EUGLYCEMIC HYPERINSULINEMIA AUGMENTS AMINO-ACID-UPTAKE BY HUMAN LEG TISSUES DURING HYPERAMINOACIDEMIA
EUGLYCEMIC HYPERINSULINEMIA AUGMENTS AMINO-ACID-UPTAKE BY HUMAN LEG TISSUES DURING HYPERAMINOACIDEMIA
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DOI：
10.1152/ajpendo.1990.259.2.e185
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发表时间：
1990-08-01
影响因子：
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通讯作者：
RENNIE, MJ
中科院分区：
文献类型：
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作者：
BENNET, WM;CONNACHER, AA;RENNIE, MJ
胰岛素对腿部和全身蛋白质周转的影响通过腿部交换以及氨基酸（AA）充足期间[15N]苯丙氨酸和[1-13C]亮氨酸的血浆动力学来确定。研究了八名健康受试者在单独 AA 输注期间以及在输注葡萄糖和胰岛素 (0.29 nmol .cntdot. m-2 .cntdot. min-1) 和额外 AA 期间的情况。胰岛素强烈刺激AA所见的正腿AA平衡（单独AA，2.6.+-.6.1对比胰岛素+AA，33.1.+-.5.8nmol苯丙氨酸.cntdot.100gleg-1.cntdot.min-1；P <0.001）。在胰岛素加 AA 期间，腿部组织对苯丙氨酸的摄取增加（47.3 .+-. 11.5 与 73.1 .+-. 7.3 nmol .cntdot. 100 g-1 .cntdot. min-1；P = 0.022），但腿部苯丙氨酸释放仅略有减少（44.7 .+-. 8.1 与 40.0） .+-. 7.9 nmol .cntdot. 100 g-1 .cntdot 分钟-1)。腿部非氧化亮氨酸加α-酮异己酸(KIC)的摄取随着胰岛素而略有增加(129.+-.26对比146.+-.21nmol.cntdot.100g-1.cntdot.min-1)，但腿部亮氨酸氧化增加四倍(P＝0.012)。腿部亮氨酸加 KIC 释放因胰岛素而减少（120.+-.17 与 84.+-.10 nmol.cntdot.100 g-1 min-1；P = 0.024）。胰岛素使全身非氧化亮氨酸处理量增加（1.90 .+-. 0.07 vs. 2.10 .+-. 0.07 .mu.mol .cntdot. kg-1 min-1；P = 0.005）；亮氨酸和苯丙氨酸的内源亮氨酸出现随着胰岛素的增加而减少（亮氨酸，1.97 .+-. 0.08 vs. 1.65 .+-. 0.10；苯丙氨酸，0.76 .+-. 0.03 vs. 0.54 .+-. 0.08 .mu.mol .cntdot. kg-1 .cntdot.分钟-1；P < 0.02)。结果表明，含有足够氨基酸的胰岛素可以通过刺激蛋白质合成和抑制蛋白质分解等机制来刺激腿部和全身蛋白质平衡。
The effect of insulin on leg and whole body protein turnover was determined by leg exchange and plasma kinetics of [15N]phenylalanine and [1-13C]leucine during amino acid (AA) sufficiency. Eight healthy subjects were studied during AA infusion alone and during infusion of glucose and insulin (0.29 nmol .cntdot. m-2 .cntdot. min-1) with additional AA. Insulin strongly stimulated the positive leg AA balance seen with AA (AA alone, 2.6 .+-. 6.1 vs. insulin + AA, 33.1 .+-. 5.8 nmol phenylalanine .cntdot. 100 g leg-1 .cntdot. min-1; P < 0.001). Phenylalanine uptake by leg tissues rose during insulin plus AA (47.3 .+-. 11.5 vs. 73.1 .+-. 7.3 nmol .cntdot. 100 g-1 .cntdot. min-1; P = 0.022) but with only a slight reduction in leg phenylalanine release (44.7 .+-. 8.1 vs. 40.0 .+-. 7.9 nmol .cntdot. 100 g-1 .cntdot. min-1). Leg nonoxidative leucine plus .alpha.-ketoisocaproate (KIC) uptake was increased slightly with insulin (129 .+-. 26 vs. 146 .+-. 21 nmol .cntdot. 100 g-1 .cntdot. min-1), but leg leucine oxidation increased fourfold (P = 0.012). Leg leucine plus KIC release was reduced by insulin (120 .+-. 17 vs. 84 .+-. 10 nmol .cntdot. 100 g-1 min-1; P = 0.024). Whole body nonoxidative leucine disposal increased with insulin (1.90 .+-. 0.07 vs. 2.10 .+-. 0.07 .mu.mol .cntdot. kg-1 min-1; P = 0.005); endogenous leucine appearance of leucine and phenylalanine decreased with insulin (leucine, 1.97 .+-. 0.08 vs. 1.65 .+-. 0.10; phenylalanine, 0.76 .+-. 0.03 vs. 0.54 .+-. 0.08 .mu.mol .cntdot. kg-1 .cntdot. min-1; P < 0.02). The results suggest that insulin, given with sufficient amino acids, may stimulate leg and whole body protein balance by mechanisms including stimulation of protein synthesis and inhibition of protein breakdown.