What Induces Diabetic Ketoacidosis or Lactic Acidosis in Diabetic Alcoholic Patients Complicated with Chronic Calcific Pancreatitis?

Diabetic ketoacidosis (DKA) and lactic acidosis (LA) are severe metabolic acidosis which develop in diabetic alcoholic patients. The insulin deficiency and elevation of glucagon leads to increased hepatic glucose output, and induces the release of free fatty acids (FFA) from ad ipose tissue, which are associated with the development of DKA. The insulin deficiency also plays a critical ro le in LA because pyruvate dehydrogenase complex (PDHc) requires insulin for activation, and increased FFA decreases PDH activ ity. Chronic calcific pancreatitis (CCP)-induced diabetes has been reported to be not prone to develop DKA because CCP leads to depletion of both insulin (β-cells) and g lucagon-producing cells (α-cells) in pancreas. Further, to our knowledge, the development of LA in patients with CCP-induced diabetes has not ever been reported. We experienced alcoholic DKA and LA patients complicated with CCP-induced diabetes. The insulin deficiency is the crit ical factor for the development of both DKA and LA. FFA release from adipose tissue may be an important factor to determine the development of DKA. The absence of DKA in patient with LA may be due to extremely small volume of visceral adipose tissue. Although FFA is associated with the development of LA, a decreased activity of PDHc by insulin deficiency may be the most crit ical factor for the development of LA. Less insulin may be required to treat or prevent LA compared with DKA.