KRIT1 and diabetes mellitus: Interestingly, although our KRIT1+/− mouse model did not show hyperglycemia, the increased expression of key markers of enhanced glucose uptake and glycolysis/mitochondrial respiration indicated that glucose metabolism was likely to be accelerated and paralleled by perturbed and deregulated gluconeogenesis, thus leading to the same exacerbated metabolism of intracellular glucose observed during diabetes, with consequent accumulation of AGEs.