Hepatic Dyrk1b regulates systemic glucose homeostasis [mouse liver]

Elucidation of the mechanisms controlling glucose homeostasis may deepen our understanding of the pathogenesis of T2DM and provide new therapeutic strategies for T2DM in the future. As reported, Dyrk1b is a pleiotropic protein and its genetic mutations are associated with blood glucose levels. However, the role of Dyrk1b in glucose metabolism is not well understood. Herein, we find that hepatic Dyrk1b overexpression in mice impairs the glucose tolerance and insulin resistance, whereas global Dyrk1b deficiency improves glucose metabolism of mcie. Dyrk1b overexpression in vitro blunts insulin signalling and glucose uptake. Collectively, our study uncovers a novel link between hepatic Dyrk1b and whole body glucose homeostasis. Overall design: For better understanding of Dyrk1b's function, RNA-seq analyses were performed on livers from C57 mice infected with adenovirus overexpressing mouse Dyrk1b (Ad-Dyrk1b) or control adenovirus (Ad-EGFP).