RNA helicase associated with AU-rich elements (RHAU) regulates hepatic glucose homeostasis via a novel...

This study elucidates the regulatory mechanism by which RHAU (RNA helicase associated with AU-rich elements) controls PPARγ (peroxisome proliferator-activated receptor-γ) expression and glucose metabolism in the mouse liver. Using liver-specific Rhau knockout mice (Rhau^cko) combined with Western blotting, immunohistochemistry, and immunofluorescence, we demonstrated that loss of RHAU significantly increased PPARγ expression, leading to reduced fasting blood glucose levels and decreased body weight. Bioinformatics analysis using QGRS identified a G-quadruplex structure within pre-miR-150, suggesting that RHAU likely facilitates miR-150 maturation by unwinding this secondary structure. This was further confirmed by RT-qPCR, which showed that knockdown of RHAU decreased miR-150 expression. Previous studies have established that miR-150 regulates Notch3 expression, and that Notch3 in turn modulates PPARγ expression. Overall, these results reveal the critical role of the RHAU-miR-150-Notch3-PPARγ signaling axis in hepatic metabolic regulation and provide novel mechanistic insights into glucose homeostasis.