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严重糖尿病会抑制大鼠急性抗阻运动后肌肉蛋白质合成的增加。

Severe diabetes prohibits elevations in muscle protein synthesis after acute resistance exercise in rats.

作者信息

Fedele M J, Hernandez J M, Lang C H, Vary T C, Kimball S R, Jefferson L S, Farrell P A

机构信息

Noll Physiological Research Center and Department of Kinesiology, Pennsylvania State University, University Park 16802, USA.

出版信息

J Appl Physiol (1985). 2000 Jan;88(1):102-8. doi: 10.1152/jappl.2000.88.1.102.

Abstract

This study determined whether rates of protein synthesis increase after acute resistance exercise in skeletal muscle from severely diabetic rats. Previous studies consistently show that postexercise rates of protein synthesis are elevated in nondiabetic and moderately diabetic rats. Severely diabetic rats performed acute resistance exercise (n = 8) or remained sedentary (n = 8). A group of nondiabetic age-matched rats served as controls (n = 9). Rates of protein synthesis were measured 16 h after exercise. Plasma glucose concentrations were >500 mg/dl in the diabetic rats. Rates of protein synthesis (nmol phenylalanine incorporated. g muscle(-1). h(-1), means +/- SE) were not different between exercised (117 +/- 7) and sedentary (106 +/- 9) diabetic rats but were significantly (P < 0.05) lower than in sedentary nondiabetic rats (162 +/- 9) and in exercised nondiabetic rats (197 +/- 7). Circulating insulin concentrations were 442 +/- 65 pM in nondiabetic rats and 53 +/- 11 and 72 +/- 19 pM in sedentary and exercised diabetic rats, respectively. Plasma insulin-like growth factor I concentrations were reduced by 33% in diabetic rats compared with nondiabetic rats, and there was no difference between exercised and sedentary diabetic rats. Muscle insulin-like growth factor I was not affected by resistance exercise in diabetic rats. The results show that there is a critical concentration of insulin below which rates of protein synthesis begin to decline in vivo. In contrast to previous studies using less diabetic rats, severely diabetic rats cannot increase rates of protein synthesis after acute resistance exercise.

摘要

本研究确定了重度糖尿病大鼠骨骼肌在急性抗阻运动后蛋白质合成速率是否增加。先前的研究一致表明,非糖尿病和中度糖尿病大鼠运动后蛋白质合成速率会升高。重度糖尿病大鼠进行急性抗阻运动(n = 8)或保持久坐(n = 8)。一组年龄匹配的非糖尿病大鼠作为对照(n = 9)。运动后16小时测量蛋白质合成速率。糖尿病大鼠的血浆葡萄糖浓度>500mg/dl。运动的糖尿病大鼠(117±7)和久坐的糖尿病大鼠(106±9)之间的蛋白质合成速率(nmol苯丙氨酸掺入量·g肌肉-1·h-1,均值±标准误)没有差异,但显著低于久坐的非糖尿病大鼠(162±9)和运动的非糖尿病大鼠(197±7)(P<0.05)。非糖尿病大鼠的循环胰岛素浓度为442±65pM,久坐和运动的糖尿病大鼠分别为53±11和72±19pM。与非糖尿病大鼠相比,糖尿病大鼠的血浆胰岛素样生长因子I浓度降低了33%,运动和久坐的糖尿病大鼠之间没有差异。糖尿病大鼠的肌肉胰岛素样生长因子I不受抗阻运动的影响。结果表明,存在一个关键的胰岛素浓度,低于该浓度时体内蛋白质合成速率开始下降。与先前使用糖尿病程度较轻的大鼠的研究不同,重度糖尿病大鼠在急性抗阻运动后无法提高蛋白质合成速率。

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