EFFECT OF CORTISOL ON ENERGY-EXPENDITURE AND AMINO-ACID-METABOLISM IN HUMANS
EFFECT OF CORTISOL ON ENERGY-EXPENDITURE AND AMINO-ACID-METABOLISM IN HUMANS
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DOI：
10.1152/ajpendo.1995.268.3.e501
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发表时间：
1995-03-01
影响因子：
5.1
通讯作者：
MATTHEWS, DE
中科院分区：
文献类型：
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作者：
BRILLON, DJ;ZHENG, B;MATTHEWS, DE
氢化可的松以0、80和200 mU·kg(-1)·h(-1)三次给9名健康成人过夜，血浆皮质醇浓度分别为10.6+/-1.2、34.0+/-2.0和64.9+/-4.3 mU/dl。在高皮质醇血症的最后7h输注L-[1-C-13]亮氨酸、L-[苯基-H-2(5)]苯丙氨酸和L-[2-N-15]谷氨酰胺，测定氨基酸动力学。在最后3.5h内，静脉滴注生长抑素、胰升糖素和胰岛素以降低皮质醇引起的血浆胰岛素升高至基础水平。高皮质醇血症可增加血糖、游离脂肪酸(FFA)和胰岛素浓度。生长抑素钳夹制度使胰岛素恢复到基础水平，但增加了血糖和游离脂肪酸。根据亮氨酸和苯丙氨酸出现率的增加，急性皮质醇血症使蛋白质分解增加5-20%。高皮质醇血症时胰岛素正常化不改变苯丙氨酸流量，但增加亮氨酸出现率，后者提示胰岛素影响高皮质醇血症时亮氨酸代谢。随着皮质醇升高，被氧化的亮氨酸通量的比例没有显著增加，但以非氧化途径摄取亮氨酸来合成蛋白质的处理增加。高皮质醇通过增加蛋白质分解和合成来增加氨基酸的循环，但这一过程的增加可能只增加静息能量消耗(REE)1-2%。高皮质醇血症通过增加从头合成以剂量依赖的方式增加谷氨酰胺流量，这可能反映了骨骼肌释放的增加。在80和200亩·kg(-1)·h(-1)的输注速率下，高皮质醇血症使REE增加9-15%。呼吸商并没有随着皮质醇的注射而上升，而是有下降的趋势，这表明REE的增加是由脂肪氧化增加所致。这些数据表明，高皮质醇血症增加了代谢率，可能是损伤时高代谢状态的部分原因。
Hydrocortisone was infused overnight into nine normal healthy adults on three occasions at 0, 80, and 200 mu g.kg(-1).h(-1), producing plasma cortisol concentrations of 10.6 +/- 1.2, 34.0 +/- 2.0, and 64.9 +/- 4.3 mu g/dl, respectively. L-[1-C-13]leucine, L-[phenyl-H-2(5)]phenylalanine, and L-[2-N-15]glutamine were infused during the last 7 h of hypercortisolemia to measure amino acid kinetics. During the last 3.5 h, somatostatin, glucagon, and insulin were infused to reduce the cortisol-induced elevation in plasma insulin to basal. Hypercortisolemia increased plasma glucose, free fatty acid (FFA), and insulin concentrations. Institution of the somatostatin clamp returned insulin to basal but increased glucose and FFA. Acute hypercortisolemia increased protein breakdown 5-20%, as measured by increases in leucine and phenylalanine appearance rates. Normalizing insulin during hypercortisolemia did not alter phenylalanine flux but en hanced leucine appearance rate, the latter result indicating that insulin was affecting leucine metabolism during hypercortisolemia. The fraction of the leucine flux that was oxidized was not significantly increased with hypercortisolemia, but disposal by the nonoxidative route of leucine uptake for protein synthesis was increased. Hypercortisolemia increased cycling of amino acids by increasing protein breakdown and synthesis, but the increase in this process could have increased resting energy expenditure (REE) only 1-2%. Hypercortisolemia increased glutamine flux in a dose-dependent fashion through an increase in de novo synthesis, which presumably reflects increased release from skeletal muscle. Hypercortisolemia increased REE 9-15% at the 80 and 200 mu g.kg(-1).h(-1) infusion rates. Respiratory quotient did not rise with cortisol infusion but tended to decrease, suggesting that the increase in REE was fueled by increased oxidation of fat. These data demonstrate that hypercortisolemia increases metabolic rate and may be in part responsible for the hypermetabolic state in injury.