Department of Physical Education, Laboratory of Exercise Physiology, College of Sports Science, Dong-A University, 840 Hadan2-dong, Saha-gu, Busan, Korea.
Lipids Health Dis. 2013 Oct 8;12:144. doi: 10.1186/1476-511X-12-144.
Nutritional imbalance-induced obesity causes a variety of diseases and in particular is an important cause of cognitive function decline. This study was performed on Sprague Dawley (SD) rats with 13-weeks of high fat diet-induced obesity in connection to the effects of regular exercise and dietary control for 8 weeks on the synaptic plasticity and cognitive abilities of brain.
Four weeks-old SD rats were adopted classified into normal-normal diet-sedentary (NNS, n = 8), obesity-high fat diet-sedentary (OHS, n = 8), obesity-high fat diet-training (OHT, n = 8), obesity-normal diet-sedentary (ONS, n = 8) and obesity- normal diet-training (ONT, n = 8). The exercise program consisted of a treadmill exercise administered at a speed of 8 m/min for 1-4 weeks, and 14 m/min for 5-8 weeks. The Western blot method was used to measure the expression of NGF, BDNF, p38MAPK and p-p38MAPK proteins in hippocampus of the brain, and expressions of NGF, BDNF, TrkA, TrkB, CREB and synapsin1 mRNA were analyzed through qRT-PCR.
The results suggest cognitive function-related protein levels and mRNA expression to be significantly decreased in the hippocampus of obese rats, and synaptic plasticity as well as cognitive function signaling sub-pathway factors were also significantly decreased. In addition, 8-weeks exercises and treatment by dietary change had induced significant increase of cognitive function-related protein levels and mRNA expression as well as synaptic plasticity and cognitive function signaling sub-pathway factors in obese rats. In particular, the combined treatment had presented even more positive effect.
Therefore, it was determined that the high fat diet-induced obesity decreases plasticity and cognitive function of the brain, but was identified as being improved by exercises and dietary changes. In particular, it is considered that regular exercise has positive effects on memory span and learning capacity unlike dietary control.
营养失衡导致的肥胖会引发多种疾病，尤其会导致认知功能下降。本研究采用高脂饮食诱导肥胖的 Sprague Dawley（SD）大鼠，观察持续 8 周的常规运动和饮食控制对肥胖大鼠大脑突触可塑性和认知能力的影响。
4 周龄 SD 大鼠按随机数字表法分为正常饮食-安静组（NNS，n=8）、肥胖-高脂饮食-安静组（OHS，n=8）、肥胖-高脂饮食-运动组（OHT，n=8）、肥胖-正常饮食-安静组（ONS，n=8）和肥胖-正常饮食-运动组（ONT，n=8）。运动方案为：1-4 周时速度为 8 m/min，5-8 周时速度为 14 m/min，跑台训练。Western blot 法检测大鼠海马 NGF、BDNF、p38MAPK 和 p-p38MAPK 蛋白表达，qRT-PCR 检测 NGF、BDNF、TrkA、TrkB、CREB 和 synapsin1mRNA 表达。
肥胖大鼠海马认知功能相关蛋白表达和 mRNA 表达显著降低，突触可塑性和认知功能信号转导亚通路相关因子也显著降低；运动和饮食改变 8 周后，肥胖大鼠海马认知功能相关蛋白表达和 mRNA 表达以及突触可塑性和认知功能信号转导亚通路相关因子均显著升高，且联合治疗效果更明显。
高脂饮食诱导肥胖降低了大脑的可塑性和认知功能，运动和饮食改变可改善肥胖大鼠的大脑可塑性和认知功能，其中运动对记忆广度和学习能力的改善作用优于饮食控制。
