Marchesini G, Bianchi G, Rossi B, Muggeo M, Bonora E
Department of Internal Medicine and Gastroenterology, Unit of Metabolic Diseases, University of Bologna, Bologna, Italy.
Int J Obes Relat Metab Disord. 2000 May;24(5):552-8. doi: 10.1038/sj.ijo.0801195.
To investigate the effects of hyperglycaemia and hyperinsulinaemia on amino acid disposal in human obesity.
Four sequential experimental conditions: (1) overnight fasting; (2) hyperglycaemia with hyperinsulinaemia (2 h hyperglycaemic clamp at 11 mmol/l); (3) hyperglycaemia with basal insulin (1 h hyperglycaemic clamp during somatostatin infusion), (4) hyperglycaemia with resuming hyperinsulinaemia (1 h hyperglycaemic clamp after somatostatin discontinuation).
Seven non-obese and seven obese non-diabetic, normo-insulinaemic subjects.
Glucose infused to maintain steady-state hyperglycaemia. Plasma insulin, glucagon, free fatty acid and amino acid concentrations in the last 20 min of the four experimental conditions. Net rates of plasma amino acid disappearance and appearance (micromol/l per hour), calculated as the slopes of the regression of amino acid concentration on time.
The amount of glucose infused to maintain hyperglycaemia was reduced by nearly 50% in obese subjects. During hyperinsulinaemia, FFA suppression was lower in obese subjects. In all experimental conditions plasma amino acid levels were slightly, non-significantly higher in obese than in non-obese subjects. In both groups plasma amino acids decreased slightly with ongoing fasting, decreased remarkably during hyperglycaemia-hyperinsulinaemia, rose promptly when insulin concentration was suppressed by somatostatin infusion, and declined again after somatostatin discontinuation. Also the time-course of plasma branched-chain amino acids, which paralleled that of total amino acids, was similar in the two groups. The net rates of amino acid disappearance from plasma did not differ in obese and non-obese subjects both at fasting and during hyperglycaemia-hyperinsulinaemia. Also plasma amino acid appearance during hyperglycaemia with basal insulin was not different in the two groups.
The net traffic of amino acids to and from plasma in relation to insulin drive and prevailing glucose is not impaired in obese subjects with normal glucose tolerance, in spite of a decreased insulin sensitivity of glucose and lipid metabolism.
研究高血糖和高胰岛素血症对人类肥胖中氨基酸代谢的影响。
四个连续的实验条件：（1）过夜禁食；（2）高血糖伴高胰岛素血症（在11 mmol/l下进行2小时高血糖钳夹）；（3）高血糖伴基础胰岛素（在生长抑素输注期间进行1小时高血糖钳夹）；（4）高血糖伴恢复高胰岛素血症（生长抑素停用后进行1小时高血糖钳夹）。
7名非肥胖和7名肥胖的非糖尿病、正常胰岛素血症受试者。
输注葡萄糖以维持稳态高血糖。在四个实验条件的最后20分钟内测定血浆胰岛素、胰高血糖素、游离脂肪酸和氨基酸浓度。计算血浆氨基酸消失和出现的净速率（微摩尔/升每小时），以氨基酸浓度对时间的回归斜率表示。
肥胖受试者为维持高血糖所需输注的葡萄糖量减少了近50%。在高胰岛素血症期间，肥胖受试者的游离脂肪酸抑制作用较低。在所有实验条件下，肥胖受试者的血浆氨基酸水平略高于非肥胖受试者，但差异无统计学意义。两组中，血浆氨基酸在持续禁食期间略有下降，在高血糖-高胰岛素血症期间显著下降，在生长抑素输注抑制胰岛素浓度时迅速上升，在生长抑素停用后再次下降。两组中血浆支链氨基酸的时间进程与总氨基酸相似。肥胖和非肥胖受试者在禁食和高血糖-高胰岛素血症期间血浆氨基酸的消失净速率没有差异。两组在基础胰岛素存在的高血糖期间血浆氨基酸的出现也没有差异。
尽管葡萄糖和脂质代谢的胰岛素敏感性降低，但糖耐量正常的肥胖受试者中，与胰岛素驱动和主要葡萄糖相关的血浆氨基酸的净转运并未受损。
