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儿茶酚胺对糖尿病大鼠骨骼肌胰岛素抵抗发生发展的间接作用。

Indirect effect of catecholamines on development of insulin resistance in skeletal muscle from diabetic rats.

作者信息

Boström M, Nie Z, Goertz G, Henriksson J, Wallberg-Henriksson H

机构信息

Department of Clinical Physiology, Karolinska Institute, Huddinge University Hospital, Stockholm, Sweden.

出版信息

Diabetes. 1989 Jul;38(7):906-10. doi: 10.2337/diab.38.7.906.

DOI:10.2337/diab.38.7.906
PMID:2567684
Abstract

The role of an increased sympathetic activation in the development of insulin resistance in diabetic skeletal muscle was investigated. Epitrochlearis muscles from rats with streptozocin-induced diabetes and from controls were incubated in vitro for 0.5-12.0 h. Diabetes decreased maximal insulin-stimulated (20 mU/ml) glucose transport capacity by 60% (P less than .001), but this decreased insulin responsiveness returned to normal on in vitro incubation (3.79 +/- 0.59 before vs. 8.92 +/- 0.64 mumol.ml-1.h-1 after 12 h of incubation). The reversal of decreased insulin responsiveness in diabetic muscles did not require the presence of insulin and was not affected by the presence of 5.0 x 10(-8) M of epinephrine. However, it was possible to partially prevent the development of insulin resistance with regard to glucose transport by treating the rats with the beta-adrenergic antagonist propranolol (0.5 mg/kg) every 12 h during the entire 72-h period in which the animals were kept diabetic (insulin responsiveness was 3.16 +/- 0.40 mumol.ml-1.h-1 for saline-injected group vs. 5.55 +/- 0.46 mumol.ml-1.h-1 for propranolol-treated group). This effect was not present after a single injection of the drug 2 h before the experiment or when propranolol treatment was withdrawn 12 h before the experiment. The beta-adrenergic blockade markedly reduced the plasma concentration of free fatty acids (0.5 +/- 0.01 mumol/ml for propranolol-treated rats vs. 1.1 +/- 0.1 mumol/ml for saline-treated rats; P less than .001).(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

研究了交感神经激活增强在糖尿病骨骼肌胰岛素抵抗发生发展中的作用。将链脲佐菌素诱导的糖尿病大鼠和对照大鼠的肱三头肌在体外孵育0.5 - 12.0小时。糖尿病使最大胰岛素刺激(20 mU/ml)的葡萄糖转运能力降低60%(P <.001),但这种降低的胰岛素反应性在体外孵育后恢复正常(孵育12小时前为3.79 ± 0.59,孵育后为8.92 ± 0.64 μmol·ml⁻¹·h⁻¹)。糖尿病肌肉中胰岛素反应性降低的逆转不需要胰岛素存在,且不受5.0×10⁻⁸ M肾上腺素存在的影响。然而,在动物保持糖尿病状态的整个72小时期间,每12小时用β - 肾上腺素能拮抗剂普萘洛尔(0.5 mg/kg)治疗大鼠,有可能部分预防葡萄糖转运方面胰岛素抵抗的发生发展(注射生理盐水组的胰岛素反应性为3.16 ± 0.40 μmol·ml⁻¹·h⁻¹,普萘洛尔治疗组为5.55 ± 0.46 μmol·ml⁻¹·h⁻¹)。在实验前2小时单次注射该药物后或在实验前12小时停止普萘洛尔治疗后,这种效果不存在。β - 肾上腺素能阻断显著降低了游离脂肪酸的血浆浓度(普萘洛尔治疗的大鼠为0.5 ± 0.01 μmol/ml,注射生理盐水的大鼠为1.1 ± 0.1 μmol/ml;P <.001)。(摘要截断于250字)

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