Piccolo Brian D, Comerford Kevin B, Karakas Sidika E, Knotts Trina A, Fiehn Oliver, Adams Sean H
Obesity and Metabolism Research Unit, USDA, Agricultural Research Service, Western Human Nutrition Research Center, Davis, CA;
Division of Endocrinology, Diabetes, and Metabolism, Department of Internal Medicine, The University of California Davis Medical Center, Sacramento, CA; and Department of Nutrition.
J Nutr. 2015 Apr;145(4):691-700. doi: 10.3945/jn.114.203943. Epub 2015 Feb 4.
It has been suggested that perturbations in branched-chain amino acid (BCAA) catabolism are associated with insulin resistance and contribute to elevated systemic BCAAs. Evidence in rodents suggests dietary protein rich in BCAAs can increase BCAA catabolism, but there is limited evidence in humans.
We hypothesize that a diet rich in BCAAs will increase BCAA catabolism, which will manifest in a reduction of fasting plasma BCAA concentrations.
The metabolome of 27 obese women with metabolic syndrome before and after weight loss was investigated to identify changes in BCAA metabolism using GC-time-of-flight mass spectrometry. Subjects were enrolled in an 8-wk weight-loss study including either a 20-g/d whey (whey group, n = 16) or gelatin (gelatin group, n = 11) protein supplement. When matched for total protein by weight, whey protein has 3 times the amount of BCAAs compared with gelatin protein.
Postintervention plasma abundances of Ile (gelatin group: 637 ± 18, quantifier ion peak height ÷ 100; whey group: 744 ± 65), Leu (gelatin group: 1210 ± 33; whey group: 1380 ± 79), and Val (gelatin group: 2080 ± 59; whey group: 2510 ± 230) did not differ between treatment groups. BCAAs were significantly correlated with homeostasis model assessment of insulin resistance at baseline (r = 0.52, 0.43, and 0.49 for Leu, Ile, and Val, respectively; all, P < 0.05), but correlations were no longer significant at postintervention. Pro- and Cys-related pathways were found discriminant of whey protein vs. gelatin protein supplementation in multivariate statistical analyses.
These findings suggest that BCAA metabolism is, at best, only modestly affected at a whey protein supplementation dose of 20 g/d. Furthermore, the loss of an association between postintervention BCAA and homeostasis model assessment suggests that factors associated with calorie restriction or protein intake affect how plasma BCAAs relate to insulin sensitivity. This trial was registered at clinicaltrials.gov as NCT00739479.
有研究表明,支链氨基酸(BCAA)分解代谢紊乱与胰岛素抵抗相关,并导致全身BCAAs水平升高。啮齿动物实验证据表明,富含BCAAs的膳食蛋白质可增加BCAA分解代谢,但人体相关证据有限。
我们假设富含BCAAs的饮食会增加BCAA分解代谢,这将表现为空腹血浆BCAA浓度降低。
采用气相色谱-飞行时间质谱法,对27名患有代谢综合征的肥胖女性在减肥前后的代谢组进行研究,以确定BCAA代谢的变化。受试者参加了一项为期8周的减肥研究,其中包括补充20克/天的乳清蛋白(乳清蛋白组,n = 16)或明胶(明胶组,n = 11)。按重量匹配总蛋白时,乳清蛋白的BCAAs含量是明胶蛋白的3倍。
干预后,异亮氨酸(明胶组:637 ± 18,定量离子峰高÷100;乳清蛋白组:744 ± 65)、亮氨酸(明胶组:1210 ± 33;乳清蛋白组:1380 ± 79)和缬氨酸(明胶组:2080 ± 59;乳清蛋白组:2510 ± 230)的血浆丰度在治疗组之间没有差异。在基线时,BCAAs与胰岛素抵抗的稳态模型评估显著相关(亮氨酸、异亮氨酸和缬氨酸的r分别为0.52、0.43和0.49;均P < 0.05),但在干预后相关性不再显著。在多变量统计分析中发现,与脯氨酸和半胱氨酸相关的途径可区分乳清蛋白与明胶蛋白补充剂。
这些发现表明,在每天补充20克乳清蛋白的剂量下,BCAA代谢充其量仅受到适度影响。此外,干预后BCAA与稳态模型评估之间关联的丧失表明,与热量限制或蛋白质摄入相关的因素会影响血浆BCAAs与胰岛素敏感性之间的关系。该试验在clinicaltrials.gov上注册,注册号为NCT00739479。