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High-Intensity Interval Training Improves Memory Deficits in Obese Mice by Enhancing Osteocalcin-Driven Astrocytic
Hyukki Chang1, Yea-Hyun Leem2, Jonghoon Park3
1Department of Sport and Exercise Science, Seoul Women's University, Seoul, South Korea.
Neurochemical Research
|July 23, 2025
Summary
High-intensity interval training (HIIT) combats diet-induced memory loss by boosting brain health. This exercise promotes neurogenesis and improves cognitive function through osteocalcin signaling.
Area of Science:
- Neuroscience
- Metabolic Disorders
- Exercise Physiology
Background:
- Obesity and high-calorie diets impair cognitive function, particularly memory.
- Physical exercise, especially high-intensity interval training (HIIT), offers a non-pharmacological strategy for weight management and cognitive enhancement.
- The precise mechanisms by which HIIT improves cognition in the context of diet-induced neurotoxicity are not fully understood.
Purpose of the Study:
- To investigate the cognitive-enhancing effects of HIIT in mice fed a high-calorie diet.
- To elucidate the role of osteocalcin (OCN)/GPR158 signaling in adult hippocampal neurogenesis as a potential mechanism for HIIT's benefits.
- To examine the impact of HIIT on neurogenesis and related molecular pathways in the hippocampus.
Main Methods:
- Mice were fed a high-fat, high-sucrose diet (HFHSD) for 12 weeks to induce obesity and cognitive deficits.
- An 8-week high-intensity interval training (HIIT) program was implemented, with intensity based on maximal running capacity (MRC).
- Cognitive function was assessed using the Y-maze test; hippocampal neurogenesis, OCN/GPR158 signaling, BDNF expression, and AKT/GSK3β pathway activation were analyzed.
Main Results:
- HIIT effectively managed body weight, feeding behavior, and improved MRC in HFHSD-fed mice.
- HIIT ameliorated memory deficits induced by the HFHSD, promoting adult hippocampal neurogenesis, particularly in the dorsal hippocampus.
- HIIT significantly increased astrocytic OCN/GPR158 signaling, elevated BDNF expression in dentate gyrus astrocytes, and activated the AKT/GSK3β pathway.
Conclusions:
- HIIT demonstrates significant cognitive-enhancing effects in combating diet-induced memory impairment.
- Astrocytic OCN/GPR158 signaling appears to be a key mediator of HIIT's memory-improving effects via proneurogenic mechanisms.
- HIIT represents a promising therapeutic strategy for mitigating cognitive decline associated with metabolic disorders.
