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

• Published in: Applied physiology, nutrition, and metabolism nutrition, and metabolism, 2018-10, Vol.43 (10), p.1083-1089
• Main Authors: Baranowski, Bradley J, MacPherson, Rebecca E.K
• Format: Article
• Language: English
• Subjects: Alzheimer's disease; Animals; BDNF; Brain-derived neurotrophic factor; Brain-Derived Neurotrophic Factor - metabolism; Care and treatment; Complications and side effects; cortex préfrontal; Cyclic AMP Response Element-Binding Protein - metabolism; Diet; Diet, Fat-Restricted; Diet, High-Fat; Disease Models, Animal; Estrogen Receptor alpha - metabolism; exercice physique; Exercise; Glucose Intolerance - metabolism; Glucose Intolerance - physiopathology; Health aspects; hippocampe; hippocampus; Hippocampus (Brain); Male; Membrane Glycoproteins - metabolism; Mice, Inbred C57BL; Neurodegenerative diseases; neurotrophin; neurotrophine; Obesity; Obesity - metabolism; Obesity - physiopathology; obésité; Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha - metabolism; Phosphorylation; Physical Exertion; Physiological aspects; Prefrontal cortex; Prefrontal Cortex - metabolism; Prefrontal Cortex - physiopathology; Prevention; Protein-tyrosine kinase; Protein-Tyrosine Kinases - metabolism; Proteins; Psychological aspects; Risk factors; Rodents; Signal Transduction; Time Factors; TrkB
• ISSN: 1715-5312; 1715-5320
• DOI: 10.1139/apnm-2018-0108

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-1α and ERα) protein content (p < 0.05). Two hours following the acute exercise bout, TrkB and CREB phosphorylation as well as PGC-1α and ER-α 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.