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Adipocyte-specific Mlkl knockout mitigates obesity-induced metabolic dysfunction by enhancing mitochondrial functions
Juliette Tokgozoglu1,2, Valeria Pistorio1,2,3, Mirko Minini1,2
1Sorbonne Université, INSERM, Centre de Recherche Saint-Antoine, CRSA, F-75012, Paris, France.
Cell Death & Disease
|October 6, 2025
Summary
Deleting the mixed lineage kinase domain-like pseudokinase (MLKL) in fat cells combats obesity. This genetic modification improves metabolism and energy expenditure, offering a new target for metabolic disorder treatments.
Area of Science:
- Metabolic regulation
- Obesity research
- Cellular signaling
Background:
- Obesity is a global epidemic linked to inflammation and metabolic dysfunction.
- Adipose tissue is central to these metabolic processes.
- Mixed lineage kinase domain-like pseudokinase (MLKL) mediates necroptosis and influences metabolism.
Purpose of the Study:
- To investigate the specific role of MLKL in adipocytes concerning obesity.
- To assess the impact of adipocyte-specific MLKL deletion on metabolic health.
Main Methods:
- Utilized adipocyte-specific Mlkl knockout (MlklAdi-KO) mice.
- Administered high-fat diet (HFD) to induce obesity.
- Performed transcriptomic and metabolomic profiling of white adipose tissue (WAT).
Main Results:
- MlklAdi-KO mice showed reduced HFD-induced obesity, improved glucose tolerance, and enhanced insulin sensitivity.
- Elevated energy expenditure, increased mitochondrial function, and reduced lipid accumulation in WAT were observed.
- WAT transcriptomics revealed modulated pathways in oxidative phosphorylation, inflammation, and lipid metabolism.
Conclusions:
- Adipocyte-specific MLKL deletion confers protection against obesity and metabolic dysfunction.
- MLKL influences adipocyte differentiation and systemic metabolic health.
- MLKL represents a potential therapeutic target for obesity and related metabolic disorders.
