Center for Human Nutrition, David Geffen School of Medicine, Division of Molecular Medicine, Department of Anesthesiology, University of California, Los Angeles, CA.
Division of Molecular Medicine, Department of Anesthesiology, David Geffen School of Medicine, University of California, Los Angeles, CA.
Am J Clin Nutr. 2019 Jun 1;109(6):1569-1577. doi: 10.1093/ajcn/nqz024.
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.
The aim of this pilot study was to determine the effects of BCAA supplementation on glucose metabolism in obese, prediabetic individuals.
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.
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%).
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.
最近的研究表明，肥胖、胰岛素抵抗个体的循环支链氨基酸（BCAA）水平升高。然而，尚不清楚额外补充 BCAA 是否会进一步损害葡萄糖代谢。
本研究旨在确定 BCAA 补充对肥胖、糖尿病前期个体葡萄糖代谢的影响。
这是一项涉及 12 名肥胖、糖尿病前期个体的随机交叉研究。参与者被随机分配接受每天补充 20 g BCAA 或低 BCAA 蛋白的补充剂，中间有 2 周的洗脱期。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葡萄糖、胰岛素和与胰岛素抵抗相关的生物标志物。
BCAA 补充剂趋于降低 OGTT 测量的血浆葡萄糖 AUC（OGTT 补充剂基线的 AUC 百分比变化，BCAA：-3.3%±3%；低 BCAA：10.0%±6%；P=0.08）。然而，BCAA 补充剂对 OGTT 期间的血浆胰岛素没有影响（BCAA：-3.9%±8%；低 BCAA：14.8%±10%；P=0.28）。与低 BCAA 对照相比，BCAA 补充剂显著降低了神经生长因子（BCAA：4.0±1 pg/mL；低 BCAA：5.7±1 pg/mL；P=0.01）和单核细胞趋化蛋白-1（BCAA：-0.4%±9%；低 BCAA：29.0%±18%；P=0.02）的血浆浓度。BCAA 补充剂显著升高了血浆白细胞介素 1β（BCAA：231.4%±187%；低 BCAA：20.6%±33%；P=0.05）。BCAA 补充剂对循环亮氨酸（BCAA：9.0%±12%；低 BCAA：9.2%±11%）、缬氨酸（BCAA：9.1%±11%；低 BCAA：12.0%±13%）或异亮氨酸（BCAA：2.5%±11%；低 BCAA：7.3%±11%）的浓度没有影响。
我们的数据表明，BCAA 补充剂对肥胖、糖尿病前期个体的葡萄糖代谢没有损害。需要进一步的研究来证实本研究中的结果。本研究在 clinicaltrials.gov 上注册为 NCT03715010。
