Effect of treadmill running on the expression of genes that are involved in neuronal differentiation in the hippocampus of adult male rats.

Gene expression in the rodent brain is dependent on exercise. However, our findings regarding this fact are inadequate. The aim of this study was to evaluate the effect of exercise intensity on changes in factors involved in neuronal differentiation and plasticity in the hippocampus of adult male rats. Thus, the effects of 2 weeks treadmill running at of low (11 m/min) and high (25 m/min) intensities, 30 min/day for 14 consecutive days on the expression of two genes, microRNA-124 and neuron restrictive silencer factor/RE1-silencing transcription factor (REST) as well as changes of two proteins of brain-derived eurotrophic factor (BDNF) and tyrosine kinase B (TrkB) were analysed. Using quantitative real-time PCR techniques have shown that both exercise intensities reduced the expression of REST (31% in low exercise intensity, 52% in high exercise intensity) and elevated the expression of miR-124 (3.8-fold in low exercise intensity, 11.9-fold in high exercise intensity)significantly (P≤0.05). This suggests that exercise probably through the changes in these genes is involved in neuronal differentiation in the hippocampus of rats. BDNF and TrkB levels were measured by ELISA. Exercise, at low intensity, increased TrkB (4.51 ng/L vs. 3.73 ng/L) and BDNF (11.97 ng/L vs. 11.08 ng/L) proteins significantly (P≤0.05), while at high intensity,the changes in comparison with the control group were not significant. Expression levels during the exercise programme with high intensity were dramatic for miR-124 and less dramatic for REST compared with low intensity exercise programme.

Consumption of a high-fat diet, but not regular endurance exercise training, regulates hypothalamic lipid accumulation in mice.

Obesity is characterised by increased storage of fatty acids in an expanded adipose tissue mass and in peripheral tissues such as the skeletal muscle and liver, where it is associated with the development of insulin resistance. Insulin resistance also develops in the central nervous system with high-fat feeding. The capacity for hypothalamic cells to accumulate/store lipids, and the effects of obesity remain undefined. The aims of this study were (1) to examine hypothalamic lipid content in mice with increased dietary fat intake and in obese ob/ob mice fed a low-fat diet, and (2) to determine whether endurance exercise training could reduce hypothalamic lipid accumulation in high-fat fed mice. Male C57BL/6 mice were fed a low- (LFD) or high-fat diet (HFD) for 12 weeks; ob/ob mice were maintained on a chow diet. HFD-exercise (HFD-ex) mice underwent 12 weeks of high-fat feeding with 6 weeks of treadmill exercise training (increasing from 30 to 70 min day(-1)). Hypothalamic lipids were assessed by unbiased mass spectrometry. The HFD increased body mass and hepatic lipid accumulation, and induced glucose intolerance, while the HFD-ex mice had reduced body weight and improved glucose tolerance. A total of 335 lipid molecular species were identified and quantified. Lipids known to induce insulin resistance, including ceramide (22%↑), diacylglycerol (25%↑), lysophosphatidylcholine (17%↑), cholesterol esters (60%↑) and dihexosylceramide (33%↑), were increased in the hypothalamus of HFD vs. LFD mice. Hypothalamic lipids were unaltered with exercise training and in the ob/ob mice, suggesting that obesity per se does not alter hypothalamic lipids. Overall, hypothalamic lipid accumulation is regulated by dietary lipid content and is refractory to change with endurance exercise training.