Everman Sarah, Mandarino Lawrence J, Carroll Chad C, Katsanos Christos S
Center for Metabolic and Vascular Biology, Arizona State University/Mayo Clinic in Arizona, Scottsdale, Arizona, United States of America.
Center for Metabolic and Vascular Biology, Arizona State University/Mayo Clinic in Arizona, Scottsdale, Arizona, United States of America; School of Life Sciences, Arizona State University,Tempe, Arizona, United States of America.
PLoS One. 2015 Mar 17;10(3):e0120049. doi: 10.1371/journal.pone.0120049. eCollection 2015.
Plasma branched-chain amino acids (BCAA) are inversely related to insulin sensitivity of glucose metabolism in humans. However, currently, it is not known whether there is a cause-and-effect relationship between increased plasma BCAA concentrations and decreased insulin sensitivity.
To determine the effects of acute exposure to increased plasma BCAA concentrations on insulin-mediated plasma glucose turnover in humans.
Ten healthy subjects were randomly assigned to an experiment where insulin was infused at 40 mU/m2/min (40U) during the second half of a 6-hour intravenous infusion of a BCAA mixture (i.e., BCAA; N = 5) to stimulate plasma glucose turnover or under the same conditions without BCAA infusion (Control; N = 5). In a separate experiment, seven healthy subjects were randomly assigned to receive insulin infusion at 80 mU/m2/min (80U) in association with the above BCAA infusion (N = 4) or under the same conditions without BCAA infusion (N = 3). Plasma glucose turnover was measured prior to and during insulin infusion.
Insulin infusion completely suppressed the endogenous glucose production (EGP) across all groups. The percent suppression of EGP was not different between Control and BCAA in either the 40U or 80U experiments (P > 0.05). Insulin infusion stimulated whole-body glucose disposal rate (GDR) across all groups. However, the increase (%) in GDR was not different [median (1st quartile - 3rd quartile)] between Control and BCAA in either the 40U ([199 (167-278) vs. 186 (94-308)] or 80 U ([491 (414-548) vs. 478 (409-857)] experiments (P > 0.05). Likewise, insulin stimulated the glucose metabolic clearance in all experiments (P < 0.05) with no differences between Control and BCAA in either of the experiments (P > 0.05).
Short-term exposure of young healthy subjects to increased plasma BCAA concentrations does not alter the insulin sensitivity of glucose metabolism.
血浆支链氨基酸(BCAA)与人体葡萄糖代谢的胰岛素敏感性呈负相关。然而,目前尚不清楚血浆BCAA浓度升高与胰岛素敏感性降低之间是否存在因果关系。
确定急性暴露于血浆BCAA浓度升高对人体胰岛素介导的血浆葡萄糖周转率的影响。
10名健康受试者被随机分配到一项实验中,在6小时静脉输注BCAA混合物(即BCAA;N = 5)的后半段,以40 mU/m2/分钟(40U)的速度输注胰岛素,以刺激血浆葡萄糖周转率,或在相同条件下不输注BCAA(对照组;N = 5)。在另一项实验中,7名健康受试者被随机分配接受80 mU/m2/分钟(80U)的胰岛素输注,同时进行上述BCAA输注(N = 4),或在相同条件下不输注BCAA(N = 3)。在胰岛素输注之前和期间测量血浆葡萄糖周转率。
胰岛素输注完全抑制了所有组的内源性葡萄糖生成(EGP)。在40U或80U实验中,对照组和BCAA组之间EGP的抑制百分比没有差异(P > 0.05)。胰岛素输注刺激了所有组的全身葡萄糖处置率(GDR)。然而,在40U([199(167 - 278)对186(94 - 308)])或80U([491(414 - 548)对478(409 - 857)])实验中,对照组和BCAA组之间GDR的增加(%)没有差异(P > 0.05)。同样,胰岛素在所有实验中均刺激了葡萄糖代谢清除率(P < 0.05),且在任何一项实验中对照组和BCAA组之间均无差异(P > 0.05)。
年轻健康受试者短期暴露于血浆BCAA浓度升高不会改变葡萄糖代谢的胰岛素敏感性。