| （华南师范大学 体育科学学院，广东 广州 510006） 摘 要：探讨肥胖及肥胖抵抗大鼠NAFLD发病机制及运动干预对不同倾向模型的效果是否存在不同之处，为更好防治NAFLD提供实验数据。通过高脂饮食诱导建模，从中遴选出肥胖和肥胖抵抗型两种大鼠，通过肝组织病理切片确定建模是否成功。而后对大鼠施加5周的游泳运动，运动结束后，通过测定体脂、脂体比，血脂、肝指数、瘦素水平、空腹血糖及胰岛素水平等指标，观察运动对不同类型NAFLD的干预效果。结果发现，肥胖抵抗组体质量与正常组相比差异无显著性，但肥胖抵抗组与肥胖组同样存在能量代谢紊乱，肥胖组存在胰岛素抵抗和瘦素抵抗，肥胖抵抗组不显示有胰岛素抵抗，存在瘦素抵抗。游泳运动改善肥胖组NAFLD的效果较肥胖抵抗组更为显著。结果表明肥胖组NAFLD与肥胖抵抗组NAFLD发病机制并不相同，游泳运动对其干预效果也不相同。游泳运动使能耗增加，减少脂质沉积，能明显改善肥胖组的瘦素抵抗，恢复脂肪-胰岛素的负反馈调节机制，进而改善IR，促进NAFLD转归。游泳运动对肥胖抵抗组的改善机制可能不同于肥胖组，主要是通过调节瘦素的受体结合率，改善瘦素抵抗，促进NAFLD的转归。 |
LIU Qian-qian，XIAO Guo-qiang
| （School of Physical Education，South China Normal University，Guangzhou 510006，China） Abstract: In order to probe into the pathogenesis of NAFLD suffered by obese and obesity resistant rats and whether there are any differences between the effects of intervention produced by exercising on different tendency models, so as to provide experimental data for controlling NAFLD better, the authors established models by means of high fat food induction, selected obese and obesity resistant rats therefrom, confirmed the success of model estab-lishment via pathological slices of liver tissues, then let the rats swim for 5 weeks, observed the effects of interven-tion produced by exercising on different types of NAFLD by measuring indexes such as body fat, fat to weight ratio, blood fat, liver index, leptin index, fastening blood glucose and insulin level etc after exercising was finished, and revealed the following findings: there was no significant difference between the body mass of the rats in the obesity resistant group and the body mass of the rats in the normal group, but the same as the rats in the obese group, the rats in the obesity resistant group had an energy metabolism disorder; the rats in the obese group had insulin resis-tance and leptin resistance, while the rats in the obesity resistant group showed no insulin resistance but leptin resis-tance; the effect of NAFLD improvement produced by swimming on the rats in the obese group was more signifi-cant than the effect of NAFLD improvement produced by swimming on the rats in the obesity resistant group. The findings indicate the followings: the pathogenesis of NAFLD suffered by the rats in the obese group is not the same as the pathogenesis of NAFLD suffered by the rats in the obesity resistant group, neither are the effects of interven-tion produced by swimming on them; swimming increases energy consumption, reduces lipid deposition, can sig-nificantly improve leptin resistance of the rats in the obese group, thus restore the fat-insulin negative feedback regulation mechanism, then improve IR, and promote the turnaround of NAFLD; the mechanism of improvement produced by swimming on the rats in the obesity resistant group may be different from the mechanism of improve-ment produced by swimming on the rats in the OB group; swimming improves leptin resistance and promotes the turnaround of NAFLD mainly by regulating the leptin receptor binding rate. |
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