1. Gyk regulates the hepatic glycerol gluconeogenesis axis and the AKT-FOXO1-PEPCK/G6Pase pathway.
Gyk regulates the hepatic glycerol gluconeogenesis axis and the AKT-FOXO1-PEPCK/G6Pase pathway. Mice infected with Ad-Gyk or Ad-GFP for 5 days were examined for hepatic Gyk mRNA and protein expression (A and G); blood glycerol and glucose levels (B and C); glucose production using glycerol (GlyTT) (D) or pyruvate (PTT) (E) as precursors; hepatic gene expression (F); and hepatic AKT, FOXO1, and CREB phosphorylation (G) (n = 6–9/group). Mice infected with adenoviruses expressing Gyk shRNA (Sh-Gyk) or control sequence (Sh-NC) were examined for hepatic Gyk expression and AKT and FOXO1 phosphorylation (H) and PTT (I) (n = 7–9/group). Mouse primary hepatocytes infected with Ad-Gyk or Ad-GFP in triplicate were examined for glucose production with various precursors (J), AKT and FOXO1 phosphorylation (K), and gluconeogenic gene expression in the presence or absence of 100 nmol/L glucagon (L). Data are mean ± SEM, representing two independent in vitro experiments and three in vivo experiments, with the number of mice included in each group in each experiment indicated. *P < 0.05, **P < 0.01 compared with Ad-GFP–infected mice (A–G) or hepatocytes (J–L) or with Sh-NC–infected mice (H and I).
Shu Zhuo et al. Diabetes 2016;65:
©2016 by American Diabetes Association