Acute exercise induced BDNF-TrkB signalling is intact in the prefrontal cortex of obese, glucose-intolerant male mice

Obesity and glucose intolerance have been directly implicated in the pathology of Alzheimer's disease. It is thought that diet-induced obesity causes a reduction in neuronal plasticity through a reduction in the neurotrophin: brain-derived neurotrophic factor (BDNF). Previous work has demonstrated that acute exercise in healthy lean animals increases BDNF-TrkB signalling in the brain. However, if this effect is intact in a state of obesity remains unknown. The purpose of this study is to determine the effects of a single bout of exercise on BDNF-TrkB signalling in the prefrontal cortex and hippocampus from obese glucose intolerant mice. Male C57BL/6 mice were fed a low-fat diet (10% kcals from lard) or a high-fat diet (HFD, 60% kcals from lard) for 7 weeks. A subset of HFD mice underwent an acute bout of exercise (treadmill running: 15 m/min, 5% incline, 120 min) followed by a recovery period of 2 h, after which point the prefrontal cortex and hippocampus were collected. The HFD increased body mass and glucose intolerance (p < 0.05). Prefrontal cortex from HFD mice demonstrated lower BDNF protein content, reduced phosphorylation of the BDNF receptor (TrkB), and its downstream effector cAMP response element-binding protein (CREB), as well as PGC-1 alpha and ER alpha) protein content (p < 0.05). Two hours following the acute exercise bout, TrkB and CREB phosphorylation as well as PGC-1 alpha and ER-alpha protein content were recovered (p < 0.05). Our findings demonstrate for the first time that an acute bout of exercise can recover BDNF-TrkB signalling in the prefrontal cortex of obese mice.