Effects of exercise training and diet on lipid kinetics during free fatty acid-induced insulin resistance in older obese humans with impaired glucose tolerance
Effects of exercise training and diet on lipid kinetics during free fatty acid-induced insulin resistance in older obese humans with impaired glucose tolerance
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DOI：
10.1152/ajpendo.00220.2009
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发表时间：
2009-08-01
影响因子：
5.1
通讯作者：
Kirwan, John P.
中科院分区：
文献类型：
--
作者：
Solomon, Thomas P. J.;Haus, Jacob M.;Kirwan, John P.
所罗门TP，豪斯JM，马切蒂CM，斯坦利WC，Kirwan JP.运动训练和饮食对糖耐量受损老年肥胖患者游离脂肪酸诱导胰岛素抵抗期间脂质动力学的影响。Am J Physiol Endocrinol Metab 297：E552-E559，2009.首次发表于2009年6月16日; doi：10.1152/ajpendo.00220.2009。- 游离脂肪酸（FFA）升高与细胞水平的胰岛素抵抗有关。然而，全身脂质动力学对FFA诱导的胰岛素抵抗的贡献还不清楚，运动和饮食对这种代谢缺陷的影响也不清楚。我们研究了在急性FFA诱导的胰岛素抵抗期间，12周的运动训练（有或无热量限制）对FFA周转和氧化（FFA（ox））的影响。16名患有糖耐量受损的肥胖受试者被随机分为两组，（n = 8; -598 +/- 125 kcal/天，66 +/- 1岁，32.8 +/- 1.8 kg/m（2））或正常热量（n = 8; 67 +/- 2岁，35.3 +/- 2.1 kg/m2）饮食和有氧运动（每天1小时，最大摄氧量为65%）方案。在整个7小时，40 mU中评估脂质动力学（[1-C-14]棕榈酸酯）。m（-2）.min（-1）高胰岛素正葡萄糖钳夹，在此期间，在最后5小时内通过持续升高血浆FFA（胰岛素/肝素输注）诱导胰岛素抵抗。尽管低热量组的体重减轻幅度更大（-7.7 +/-0.5vs.-3.3 +/-0.7%，P < 0.001），但FFA诱导的外周胰岛素抵抗在两组中得到了同等程度的改善。然而，仅在低热量组中，低血糖期间循环FFA浓度（2，123 +/- 261 vs. 1，764 +/- 194 mu mol/l，P < 0.05）和FFA转换（3.20 +/- 0.58 vs. 2.19 +/- 0.58 mu mol.kg-1.min（-1），P < 0.01）受到抑制。相比之下，两组在休息时和高血压期间的全身FFA（ox）均有所改善。这些变化是由细胞内脂质衍生的FFAox增加驱动的12.3是由细胞内脂质衍生的FFAox增加驱动的（12.3 +/- 7.7和14.7 +/-7.8%，P < 0.05）。我们的结论是，FFA诱导的胰岛素抵抗运动引起的改善是独立的重量损失和FFA营业额的幅度，但它是与细胞内FFA利用率增加。
Solomon TP, Haus JM, Marchetti CM, Stanley WC, Kirwan JP. Effects of exercise training and diet on lipid kinetics during free fatty acid-induced insulin resistance in older obese humans with impaired glucose tolerance. Am J Physiol Endocrinol Metab 297: E552-E559, 2009. First published June 16, 2009; doi:10.1152/ajpendo.00220.2009. - Elevated free fatty acids (FFA) are implicated with insulin resistance at the cellular level. However, the contribution of whole body lipid kinetics to FFA-induced insulin resistance is not well understood, and the effect of exercise and diet on this metabolic defect is not known. We investigated the effect of 12 wk of exercise training with and without caloric restriction on FFA turnover and oxidation (FFA(ox)) during acute FFA-induced insulin resistance. Sixteen obese subjects with impaired glucose tolerance were randomized to either a hypocaloric (n = 8; -598 +/- 125 kcal/day, 66 +/- 1 yr, 32.8 +/- 1.8 kg/m(2)) or a eucaloric (n = 8; 67 +/- 2 yr, 35.3 +/- 2.1 kg/m(2)) diet and aerobic exercise (1 h/day at 65% of maximal oxygen uptake) regimen. Lipid kinetics ([1-C-14] palmitate) were assessed throughout a 7-h, 40 mU. m(-2).min(-1) hyperinsulinemic euglycemic clamp, during which insulin resistance was induced in the last 5 h by a sustained elevation in plasma FFA (intralipid/heparin infusion). Despite greater weight loss in the hypocaloric group (-7.7 +/- 0.5 vs. -3.3 +/- 0.7%, P < 0.001), FFA-induced peripheral insulin resistance was improved equally in both groups. However, circulating FFA concentrations (2,123 +/- 261 vs. 1,764 +/- 194 mu mol/l, P < 0.05) and FFA turnover (3.20 +/- 0.58 vs. 2.19 +/- 0.58 mu mol.kg FFM-1.min(-1), P < 0.01) during hyperlipemia were suppressed only in the hypocaloric group. In contrast, whole body FFA(ox) was improved in both groups at rest and during hyperlipemia. These changes were driven by increases in intracellular lipid-derived FFAox 12.3 were driven by increases in intracellular lipid-derived FFAox (12.3 +/- 7.7 and 14.7 +/- 7.8%, P < 0.05). We conclude that the exercise-induced improvement in FFA-induced insulin resistance is independent of the magnitude of weight loss and FFA turnover, yet it is linked to increased intracellular FFA utilization.