥饿素浓度并增加了餐后厌食激素浓度。这些影响在代偿性暴饮暴食之前出现,表明在无肥胖的成年人中,对食欲调节激素敏感性的改变可能在负能量平衡的初始阶段促成适应性反调节反应。该试验在clinicaltrials.gov上注册为NCT01603550。