Sammanfattning
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 myocytes 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 signaling to efficient mitochondrial respiratory function and metabolism in muscle.
Originalspråk | Engelska |
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Tidskrift | International Journal of Molecular Sciences |
Volym | 24 |
Nummer | 4 |
DOI | |
Status | Publicerad - 8 feb. 2023 |
MoE-publikationstyp | A1 Tidskriftsartikel-refererad |
Nyckelord
- CBL
- mitochondria
- insulin signalling
- insulin resistance
- glucose transport
- SORBS1