Benn J J, Brown P M, Beckwith L J, Farebrother M, Sönksen P H
Department of Medicine, United Medical School, St. Thomas's Hospital, London, United Kingdom.
Diabetes Care. 1992 Nov;15(11):1721-6. doi: 10.2337/diacare.15.11.1721.
To assess the effect of selective beta 1-blockade (atenolol and betaxolol) and nonselective beta-blockade (propranolol) on glucose turnover in subjects with insulin-dependent (type I) diabetes mellitus during moderate exercise.
Five subjects with type I diabetes were infused with insulin and then exercised for 1 h, after pretreatment with each of the three drugs or saline and, on a separate day, after withdrawal of insulin. Glucose turnover was measured using tritiated glucose.
Plasma glucose, initially 9.2 +/- 0.5 mmol/L (mean +/- SE) when insulin infused and 14.0 +/- 0.8 when insulin was withdrawn, fell on exercise by 3.4 +/- 1.1 mmol/L (P < 0.05) saline, 4.0 +/- 0.8 mmol/L (P < 0.01) with betaxolol, 3.8 +/- 0.7 mmol/L (P < 0.01) with atenolol, 5.0 +/- 0.6 mmol/L (P < 0.005) with propranolol, and 1.7 +/- 1.0 mmol/L (NS) when insulin was withdrawn. Propranolol, but not the other beta-blockers, caused a significantly greater fall in glucose on exercise than during the control study. Glucose appearance rate (Ra) was similar basally and rose to an almost identical level in all five groups during exercise. Glucose disappearance rate (Rd) rose similarly during exercise, except after propranolol when the rise was significantly greater than with saline (P < 0.01). Failure of glucose to change significantly during exercise when insulin had been withdrawn was associated with the smallest rise in Rd and the highest nonesterified fatty acid concentrations. Propranolol and betaxolol, but not atenolol, reduced nonesterified fatty acids.
We conclude that the greater fall in glucose on exercise after beta-blocking drugs is probably largely a direct effect of beta 2-blockade on muscle, increasing the exercise-induced rise in Rd glucose. This offers support to the use of beta 1-specific drugs, where beta-blockade is necessary in type I diabetes.
评估选择性β1受体阻滞剂(阿替洛尔和美托洛尔)及非选择性β受体阻滞剂(普萘洛尔)对胰岛素依赖型(I型)糖尿病患者在中等强度运动期间葡萄糖代谢的影响。
五名I型糖尿病患者在分别接受三种药物或生理盐水预处理后,以及在单独一天停用胰岛素后,先输注胰岛素,然后运动1小时。使用氚标记葡萄糖测量葡萄糖代谢率。
输注胰岛素时血浆葡萄糖初始值为9.2±0.5 mmol/L(均值±标准误),停用胰岛素时为14.0±0.8 mmol/L,运动期间生理盐水组下降3.4±1.1 mmol/L(P<0.05),美托洛尔组下降4.0±0.8 mmol/L(P<0.01),阿替洛尔组下降3.8±0.7 mmol/L(P<0.01),普萘洛尔组下降5.0±0.6 mmol/L(P<0.005),停用胰岛素时下降1.7±1.0 mmol/L(无显著性差异)。与对照研究相比,普萘洛尔而非其他β受体阻滞剂导致运动期间葡萄糖下降幅度显著更大。基础葡萄糖出现率(Ra)相似,运动期间所有五组均升至几乎相同水平。运动期间葡萄糖消失率(Rd)同样上升,但普萘洛尔组上升幅度显著大于生理盐水组(P<0.01)。停用胰岛素后运动期间葡萄糖无显著变化与Rd最小上升及最高非酯化脂肪酸浓度相关。普萘洛尔和美托洛尔而非阿替洛尔降低了非酯化脂肪酸。
我们得出结论,β受体阻滞剂后运动期间葡萄糖下降幅度更大可能主要是β2受体阻滞剂对肌肉的直接作用,增加了运动诱导的Rd葡萄糖上升。这为I型糖尿病中需要β受体阻滞剂时使用β1特异性药物提供了支持。