Shilo S, Sotsky M, Shamoon H
Albert Einstein College of Medicine, Bronx, New York 10561.
J Clin Endocrinol Metab. 1990 Jan;70(1):162-72. doi: 10.1210/jcem-70-1-162.
A decline in plasma insulin and an increase in glucagon are known to occur during intense and/or prolonged exercise. However, it is not established whether changes in insulin and glucagon secretion are involved in the precise matching of hepatic glucose production to the enhanced glucose uptake by muscle during brief, low intensity exercise. We studied the effects of 30-min cycle exercise at 40% of maximal aerobic capacity in healthy subjects and C-peptide-deficient subjects with type 1 diabetes (IDDM) using [3-3H]glucose to estimate glucose turnover. Diabetic subjects were studied during continuous iv insulin infusion, which normalized glucose kinetics before experimental perturbations. In control (saline-infused) experiments, endogenous glucose appearance (Ra) increased by 80-90% above baseline to match the increase in glucose disappearance in both normal and IDDM subjects, even though the latter exercised at fixed levels of plasma free insulin, averaging 203 +/- 19 pmol/L. In other experiments, somatostatin was infused, and glucagon (1.0 ng/kg.min) and insulin (at two different rates) were maintained at constant levels. Infusion of insulin in normal subjects at doses sufficient to maintain constant peripheral plasma insulin was associated with no apparent effect on glucose turnover (plasma insulin, 80 +/- 21 pmol/L, compared to 52 +/- 5 pmol/L during saline; P = NS). However, insulin infusion at doses that normalized the portal insulin concentration (approximately 208 pmol/L) together with glucagon replacement inhibited the rise in glucose production in both normal and IDDM subjects. There were similar 45-55% reductions (P less than 0.03) of the increase in Ra seen with exercise in control experiments. When peripheral plasma free insulin (and presumably portal levels as well) were increased by about 20% in this experimental setting in IDDM (278 +/- 43 pmol/L), the suppression of Ra was even more profound, and Ra failed to increase at all with exercise. We conclude that the hormonal regulation of Ra in brief duration exercise in man does not necessitate the decrements in portal venous insulin observed under more intense exercise conditions as long as an exercise-induced glucagon secretory response can occur. Glucagon secretion alone cannot prevent hypoglycemia when portal venous insulin concentrations are increased by minimal amounts, such as in insulin-treated diabetics.
已知在剧烈和/或长时间运动期间，血浆胰岛素水平会下降，胰高血糖素水平会升高。然而，在短暂的低强度运动期间，胰岛素和胰高血糖素分泌的变化是否参与肝脏葡萄糖生成与肌肉增强的葡萄糖摄取的精确匹配，目前尚无定论。我们使用[3-3H]葡萄糖来估计葡萄糖周转率，研究了健康受试者和1型糖尿病（IDDM）的C肽缺乏受试者在最大有氧能力的40%下进行30分钟自行车运动的影响。在连续静脉输注胰岛素期间对糖尿病受试者进行研究，胰岛素使葡萄糖动力学在实验干扰前恢复正常。在对照（输注生理盐水）实验中，内源性葡萄糖出现率（Ra）比基线水平升高80-90%，以匹配正常和IDDM受试者中葡萄糖消失的增加，尽管后者在固定的血浆游离胰岛素水平下运动，平均为203±19 pmol/L。在其他实验中，输注生长抑素，并将胰高血糖素（1.0 ng/kg·min）和胰岛素（以两种不同速率）维持在恒定水平。在正常受试者中输注足以维持外周血浆胰岛素恒定的剂量的胰岛素，对葡萄糖周转率没有明显影响（血浆胰岛素，80±21 pmol/L，而输注生理盐水期间为52±5 pmol/L；P=无显著性差异）。然而，输注使门静脉胰岛素浓度正常化（约208 pmol/L）的剂量的胰岛素并补充胰高血糖素，可抑制正常和IDDM受试者中葡萄糖生成的增加。在对照实验中，运动时观察到的Ra增加有类似的45-55%的降低（P<0.03）。在这种实验设置下，当IDDM受试者的外周血浆游离胰岛素（可能门静脉水平也一样）增加约20%（278±43 pmol/L）时，对Ra的抑制作用更显著，并且运动时Ra根本没有增加。我们得出结论，只要能发生运动诱导的胰高血糖素分泌反应，在人类短暂运动中对Ra的激素调节并不需要在更剧烈运动条件下观察到的门静脉胰岛素的减少。当门静脉胰岛素浓度仅少量增加时，如在胰岛素治疗的糖尿病患者中，仅胰高血糖素分泌不能预防低血糖。
