Figure 7.

Schematic representation of CYC31 regulation on palmitate-induced insulin resistance and fatty acid oxidation: CYC31 binds to the catalytic domain of PTP1B and inactivates PTP1B, which further recovered palmitate-induced insulin resistance by increasing tyrosine phosphorylation of IRβ and IRS1. Akt was activated by increased upstream signaling of IR and IRS1, thereby promoting GLUT4 translocation to the cell membrane and increasing glucose uptake. Phosphorylated Akt also increases GSK3 phosphorylation and inhibits GS phosphorylation, suggesting potential for enhancing glycogen synthesis. On the other hand, CYC31 enhances AMPK phosphorylation and increases the expression of mitochondrial CPT1, indicating an increased signaling of mitochondrial fatty acid oxidation.