2026-04-14T03:09:11Zhttps://recercat.cat/oai/request

oai:recercat.cat:2445/1972232025-12-04T21:15:16Zcom_2072_1057col_2072_478781col_2072_478917

00925njm 22002777a 4500 dc Aye, Cho-Cho author Hammond, Dean E. author Rodriguez-Cuenca, Sergio author Doherty, Mary K. author Whitfield, Phillip D. author Phelan, Marie M. author Yang, Chenjing author Perez-Perez, Rafael author Li, Xiaoxin author Diaz-Ramos, Angels author Peddinti, Gopal author Oresic, Matej author Vidal Puig, Antonio author Zorzano Olarte, Antonio author Ugalde, Cristina author Mora Fayos, Sílvia author 2023-04-25T08:39:50Z 2023-04-25T08:39:50Z 2023-02-04 2023-04-25T08:39:50Z CBL is rapidly phosphorylated upon insulin receptor activation. Mice whole body CBL depletion improved insulin sensitivity and glucose clearance, however, the precise mechanisms remain unknown. We depleted either CBL or its associated protein SORBS1/CAP independently in my-ocytes and assessed mitochondrial function and metabolism compared to control cells. CBL and CAP-depleted cells showed increased mitochondrial mass with greater proton leak. Mitochondrial respiratory complex I activity and assembly into respirasomes were reduced. Proteome profiling revealed alterations in proteins involved in glycolysis and fatty acid degradation. Our findings demonstrate CBL/CAP pathway couples insulin signalling to efficient mitochondrial respiratory function and metabolism in muscle. Mitocondris Resistència a la insulina Glucosa Mitochondria Insulin resistance Glucose CBL/CAP is essential for mitochondria respiration complex I assembly and bioenergetics efficiency in muscle cells.