In more detail, impaired insulin ability to inhibit lipolysis processes in peripheral adipose tissue leads to increased levels of FFAs and elevated intrahepatic diacylglycerol concentrations, which are associated with activation of the protein kinase C epsilon (PKC-ε) and c-Jun N-terminal kinases 1 (JNK1) pathways, affecting insulin receptor substrates 1 and 2 and eventually aggravating insulin resistance and liver steatosis [50,51]. This evidence concerns the gene PRKCE and fatty liver disease.