PhD, Department of Biomedical Sciences, Panum Institute 4.5.13, University of Copenhagen, Blegdamsvej 3B, Copenhagen 2200, Denmark.
J Clin Endocrinol Metab. 2013 Oct;98(10):4176-86. doi: 10.1210/jc.2013-2232. Epub 2013 Aug 21.
Understanding intersubject variability in glycemic control following exercise training will help individualize treatment.
Our aim was to determine whether this variability is related to training-induced changes in insulin sensitivity or pancreatic β-cell function.
DESIGN, SETTING, AND PARTICIPANTS: We conducted an observational clinical study of 105 subjects with impaired glucose tolerance or type 2 diabetes.
Individual subject changes in fitness (VO2max), glycemia (glycosylated hemoglobin, fasting glucose, oral glucose tolerance test), insulin sensitivity (hyperinsulinemic-euglycemic clamp), oral glucose-stimulated insulin secretion (GSIS), and disposition index (DI) were measured following 12 to 16 weeks of aerobic exercise training. Regression analyses were used to identify relationships between variables.
After training, 86% of subjects increased VO2max and lost weight. Glycosylated hemoglobin, fasting glucose, and 2-hour oral glucose tolerance test were reduced in 69%, 62%, and 68% of subjects, respectively, while insulin sensitivity improved in 90% of the participants. Changes in glycemic control were congruent with changes in GSIS such that 66% of subjects had a reduction in first-phase GSIS, and 46% had reduced second-phase GSIS. Training increased first- and second-phase DI in 83% and 74% of subjects. Training-induced changes in glycemic control were related to changes in GSIS (P < .05), but not insulin sensitivity or DI, and training-induced improvements in glycemic control were largest in subjects with greater pretraining GSIS.
Intersubject variability in restoring glycemic control following exercise is explained primarily by changes in insulin secretion. Thus, baseline and training-induced changes in β-cell function may be a key determinant of training-induced improvements in glycemic control.
了解运动训练后血糖控制的个体差异将有助于实现个体化治疗。
我们旨在确定这种变异性是否与胰岛素敏感性或胰岛β细胞功能的训练诱导变化有关。
设计、设置和参与者：我们对 105 例糖耐量受损或 2 型糖尿病患者进行了一项观察性临床研究。
在 12 至 16 周的有氧运动训练后，测量个体对健身（VO2max）、血糖（糖化血红蛋白、空腹血糖、口服葡萄糖耐量试验）、胰岛素敏感性（高胰岛素正葡萄糖钳夹）、口服葡萄糖刺激的胰岛素分泌（GSIS）和处置指数（DI）的个体变化。回归分析用于确定变量之间的关系。
训练后，86%的患者增加了 VO2max 并减轻了体重。糖化血红蛋白、空腹血糖和 2 小时口服葡萄糖耐量试验分别降低了 69%、62%和 68%，而 90%的参与者胰岛素敏感性提高。血糖控制的变化与 GSIS 的变化一致，即 66%的患者第一相 GSIS 减少，46%的患者第二相 GSIS 减少。83%和 74%的患者第一相和第二相 DI 增加。血糖控制的训练诱导变化与 GSIS 的变化有关（P<0.05），但与胰岛素敏感性或 DI 无关，并且在训练前 GSIS 较高的患者中，血糖控制的改善最大。
运动后恢复血糖控制的个体差异主要由胰岛素分泌的变化解释。因此，β细胞功能的基线和训练诱导变化可能是训练诱导血糖控制改善的关键决定因素。
