Nature communications · 2025
MTCH2 modulates CPT1 activity to regulate lipid metabolism of adipocytes.
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Wu Chunyan, Wang Tongtong, Ghosh Adhideb, Long Fen, Sharma Anand Kumar, Dahlby Tina, Noé Falko, Severi Ilenia, Colleluori Georgia, Cinti Saverio, Giordano Antonio, Ding Lianggong, Khandelwal Radhika, Kostidis Sarantos, Giera Martin, Balazova Lucia, Gardeux Vincent, Abu-Nawwas Laith, Deplancke Bart, Chourasia Sabita, Kleiner Sandra, Hamilton Bradford S, Alcántara Juan Manuel Alcántara, Ruiz Jonatan R, Blüher Matthias, Pekcec Anton, Balaz Miroslav, Gross Atan, Neubauer Heike, Wolfrum Christian
Аннотация
Metabolic disorders, including obesity and metabolic-associated steatohepatitis, arise from a chronic energy surplus. Thus, enhancing energy dissipation through increased respiration holds significant therapeutic potential for metabolic disorders. Through a comprehensive analysis of human and murine adipose tissues, along with a functional screen, we identify mitochondrial carrier homolog 2, a mitochondrial outer membrane protein, as a pivotal regulator of mitochondrial metabolism. Intriguingly, its expression in adipose tissue is a strong determinant of obesity in humans. Adipocyte-specific ablation of mitochondrial carrier homolog 2 improves mitochondrial function and whole-body energy expenditure, independent of uncoupling protein 1. Furthermore, mitochondrial carrier homolog 2 regulates mitochondrial influx of free fatty acids by modulating the sensitivity of carnitine palmitoyltransferase 1 to malonyl-CoA through direct physical interaction, leading to enhanced energy expenditure in adipocytes/adipose tissue. Here we show mitochondrial carrier homolog 2 functions as a negative regulator of energy metabolism in adipocytes and represents a potential target for treating obesity and related metabolic disorders.