Abstract
Two concepts are advanced to explain some of the puzzling biochemical features found in nonketotic hyperosmolar diabetic coma. It is firstly suggested that an insulinised liver (reflecting residual beta-cell secretory activity) coexists with a diabetic periphery, thereby inactivating intrahepatic oxidation of incoming free fatty acids, which are directed largely along nonketogenic metabolic pathways such as triglyceride synthesis. This could account for the lack of hyperketonæmia. Secondly, it is hypothesised that within the liver enhanced neoglucogenesis occurs, due to the prevailing portal-vein ratio of glucagon to insulin, and is mainly responsible for the development of massive hyperglycæmia.