Exercise Intensity Modulates Glucose-Stimulated Insulin Secretion when Adjusted for Adipose, Liver and Skeletal Muscle Insulin Resistance

Exercise Intensity Modulates Glucose-Stimulated Insulin Secretion when Adjusted for Adipose, Liver and Skeletal Muscle Insulin Resistance
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DOI:
10.1371/journal.pone.0154063
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发表时间:
2016-04-25
期刊:
影响因子:
3.7
通讯作者:
Weltman, Arthur
Weltman, Arthur
中科院分区:
综合性期刊3区
文献类型:
--
作者:
Malin, Steven K.;Rynders, Corey A.;Weltman, Arthur

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当调整脂肪、肝脏和骨骼肌胰岛素抵抗(IR)时,运动强度对葡萄糖刺激的胰岛素分泌(GSIS)代偿性变化的影响知之甚少。15名与会者(8名女性,年龄:49.9 +/-3.6岁; BMI:31.0 +/- 1.5kg/m2; VO(2)峰值:23.2 +/- 1.2mg/kg/min)伴前驱糖尿病(ADA标准,75 g OGTT和/或HbA(1c))进行时间过程匹配的控制,并在中等强度下进行等热量(200 kcal)运动(MIE;乳酸阈值(LT))和高强度(HIE; LT和VO(2)峰值之间差异的75%)。在运动/对照后1小时进行75 g OGTT,并测定血浆葡萄糖、胰岛素、C肽和游离脂肪酸以计算骨骼肌(1/口服最小模型; SMIR)、肝脏(HOMA(IR))和脂肪(ADIPOSE(IR))IR。通过GSIS的去卷积建模和处置指数(DI; GSIS/IR; DISMIR、DIHOMAIR、DIADIPOSEIR)计算来测定胰岛素分泌速率。与对照组相比,运动组SMIR降低(P< 0.05),且与运动强度无关;与对照组相比,运动组HOMA(IR)和ADIPOSE(IR)升高(P< 0.05)。运动后GSIS无明显下降,但DIHOMAIR和DIADIPOSEIR在HIE后较对照组下降更明显(P< 0.05)。然而,DISMIR相对于对照以基于强度的方式增加(P< 0.05),这对应于较低的餐后血糖水平。总之,胰腺胰岛素分泌以运动强度依赖性方式调节,以匹配骨骼肌、肝脏和脂肪组织中的胰岛素抵抗水平。进一步的工作是必要的,以了解运动影响的机制之间的串扰调节血糖的前驱糖尿病患者的组织。
Little is known about the effects of exercise intensity on compensatory changes in glucose-stimulated insulin secretion (GSIS) when adjusted for adipose, liver and skeletal muscle insulin resistance (IR). Fifteen participants (8F, Age: 49.9 +/- 3.6yr; BMI: 31.0 +/- 1.5kg/m(2); VO(2)peak: 23.2 +/- 1.2mg/kg/min) with prediabetes (ADA criteria, 75g OGTT and/or HbA(1c)) underwent a time-course matched Control, and isocaloric (200kcal) exercise at moderate (MIE; at lactate threshold (LT)), and high-intensity (HIE; 75% of difference between LT and VO(2)peak). A 75g OGTT was conducted 1 hour post-exercise/Control, and plasma glucose, insulin, C-peptide and free fatty acids were determined for calculations of skeletal muscle (1/Oral Minimal Model; SMIR), hepatic (HOMA(IR)), and adipose (ADIPOSE(IR)) IR. Insulin secretion rates were determined by deconvolution modeling for GSIS, and disposition index (DI; GSIS/IR; DISMIR, DIHOMAIR, DIADIPOSEIR) calculations. Compared to Control, exercise lowered SMIR independent of intensity (P< 0.05), with HIE raising HOMA(IR) and ADIPOSE(IR) compared with Control (P< 0.05). GSIS was not reduced following exercise, but DIHOMAIR and DIADIPOSEIR were lowered more following HIE compared with Control (P< 0.05). However, DISMIR increased in an intensity based manner relative to Control (P< 0.05), which corresponded with lower post-prandial blood glucose levels. Taken together, pancreatic insulin secretion adjusts in an exercise intensity dependent manner to match the level of insulin resistance in skeletal muscle, liver and adipose tissue. Further work is warranted to understand the mechanism by which exercise influences the cross-talk between tissues that regulate blood glucose in people with prediabetes.