Pancreatic β-cell function increases in a linear dose-response manner following exercise training in adults with prediabetes

Pancreatic β-cell function increases in a linear dose-response manner following exercise training in adults with prediabetes
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DOI:
10.1152/ajpendo.00260.2013
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发表时间:
2013-11-01
影响因子:
5.1
通讯作者:
Kirwan, John P.
Kirwan, John P.
中科院分区:
医学2区
文献类型:
--
作者:
Malin, Steven K.;Solomon, Thomas P. J.;Kirwan, John P.

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尽管一些研究表明,运动和胰岛素敏感性之间存在线性剂量-反应关系,但增强胰岛β细胞功能所需的运动剂量尚不清楚。35名患有前驱糖尿病的老年肥胖成年人接受了持续12周的有监督的运动干预(5天/周,60分钟,最大心率类似于85%)。胰岛素和C-肽对OGTT的反应被用来定义第一相和第二相倾向指数(DI;β细胞功能=葡萄糖刺激的胰岛素分泌×钳夹衍生的胰岛素敏感性)。干预前后分别测量最大耗氧量(V)/DOTO(2max)和身体成分(双能X线骨密度仪和计算机断层扫描)。使用(V)对Doto(2max)心率导出的线性回归方程计算运动剂量。受试者在干预期间消耗了474.5+/-8.8千卡/次(2,372.5+/-44.1千卡/周),并减去了类似8%的体重。运动使第一时相和第二时相DI增加,且这些变化与运动剂量呈线性相关(第一时相:r=0.54P&t;0.001;第二时相:r=0.56P=0.0005)。强化的DI与训练后DOTO(2max)增加(V)(DI第一阶段:R=0.36,P=0.04;DI第二阶段:R=0.41,P<0.02)有关,但不与降低体脂有关(DI第一阶段:R=-0.21,P=0.25;DI第二阶段:R=-0.30,P=0.10)。低基线DI预示着干预后DI的增加(DI第一阶段:R=-0.37;DI第二阶段:R=-0.41,每个P<0.04)。因此,在患有糖尿病前期的成年人中,运动训练和减肥以线性剂量-反应方式增加胰岛β细胞功能。我们的数据表明,对于胰岛素分泌能力较差的成年人来说,更高的运动量(即2000千卡/周)对于增强β细胞功能是必要的。
Although some studies suggest that a linear dose-response relationship exists between exercise and insulin sensitivity, the exercise dose required to enhance pancreatic beta-cell function is unknown. Thirty-five older obese adults with prediabetes underwent a progressive 12-wk supervised exercise intervention (5 days/wk for 60 min at similar to 85% HRmax). Insulin and C-peptide responses to an OGTT were used to define the first- and second-phase disposition index (DI; beta-cell function = glucose-stimulated insulin secretion X clamp-derived insulin sensitivity). Maximum oxygen consumption ((V) over dotO(2max)) and body composition (dual-energy X-ray absorptiometry and computed tomography) were also measured before and after the intervention. Exercise dose was computed using (V) over dotO(2max) heart-rate derived linear regression equations. Subjects expended 474.5 +/- 8.8 kcal/session (2,372.5 +/- 44.1 kcal/wk) during the intervention and lost similar to 8% body weight. Exercise increased first- and second-phase DI (P < 0.05), and these changes in DI were linearly related to exercise dose (DIfirst phase: r =0.54, P < 0.001; DIsecond phase: r = 0.56, P = 0.0005). Enhanced DI was also associated with increased (V) over dotO(2max) (DIfirst phase: r = 0.36, P = 0.04; DIsecond phase: r = 0.41, P < 0.02) but not lower body fat (DIfirst phase: r = -0.21, P = 0.25; DIsecond phase: r = -0.30, P = 0.10) after training. Low baseline DI predicted an increase in DI after the intervention (DIfirst phase: r = -0.37; DIsecond phase: r = -0.41, each P < 0.04). Thus, exercise training plus weight loss increased pancreatic beta-cell function in a linear dose-response manner in adults with prediabetes. Our data suggest that higher exercise doses (i.e., >2,000 kcal/wk) are necessary to enhance beta-cell function in adults with poor insulin secretion capacity.