ArticleFrontiers in endocrinology2025
Brown adipose tissue-derived extracellular vesicles regulate hepatocyte mitochondrial activity to alleviate high-fat diet-induced jawbone osteoporosis in mice.
Article in Frontiers in endocrinology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Molecular Mechanisms of Obesity-Associated Oxidative Stress and Therapeutic Strategies.Antioxidants (Basel, Switzerland) · 2026Review
- Therapeutic effect of mitochondrial transfer on bone tissue diseases: treatment strategy of mitochondrial transplantation and delivery technology.Journal of orthopaedic translation · 2026Review
- Physical Exercise Counteracts Impaired Cognition by Improving Mitochondrial Function.International journal of molecular sciences · 2026Review
- Pathophysiological Roles of Obesity-Induced Alterations in Extracellular Vesicles Derived from Adipose Tissue and Adipocytes.Current obesity reports · 2026Review
- Progress in multiaxial coupling mechanisms of osteoporosis: insights from systems medicine on immune-inflammatory interactions, hormonal regulation, and metabolic imbalance.Frontiers in endocrinology · 2025Review
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Authors and funding
10 authors.
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Abstract
Background: Lipid metabolic disorder (LMD) serves as a systemic driver of osteoporosis (OP), with jawbone osteoporosis (JOP) representing a clinically significant yet underexplored complication. Current clinical treatments for JOP remain suboptimal, highlighting the need for innovative approaches. The use of metabolic regulators represents a promising therapeutic strategy for OP management. While brown adipose tissue-derived extracellular vesicles (BEV) exhibit metabolic regulatory potential, their capacity to mitigate LMD-associated OP remains unclear. Methods: A high-fat diet (HFD)-induced LMD mouse model was established to identify the JOP phenotype through micro-computed tomography (micro-CT) and transcriptomic profiling. BEV isolation was optimized using liberase enzyme-enhanced differential centrifugation, with Results: Sixteen weeks of HFD successfully induced typical LMD and JOP manifestations in mice. Transcriptomic sequencing revealed downregulation of osteogenic-related genes concomitant with upregulation of lipid metabolism-associated genes in the jawbone of LMD mice. Conclusion: This study establishes LMD as a crucial driver factor in JOP and identifies BEV-mediated mitochondrial transferring in hepatocytes as a therapeutic strategy for LMD-related JOP.
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