Exercise Alleviates Cognitive Functions by Enhancing Hippocampal Insulin Signaling and Neuroplasticity in High-Fat Diet-Induced Obesity

• Published in: Nutrients 2019-07, Vol.11 (7), p.1603
• Main Authors: Park, Hye-Sang, Park, Sang-Seo, Kim, Chang-Ju, Shin, Mal-Soon, Kim, Tae-Woon
• Format: Article
• Language: English
• Subjects: Alzheimer's disease; Animal Feed; Animals; Brain; Brain damage; Brain research; Brain-derived neurotrophic factor; Cardiovascular diseases; Cognition; Cognitive ability; Complications; Dementia; Dementia disorders; Diabetes; Diabetes mellitus; Diet - veterinary; Diet, High-Fat - adverse effects; exercise; Fitness equipment; Glucose; Health risks; High fat diet; Hippocampal plasticity; Hippocampus; Hippocampus - cytology; Hippocampus - physiology; Homeostasis; Hypertension; Insulin; Insulin - metabolism; Insulin resistance; Kinases; Male; males; Memory; Mice; Mice, Inbred C57BL; Neurodegeneration; Neurogenesis; Neuronal Plasticity - drug effects; Neuroplasticity; Obesity; Obesity - chemically induced; Organic chemistry; Physical Conditioning, Animal; Regulation; Risk analysis; Risk factors; Signal transduction; Signal Transduction - drug effects; Signal Transduction - physiology; Synaptic plasticity
• ISSN: 2072-6643; 2072-6643
• DOI: 10.3390/nu11071603

Obesity, caused by a high-fat diet (HFD), leads to insulin resistance, which is a precursor of diabetes and a risk factor for impaired cognitive function, dementia, and brain diseases, such as Alzheimer's disease. Physical exercise has positive effects on obesity and brain functions. We investigated whether the decline in cognitive function caused by a HFD could be improved through exercise by examining insulin signaling pathways and neuroplasticity in the hippocampus. Four-week-old C57BL/6 male mice were fed a HFD or a regular diet for 20 weeks, followed by 12 weeks of treadmill exercise. To ascertain the effects of treadmill exercise on impaired cognitive function caused by obesity, the present study implemented behavioral testing (Morris water maze, step-down). Moreover, insulin-signaling and neuroplasticity were measured in the hippocampus and dentate gyrus. Our results demonstrated that HFD-fed obesity-induced insulin resistance was improved by exercise. In addition, the HFD group showed a decrease in insulin signaling and neuroplasticity in the hippocampus and the dentate gyrus and increased cognitive function impairment, which were reversed by physical exercise. Overall, our findings indicate that physical exercise may act as a non-pharmacologic method that protects against cognitive dysfunction caused by obesity by improving hippocampal insulin signaling and neuroplasticity.