PUBLICATION
Swimming Training in a T2DM Zebrafish Model Restores Mitochondrial Function to Alleviate Anxiety-Like Behaviors and Metabolic Dysregulation
- Authors
- Fang, Y., Qu, J., Zhao, J., Qu, L., Wang, L., Luo, C., Yang, Q., Wu, W., Sun, D., He, D.
- ID
- ZDB-PUB-250605-3
- Date
- 2025
- Source
- Frontiers in bioscience (Landmark edition) 30: 3710037100 (Journal)
- Registered Authors
- Keywords
- T2DM, anxiety, mitochondrial damage, oxidative stress, swimming training
- MeSH Terms
-
- Swimming*/physiology
- Membrane Potential, Mitochondrial
- Mitochondria*/metabolism
- Anxiety*/metabolism
- Anxiety*/therapy
- Lipid Metabolism
- Disease Models, Animal
- Oxidative Stress
- Zebrafish
- Reactive Oxygen Species/metabolism
- Behavior, Animal
- Blood Glucose/metabolism
- Animals
- Diabetes Mellitus, Type 2*/metabolism
- Diabetes Mellitus, Type 2*/psychology
- Diabetes Mellitus, Type 2*/therapy
- Physical Conditioning, Animal*
- PubMed
- 40464517 Full text @ Front Biosci (Landmark Ed)
Citation
Fang, Y., Qu, J., Zhao, J., Qu, L., Wang, L., Luo, C., Yang, Q., Wu, W., Sun, D., He, D. (2025) Swimming Training in a T2DM Zebrafish Model Restores Mitochondrial Function to Alleviate Anxiety-Like Behaviors and Metabolic Dysregulation. Frontiers in bioscience (Landmark edition). 30:3710037100.
Abstract
Introduction Anxiety and depression-like behaviors are common in patients with type 2 diabetes mellitus (T2DM). This study explored the potential of swimming training (ST) to alleviate these symptoms by restoring mitochondrial function. While aerobic exercise is known to influence mitochondrial dysfunction and behavioral abnormalities, the mechanism by which ST achieves this remains unclear.
Objective To investigate how ST improves T2DM and associated anxiety-like behaviors by regulating mitochondrial structure and function.
Methods T2DM was induced in zebrafish with a high-sugar diet, followed by 20 days of ST. Behavioral analysis assessed anxiety-like behaviors, while ELISA and microscopic imaging techniques were used to evaluate changes in mitochondrial structure and function in liver tissue.
Results ST significantly alleviated anxiety-like behavior and mitigated mitochondrial damage. Furthermore, ST counteracted mitochondrial dysfunction induced by oxidative stress through regulation of reactive oxygen species levels (p < 0.01), stabilization of mitochondrial membrane potential (p < 0.0001), and increasing the production of adenosine triphosphate (p < 0.01). ST also improved T2DM markers, including blood glucose regulation (p < 0.001), insulin level (p < 0.05), and lipid metabolism (p < 0.01 for low-density lipoprotein cholesterol (LDL-C), p < 0.01 for high-density lipoprotein cholesterol (HDL-C), p < 0.01 for total cholesterol (T-CHO)).
Conclusions This research provides insights into the intricate interplay between mitochondrial dysfunction in T2DM and behavioral outcomes while highlighting the potential of ST as a holistic therapeutic strategy for T2DM patients.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping