Effects of branched-chain amino acids on glucose metabolism in obese, prediabetic men and women: a randomized, crossover study.
Effects of branched-chain amino acids on glucose metabolism in obese, prediabetic men and women: a randomized, crossover study.
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DOI：
10.1093/ajcn/nqz024
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发表时间：
2019-06
期刊：
影响因子：
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通讯作者：
S. Woo;Jieping Yang;Mark Hsu;Alicia Yang;Lijun Zhang;Ru-po Lee;Irene Gilbuena;G. Thames;Jianjun Huang;Anna Rasmussen;C. Carpenter;S. Henning;D. Heber;Yibin Wang;Zhaoping Li
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文献类型：
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作者：
S. Woo;Jieping Yang;Mark Hsu;Alicia Yang;Lijun Zhang;Ru-po Lee;Irene Gilbuena;G. Thames;Jianjun Huang;Anna Rasmussen;C. Carpenter;S. Henning;D. Heber;Yibin Wang;Zhaoping Li
背景：最近的研究表明，肥胖、胰岛素抵抗的个体循环中的支链氨基酸(BCAA)水平升高。然而，补充额外的支链氨基酸是否会进一步损害葡萄糖代谢尚不清楚。目的研究补充支链氨基酸对肥胖、糖尿病前期人群糖代谢的影响。方法这是一项随机交叉研究，涉及12名患有糖尿病前期的肥胖者。参与者被随机分配到每天服用含有20g支链氨基酸或低支链氨基酸蛋白质的补充剂，持续4wk，其间进行2wk的洗涤。每次就诊时，进行口服葡萄糖耐量试验(OGTT)。采集的血液样本用于测量血糖、胰岛素和胰岛素抵抗相关生物标记物。结果补充支链氨基酸有降低OGTT测得的血糖曲线下面积(AUC)的趋势(AUC较补充前：-3.3%±3%；低BCAA：10.0%±6%；P=0.08)。然而，补充支链氨基酸对OGTT激发时的血浆胰岛素没有影响(支链氨基酸：-3.9%±8%；低支链氨基酸：14.8%±10%；P=0.28)。补充支链氨基酸后，血浆神经生长因子(支链氨基酸：4.0±1pg/mL；低支链支链氨基酸：5.7±1pg/mL；P=0.01)和单核细胞趋化蛋白-1(支链支链氨基酸：-0.4%±9%；低支链支链氨基酸：29.0%±18%；P=0.02)的浓度明显低于低支链氨基酸对照组。补充支链氨基酸后，血浆IL-1β水平显著升高(支链氨基酸：231.4%±187%；低支链氨基酸：20.6%±33%；P=0.05)。补充支链氨基酸不影响支链氨基酸循环中亮氨酸(支链氨基酸：9.0%±12%；低支链氨基酸：9.2%±11%)、缬氨酸(支链氨基酸：9.1%±11%；低支链氨基酸：12.0%±13%)或异亮氨酸(支链氨基酸：2.5%±11%；低支链氨基酸：7.3%±11%)的循环浓度。结论我们的数据表明，补充支链氨基酸不会损害肥胖、糖尿病前期受试者的糖代谢。还需要进一步的研究来证实本研究的结果。这项研究在Clinicaltrials.gov上注册为NCT03715010。
BACKGROUND Recent studies have shown that circulating branched-chain amino acids (BCAAs) are elevated in obese, insulin-resistant individuals. However, it is not known if supplementation of additional BCAAs will further impair glucose metabolism. OBJECTIVES The aim of this pilot study was to determine the effects of BCAA supplementation on glucose metabolism in obese, prediabetic individuals. METHODS This is a randomized crossover study involving 12 obese individuals with prediabetes. Participants were randomly assigned to receive a daily supplement containing either 20 g BCAA or protein low in BCAAs for 4 wk with a 2-wk washout in between. At each visit, an oral-glucose-tolerance test (OGTT) was performed. Collected blood samples were used to measure glucose, insulin, and insulin resistance-associated biomarkers. RESULTS BCAA supplementation tended to decrease the plasma glucose area under the curve (AUC) measured by the OGTT (AUC percentage change from supplementation baseline, BCAA: -3.3% ± 3%; low-BCAA: 10.0% ± 6%; P = 0.08). However, BCAA supplementation did not affect plasma insulin during OGTT challenge (BCAA: -3.9% ± 8%; low-BCAA: 14.8% ± 10%; P = 0.28). The plasma concentrations of nerve growth factor (BCAA: 4.0 ± 1 pg/mL; low-BCAA: 5.7 ± 1 pg/mL; P = 0.01) and monocyte chemoattractant protein-1 (BCAA: -0.4% ± 9%; low-BCAA: 29.0% ± 18%; P = 0.02) were significantly lowered by BCAA supplementation compared to low-BCAA control. Plasma interleukin 1β was significantly elevated by BCAA supplementation (BCAA: 231.4% ± 187%; low-BCAA: 20.6% ± 33%; P = 0.05). BCAA supplementation did not affect the circulating concentrations of the BCAAs leucine (BCAA: 9.0% ± 12%; low-BCAA: 9.2% ± 11%), valine (BCAA: 9.1% ± 11%; low-BCAA: 12.0% ± 13%), or isoleucine (BCAA: 2.5% ± 11%; low-BCAA: 7.3% ± 11%). CONCLUSIONS Our data suggest that BCAA supplementation did not impair glucose metabolism in obese, prediabetic subjects. Further studies are needed to confirm the results seen in the present study. This study was registered at clinicaltrials.gov as NCT03715010.