High-energy demand and nutrient exhaustion in MTCH2 knockout cells DOI Creative Commons

Sabita Chourasia,

Christopher Petucci,

Hu Wang

et al.

bioRxiv (Cold Spring Harbor Laboratory), Journal Year: 2023, Volume and Issue: unknown

Published: Dec. 16, 2023

Abstract Mitochondrial carrier homolog 2 (MTCH2) is a regulator of apoptosis, mitochondrial dynamics, and metabolism. Loss MTCH2 results in fragmentation, an increase whole-body energy utilization, protection from diet-induced obesity. We now show using temporal metabolomics that deletion high ATP demand, oxidized environment, lipid/amino acid/carbohydrate metabolism, the decrease many metabolites. Lipidomics analyses strategic adaptive membrane lipids storage knockout cells. Importantly, all metabolic changes cells were rescued by re-expression. Interestingly, this imbalance metabolism reductive potential triggered MTCH2-deletion inhibits adipocyte differentiation, consuming biosynthetic process. In summary, loss demand triggers catabolic oxidizing which fails to fuel anabolic processes during differentiation.

Language: Английский

High-energy demand and nutrient exhaustion in MTCH2 knockout cells DOI Creative Commons

Sabita Chourasia,

Christopher Petucci,

Hu Wang

et al.

bioRxiv (Cold Spring Harbor Laboratory), Journal Year: 2023, Volume and Issue: unknown

Published: Dec. 16, 2023

Abstract Mitochondrial carrier homolog 2 (MTCH2) is a regulator of apoptosis, mitochondrial dynamics, and metabolism. Loss MTCH2 results in fragmentation, an increase whole-body energy utilization, protection from diet-induced obesity. We now show using temporal metabolomics that deletion high ATP demand, oxidized environment, lipid/amino acid/carbohydrate metabolism, the decrease many metabolites. Lipidomics analyses strategic adaptive membrane lipids storage knockout cells. Importantly, all metabolic changes cells were rescued by re-expression. Interestingly, this imbalance metabolism reductive potential triggered MTCH2-deletion inhibits adipocyte differentiation, consuming biosynthetic process. In summary, loss demand triggers catabolic oxidizing which fails to fuel anabolic processes during differentiation.

Language: Английский

Citations

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