Mitofusin-2 induced by exercise modifies lipid droplet-mitochondria communication, promoting fatty acid oxidation in male mice with NAFLD
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Background and aim The excessive accumulation of lipid droplets (LDs) is a defining characteristic of nonalcoholic fatty liver disease (NAFLD). The interaction between LDs and mitochondria is functionally important for lipid metabolism homeostasis. Exercise improves NAFLD, but it is not known if it has an effect on hepatic LD-mitochondria interactions. Here, we investigated the influence of exercise on LD-mitochondria interactions and its significance in the context of NAFLD. Approach and results Mice were fed high-fat diet (HFD) or HFD-0.1 % methionine and choline-deficient diet (MCD) to emulate simple hepatic steatosis or non-alcoholic steatohepatitis, respectively. In both models, aerobic exercise decreased the size of LDs bound to mitochondria and the number of LD-mitochondria contacts. Analysis showed that the effects of exercise on HOMA-IR and liver triglyceride levels were independent of changes in body weight, and a positive correlation was observed between the number of LD-mitochondria contacts and NAFLD severity and with the lipid droplet size bound to mitochondria. Cellular fractionation studies revealed that ATP-coupled respiration and fatty acid oxidation (FAO) were greater in hepatic peridroplet mitochondria (PDM) from HFD-fed exercised mice than from equivalent sedentary mice. Finally, exercise increased FAO and mitofusin-2 abundance exclusively in PDM through a mechanism involving the curvature of mitochondrial membranes and the abundance of saturated lipids. Accordingly, hepatic mitofusin-2 ablation prevented exercise-induced FAO in PDM. Conclusions This study demonstrates that aerobic exercise has beneficial effects in murine NAFLD models by lessening the interactions between hepatic LDs and mitochondria, and by decreasing LD size, correlating with a reduced severity of NAFLD. Additionally, aerobic exercise increases FAO in PDM and this process is reliant on Mfn-2 enrichment, which modifies LD-mitochondria communication.
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The MCD diet lacks key metabolic features of human MASLD, such as obesity and insulin resistance.
“While the MCD diet lacks key metabolic features of human MASLD, such as obesity and insulin resistance [30, 31, 32]”
From Liver Stiffness Rises Early in MASLD and Drives Inflammation, Lipid Dysmetabolism, and Fibrosis via Piezo1–YAP Mechanotransduction (2026) · cites this paper as [31]
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- Authors
- Bórquez, J. C., Díaz-Castro, F., La Fuente, F. P.-D., Espinoza, K., Figueroa, A. M., Martínez-Ruíz, I., Hernández, V., López-Soldado, I., Ventura, R., Domingo, J. C., Bosch, M., Fajardo, A., Sebastián, D., Espinosa, A., Pol, A., Zorzano, A., Cortés, V., Hernández-Alvarez, M. I., & Troncoso, R.
- Affiliations
- University of Chile (CL)
- Pontificia Universidad Católica de Chile (CL)
- Institut de Biomedicina de la Universitat de Barcelona (ES)
- Universitat de Barcelona (ES)
- Consorci Institut D'Investigacions Biomediques August Pi I Sunyer (ES)
- Advanced Center for Chronic Diseases (CL)
- Corresponding author
- Troncoso, Rodrigo
- ORCID
- Venue
- Metabolism
- Publisher
- Elsevier BV
- Published
- 2024-03
- Volume
- 152
- Pages
- 155765
- ISSN
- 0026-0495 (ISSN-L)
- OpenAlex
- W4390128083
- Cited by
- 54
- References
- 62
- Citations by year
- 2026: 21 · 2025: 25 · 2024: 8
- FWCI
- 10.77
- Type
- journal article
- Language
- en
- Open access
- green
- hdl.handle.net
- Licence
- Locations
- Metabolism (publishedVersion)
- PubMed (publishedVersion)
- Dipòsit Digital de la Universitat de Barcelona (Universitat de Barcelona) (submittedVersion, cc-by-nc-nd)
- Universidad de Chile (submittedVersion, cc-by-nc-nd)
- Topics
- Health Sciences › Medicine › Epidemiology › Liver Disease Diagnosis and Treatment
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
- Keywords
- mitofusin 2, non-alcoholic fatty liver disease, fatty acid oxidation, aerobic exercise, hepatic steatosis, nonalcoholic steatohepatitis, saturated lipids, insulin resistance, high-fat diet
- MeSH terms
- Animals, Fatty Acids, Liver, Male, Mice, Inbred C57BL, Mitochondria, GTP Phosphohydrolases, Lipid Metabolism, Mice, Diet, High-Fat, Non-alcoholic Fatty Liver Disease, Lipid Droplets
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