High-intensity exercise improves cognitive function and hippocampal brain-derived neurotrophic factor expression in obese mice maintained on high-fat diet

Abstract

We wanted to find the intensity of exercise that could increase brainderived neurotrophic factor (BDNF) expression and improve spatial learning and memory without dietary control. C57BL/6 mice were fed a 60% high-fat diet (HFD) for 6 weeks to induce obesity. Obesity-induced mice were exercised on a treadmill for 8 weeks at various exercise intensities: HFD-control (n= 7), HFD-low-intensity exercise (HFD-LIE, n= 7, 12 m/min for 75 min), HFD-middle intensity exercise (HFD-MIE, n= 7, 15 m/min for 60 min) and HFD-high-intensity exercise (HFD-HIE, n= 7, 18 m/min for 50 min). One week before sacrificing mice, the Morris water maze test was performed, and the hippocampus was immediately removed after sacrifice. The expression levels of BDNF (encoded by the gene Bdnf) and tropomyosin receptor kinase B (TrkB) in the hippocampus were analyzed by quantitative real-time reverse transcription-polymerase chain reaction and western blot. In the last probe test of the Morris water maze test, occupancy in the target quadrant was significantly higher in the HFD-HIE group (P< 0.05) than in the other groups. In addition, mRNA expression from the Bdnf promoter region was found to be significantly higher in the HFD-HIE group than in the other groups (P< 0.001). Although there were some differences in the levels of significance, the expression levels of both BDNF and TrkB were significantly higher in the HFD-HIE group than in the other groups. Therefore, relatively high-intensity aerobic exercise can resist the adverse effects of a high-fat diet on the brain without dietary control.

Swimming Suppresses Cognitive Decline of HFD-Induced Obese Mice through Reversing Hippocampal Inflammation, Insulin Resistance, and BDNF Level

“…As an intracellular protein, PSD95 plays a vital role in neuronal synaptic plasticity and learning and memory functions [46]. A previous study has also found that exercise can inhibit the reduction of BNDF in the hippocampal tissue of an obesity model [47]. The feeding of high-fat diets for 3-month-old mice can trigger the reduction of the PSD95 level [48], and both aerobic exercise and resistance exercise training can up-regulate hippocampal PSD95 expression [49,50].…”

From Obesity to Hippocampal Neurodegeneration: Pathogenesis and Non-Pharmacological Interventions

“…Wheel running is also shown to ameliorate memory deficit and amyloid deposition in HFD-fed AD mouse model [ 293 ]. Notably, physical exercise is not only useful in combating a wide range of neurocognitive and neuropsychiatric symptoms in obese and diabetic rodents, including improving learning and memory deficits [ 294 , 295 , 296 , 297 , 298 , 299 , 300 , 301 , 302 , 303 ], reducing depression-like behaviours [ 90 , 304 ], and improving uncontrolled appetitive behaviours in hyperphagia suppression test [ 305 , 306 , 307 ]. Restored adult neurogenesis, improved synaptic plasticity, and reduced neuroinflammation may altogether contribute to cognitive improvements in obese and diabetic rodents [ 66 , 67 , 295 , 308 , 309 , 310 , 311 , 312 ].…”

Treadmill Running Improves Spatial Learning Memory Through Inactivation of Nuclear Factor Kappa B/Mitogen-Activated Protein Kinase Signaling Pathway in Amyloid-β-Induced Alzheimer Disease Rats

“…Voluntary wheel running following brain inflammation inhibited proinflammatory cytokine production and apoptosis, then improved spatial learning memory [13]. Performing treadmill running improved spatial learning memory, short-term memory, and recognition memory [26][27][28]. In the current study, induction of AD was found to worsen the spatial learning memory in the Morris water maze task, whereas treadmill running improved AD-induced spatial learning memory.…”