ArticleDiabetes2025
Ablation of FAM210A in Brown Adipocytes of Mice Exacerbates High-Fat Diet-Induced Metabolic Dysfunction.
Article in Diabetes, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed.
- Energy's long game: thermogenic adipocytes and the metabolic diseases of modern life.Academia biology · 2026Article
- Microproteins in Metabolic Biology: Emerging Functions and Potential Roles as Nutrient-Linked Biomarkers.International journal of molecular sciences · 2025Review
- Hepatocyte FAM210A deficiency disrupts mitochondrial function and triggers juvenile steatosis with compensatory repair in adulthood.bioRxiv : the preprint server for biology · 2025Article
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Authors and funding
9 authors.
Funding
Abstract
Thermogenesis of brown adipose tissue (BAT) provides metabolic benefits against pathologic conditions, such as type 2 diabetes, obesity, cardiovascular disease, and cancer. The thermogenic function of BAT relies on mitochondria, but whether mitochondrial remodeling is required for the beneficial effects of BAT remains unclear. We recently identified FAM210A as a BAT-enriched mitochondrial protein essential for cold-induced thermogenesis through the modulation of OPA1-dependent cristae remodeling. Here, we report a key role of FAM210A in the systemic response to a high-fat diet (HFD). We discovered that an HFD suppressed FAM210A expression, associated with excessive OPA1 cleavage in BAT. Ucp1-Cre-driven BAT-specific Fam210a knockout (Fam210aUKO) similarly elevated OPA1 cleavage, accompanied by whitening of BAT. When subjected to an HFD, Fam210aUKO mice gained similar fat mass as sibling control mice but developed glucose intolerance, insulin resistance, and liver steatosis. The metabolic dysfunction was associated with overall increased lipid content in both the liver and BAT. Additionally, Fam210aUKO leads to inflammation in white adipose tissue. These data demonstrate that FAM210A in BAT is necessary for counteracting HFD-induced metabolic dysfunction but not obesity. ARTICLE HIGHLIGHTS: FAM210A regulates cold-induced mitochondrial remodeling through control of OPA1 cleavage, but whether it also plays a role in high-fat diet (HFD)-induced cristae remodeling is unknown. We asked if an HFD would alter the FAM210A level and OPA1 cleavage in brown adipose tissue (BAT) and how FAM210A loss of function would affect diet-induced obesity in mice. We found that an HFD diminished FAM210A expression and accelerated OPA1 cleavage in BAT, and Fam210a knockout exacerbated HFD-induced whitening of BAT, cold intolerance, liver steatosis, white adipose tissue inflammation, and metabolic dysfunction. Our work reveals a physiologic role of FAM210A-mediated BAT mitochondrial remodeling in systemic adaptation to an HFD and suggests that BAT mitochondria may be targeted to treat diet-induced metabolic dysfunction.
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