Abstract

BackgroundNutritional 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.MethodsFour 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.ResultsThe 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.ConclusionsTherefore, 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.

Highlights

  • Obesity-induced oxidative stress causes inflammatory reactions resulting in abnormalities of the immune system [1] and transforms functions of protein, lipid and DNA, triggering neurodegenerative diseases such as Alzheimer’s disease and Parkinson’s disease [2,3] as well as aging of brain function, cognitive impairment [4], and is reported to affect apoptosis of in understanding the mechanism between obesity and cognitive function.Regular exercise prevents and treats obesityinduced metabolic imbalance and prevents brain damage

  • The studies that had observed changes of synaptic plasticity such as nerve growth factor (NGF), brain-drived neurotrophic factor (BDNF), p38MAPK, cAMP response elementbinding protein (CREB) and synapsin 1 in rats with obesity triggered by the energy imbalance from high fat diet, are still scarce, and in particular, there is no study to this date implementing the use of regular exercise and dietary change in these obese models

  • This study aimed to define the relationship between obesity and neurogenesis in rats with acquired obesity caused by high fat diet, and to identify the effects of regular aerobic exercise and dietary change on synaptic plasticity markers and cognitive function

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Summary

Introduction

Obesity-induced oxidative stress causes inflammatory reactions resulting in abnormalities of the immune system [1] and transforms functions of protein, lipid and DNA, triggering neurodegenerative diseases such as Alzheimer’s disease and Parkinson’s disease [2,3] as well as aging of brain function, cognitive impairment [4], and is reported to affect apoptosis of in understanding the mechanism between obesity and cognitive function.Regular exercise prevents and treats obesityinduced metabolic imbalance and prevents brain damage. The studies that had observed changes of synaptic plasticity such as NGF, BDNF, p38MAPK, cAMP response elementbinding protein (CREB) and synapsin 1 in rats with obesity triggered by the energy imbalance from high fat diet, are still scarce, and in particular, there is no study to this date implementing the use of regular exercise and dietary change in these obese models. This study aimed to define the relationship between obesity and neurogenesis in rats with acquired obesity caused by high fat diet, and to identify the effects of regular aerobic exercise and dietary change on synaptic plasticity markers and cognitive function. 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

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