Journal article
Endurance exercise prevents metabolic distress-induced senescence in the hippocampus
Medicine and Science in Sports and Exercise, Vol.51, pp.2012-2024
51
2019
PMID: 30998584
Web of Science ID: WOS:000485908300005
Metrics
99 Record Views
Abstract
Purpose
Metabolic disorder such as obesity and type 2 diabetes caused by excess caloric intake is associated with an increased risk of neurodegenerative diseases. Endurance exercise (EXE) has been suggested to exert neuroprotective effects against the metabolic distress. However, the exact underlying molecular mechanisms responsible for the exercise-induced neuroprotection have not been fully elucidated. In this study, we investigated whether EXE-induced neuroprotection is associated with cellular senescence, neuroinflammation, and oxidative stress using a mouse model of obesity induced by a high-fat/high-fructose diet.
Methods
C57BL/6 female mice (10 wk old) were randomly divided to three groups: normal chow diet group (CON, n = 11), high-fat diet/high-fructose (HFD/HF) group (n = 11), and high-fat diet/high-fructose + endurance exercise (HFD/HF + EXE) group (n = 11). HFD/HF + EXE mice performed treadmill running exercise for 60 min·d⁻¹, 5 d·wk⁻¹ for 12 wk.
Results
Our data showed that EXE ameliorated HFD/HF-induced weight gain, fasting blood glucose levels, and visceral fat gain. More importantly, HFD/HF diet promoted cellular senescence, whereas EXE reversed it, evidenced by a reduction in the levels of p53, p21, p16, beta-galactosidase (SA-β-gal), and lipofuscin. Furthermore, EXE prevented HFD/HF-induced neuroinflammation (e.g., tumor necrosis factor-α and interleukin-1β) by inhibiting toll-like receptor 2 downstream signaling cascades (e.g., tumor necrosis factor receptor–associated factor 6, c-Jun N-terminal kinase, and c-Jun) in parallel with reduced reactive glial cells. This anti-inflammatory effect of EXE was associated with the reversion of HFD/HF-induced cellular oxidative stress.
Conclusion
Our study provides novel evidence that EXE-induced antisenescence against metabolic distress in the hippocampus may be a key neuroprotective mechanism, preventing neuroinflammation and oxidative stress.
Related links
Details
- Title
- Endurance exercise prevents metabolic distress-induced senescence in the hippocampus
- Publication Details
- Medicine and Science in Sports and Exercise, Vol.51, pp.2012-2024
- Resource Type
- Journal article
- Publisher
- Lippincott Williams & Wilkins; Hagerstown, MD
- Series
- 51
- Copyright
- © 2019 by the American College of Sports Medicine
- Identifiers
- WOS:000485908300005; 99380090769906600
- Academic Unit
- Movement Sciences and Health; Usha Kundu, MD College of Health
- Language
- English