GCKR and Insulin resistance: On the other hand, because the glucose-dependent glucokinase−GKRP dissociation was restored and 2-DG uptake was augmented by deacetylation-mimicking GKRP mutant (K126R) overexpression in db/db mouse-derived hepatocytes, deacetylation-mimicking GKRP (K126R) transduction in the livers of HFD-fed mice and db/db mice increased hepatic 2-DG uptake and improved glucose tolerance and insulin resistance, even though their hepatic NAD+ levels were unaffected.