BOTH GLUCOSE PRODUCTION AND DISAPPEARANCE MODULATE FASTING AND

hyperglycemia. Abnormalities in hepatic glucose metabolism i.e. excessive glucose production and decreased glucose uptake have been shown to contribute to both fasting and post-prandial hyperglycemia in individuals with T2DM. Insulin induced suppression of endogenous glucose production (EGP) and splanchnic glucose uptake (SGU) are considerably impaired in T2DM when compared to nondiabetic subjects (ND) matched for age, gender and degree of body fatness. Additionally, the effect of glucose per se on suppression of endogenous glucose production is also impaired in people with T2DM. Furthermore, it has been shown that the “nonsuppressability ” of post-prandial glucagon concentrations in people with T2DM contributes to post-prandial hyperglycemia through stimulation of hepatic glucose production. Additionally both higher rates of gluconeogenesis (GNG) and lack of suppression of glycogenolysis (GGL) contribute to excessive hepatic glucose production in T2DM. Therefore, dysregulation of hepatic glucose metabolism contributes significantly to both fasting and post-prandial hyperglycemia typically observed in individuals wit