However, in the presence of insulin resistance, impaired insulin action results in a lack of efficient suppression of gluconeogenesis even in the fed state due to aberrant expressions of gluconeogenic genes, such as glucose-6-phosphatase (G6PC) and phosphoenolpyruvate carboxykinase 1 (PCK1), in the liver as well as an increased supply of gluconeogenic substrates, such as glycerol, to the liver caused by enhanced lipolysis in adipose tissue. This evidence concerns the gene INS and Insulin resistance.