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Impaired unsaturated fatty acid elongation alters mitochondrial function and accelerates metabolic dysfunction-associated steatohepatitis progression
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Impaired unsaturated fatty acid elongation alters mitochondrial function and accelerates metabolic dysfunction-associated steatohepatitis progression

Adrien Vouilloz, Thibaut Bourgeois, Marc Diedisheim, Thomas Pilot, Antoine Jalil, Naig Le Guern, Victoria Bergas, Noéline Rohmer, Florence Castelli, Damien Leleu, …
Metabolism, Vol.162
01/2025
DOI: https://doi.org/10.1016/j.metabol.2024.156051
PMID: 39454822

Résumé

Steatosis PUFAs MASLD MASH ELOVL5 Cardiolipins Animals Fatty Acid Elongases Humans Mice, Knockout Male Liver Mitochondria Fatty Liver Mice, Inbred C57BL Mitochondria, Liver Lipid Metabolism Triglycerides Mice Fatty Acids, Unsaturated Disease Progression
Although qualitative and quantitative alterations in liver Polyunsaturated Fatty Acids (PUFAs) are observed in MASH in humans, a causal relationship of PUFAs biosynthetic pathways is yet to be clarified. ELOVL5, an essential enzyme in PUFA elongation regulates hepatic triglyceride metabolism. Nonetheless, the long-term consequences of elongase disruption, particularly in murine models of MASH, have not been evaluated.

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