First Author | Jardim NS | Year | 2021 |
Journal | Neuroscience | Volume | 452 |
Pages | 311-325 | PubMed ID | 33246070 |
Mgi Jnum | J:302008 | Mgi Id | MGI:6501410 |
Doi | 10.1016/j.neuroscience.2020.11.023 | Citation | Jardim NS, et al. (2021) Nuclear Factor [Erythroid-derived 2]-like 2 and Mitochondrial Transcription Factor A Contribute to Moderate-intensity Swimming Effectiveness against Memory Impairment in Young Mice Induced by Concomitant Exposure to a High-calorie Diet during the Early Life Period. Neuroscience 452:311-325 |
abstractText | Increased energy food consumption during early-life has been associated with memory impairment. Swimming training has been reported to improve memory processes in rodent models. This study aimed to evaluate whether moderate-intensity swimming training counteracts learning and memory impairment in young mice fed a high-calorie diet during the early-life period. The contribution of hippocampal oxidative stress, as well as nuclear factor [erythroid-derived 2]-like 2/Kelch-like ECH-associated protein (NRF2/Keap-1/HO-1) and peroxisome proliferator-activated receptor gamma co-activator 1-alpha/mitochondrial transcription factor A (PCG-1alpha/mtTFA) signaling, in memory effects was also investigated. Three-week-old male Swiss mice received a high-calorie diet (20% fat; 20% carbohydrate enriched) or a standard diet from 21 to 49 postnatal days. Mice performed a moderate-intensity swimming protocol (5days/week) and behavioral tests predictive of memory function. Mice fed a high-calorie diet and subjected to the swimming protocol performed better on short- and long-term spatial and object recognition memory tests than those fed a high-calorie diet. The swimming protocol modulated the hippocampal NRF2/Keap-1/HO-1 and mtTFA pathways in mice fed a high-calorie diet. Swimming training positively affected location and long-term memory, fat mass content, as well as NRF2/Keap-1/HO-1 and mtTFA proteins of control-diet-fed mice. In conclusion, a moderate-intensity swimming training evoked an adaptive response in mice fed a high-calorie diet by restoring different types of memory-impaired and hippocampal oxidative stress as well as upregulated the NRF2/Keap-1/HO-1 and mtTFA pathways. |