Hence, this suggests a plausible role in that p38 signalling may be able to explain insulin resistance and the lack of glucose uptake in type II diabetes.[95] Furthermore, another study found the activation of p38 signalling through hepatic neuronal nitric oxide synthase (nNOS) overexpression in HFD obese mice exacerbated glucose tolerance, intrahepatic lipid accumulation through increased triglyceride production, as well as decreased glycogen storage. This evidence concerns the gene MAPK1 and type 2 diabetes mellitus.