Low-intensity exercise exerts beneficial effects on plasma lipids via PPARγ
Low-intensity exercise exerts beneficial effects on plasma lipids via PPARγ
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DOI：
10.1249/mss.0b013e31816c091d
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发表时间：
2008-07-01
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影响因子：
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通讯作者：
Morris, Keith
中科院分区：
文献类型：
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作者：
Butcher, Lee R.;Thomas, Andrew;Morris, Keith
前言：体力活动降低心血管疾病风险的一个重要机制是通过调节血脂。我们研究了低强度运动是否调节脂质代谢以及负责控制胆固醇逆向转运（RCT）的转录因子过氧化物酶体增殖物激活受体γ（PPAR γ）和肝脏X受体α（LXR α）。研究方法：34名久坐不动的成年人，平均年龄45.6 ± 11.1岁，参加了为期8周的低强度运动计划，包括步行10，000步，每周三次。受试者被随机分配到运动组或久坐对照组，并测定血清脂质或脂蛋白浓度。结果如下：与对照组相比，运动后总胆固醇显著降低（运动前，5.73 +/-1.39 mmol. L-1;运动后，5.32 +/-1.28 mmol. L-1），HDL显著升高（运动前，1.46 +/-0.47 mmol. L-1;运动后，1.56 +/-0.50 mmol. L-1）。运动组运动前后血清氧化低密度脂蛋白（oxLDL）浓度显著升高（0周，554 +/-107 ng. mL（-1）; 4周，698 +/-134 ng. mL（-1）; 8周，588 +/-145 ng. mL（-1））。观察到白细胞PPAR-γ mRNA表达显著增加（4周，1.8 +/-0.9倍; 8周，4.3 +/-1.9倍），运动后增加的PPAR-γ DNA结合活性（运动前，0.22 +/-0.09 OD单位;运动后，1.13 0.29 OD单位）加强了这一点。观察到oxLDL清道夫受体CD36（4周，3.8 +/-0.6倍; 8周，2.7 +/-0.5倍）和LXR α（8周，3.5 +/-0.8倍）的基因表达显著增加。RCT中涉及的两个LXR α调节基因，即ATP结合盒转运体A1和G1（分别为ABCA 1和ABCG 1），在运动后显著上调（8周：ABCAI，3.46 +/-0.56倍; ABCG 1，3.06 +/-0.47倍）。结论：我们认为，这些变化的净效应可能是增加oxLDL摄取，刺激RCT，从而促进血管系统中致动脉粥样硬化脂质的清除，最终有助于低强度有氧运动的心血管益处。
Introduction: An important mechanism by which physical activity reduces the risk of cardiovascular disease is through regulating plasma lipids. We investigated whether low-intensity exercise modulates lipid metabolism and the transcription factors peroxisome proliferator-activated receptor gamma (PPAR gamma) and liver X receptor a (LXR alpha) responsible for controlling reverse cholesterol transport (RCT). Methods: Thirty-four sedentary adults, mean age 45.6 +/- 11.1 yr, participated in an 8-wk low-intensity exercise program consisting of walking 10,000 steps, three times a week. Subjects were randomly allocated to either an exercise group or a sedentary control group, and serum lipid or lipoprotein concentrations were determined. Results: Compared with controls, there was a significant decrease in total cholesterol (preexercise, 5.73 +/- 1.39 mmol.L-1; postexercise, 5.32 +/- 1.28 mmol.L-1) and a significant increase in HDL (preexercise, 1.46 +/- 0.47 mmol.L-1; postexercise, 1.56 +/- 0.50 mmol.L-1) after the exercise program. There was a significant increase in serum oxidized LDL (oxLDL) concentrations in the exercise group before and after exercise (0 wk, 554 +/- 107 ng.mL(-1); 4 wk, 698 +/- 134 ng.mL(-1); 8 wk, 588 +/- 145 ng.mL(-1)). A significant increase in leukocyte mRNA expression for PPAR-gamma (4 wk, 1.8 +/- 0.9-fold; 8 wk, 4.3 +/- 1.9-fold) was observed, which was reinforced by increased PPAR-gamma DNA-binding activity postexercise (preexercise, 0.22 +/- 0.09 OD units; postexercise, 1.13 0.29 OD units). A significant increase in gene expression was observed for the oxLDL scavenger receptor CD36 (4 wk, 3.8 +/- 0.6-fold; 8 wk, 2.7 +/- 0.5-fold) and LXR alpha (8 wk, 3.5 +/- 0.8-fold). Two LXR alpha-regulated genes involved in RCT, namely, ATP-binding cassette transporters A1 and G1 (ABCA1 and ABCG1, respectively), were significantly up-regulated postexercise (8 wk: ABCAI, 3.46 +/- 0.56-fold; ABCG1, 3.06 +/- 0.47-fold). Conclusion: We propose that the net effect of these changes may be to increase oxLDL uptake, to stimulate RCT, and thus to promote clearance of proatherogenic lipids from the vasculature, ultimately contributing to the cardiovascular benefits of low-intensity aerobic exercise.