Pathogenesis of Prediabetes: Role of the Liver in Isolated Fasting Hyperglycemia and Combined Fasting and Postprandial Hyperglycemia

摘要

People with impaired fasting glucose (IFG) (ie, fasting glucose 100–125 mg/dL) have an increased likelihood of developing diabetes with the risk being particularly high in people with combined IFG and impaired glucose tolerance (IGT) (ie, a 2-hour oral glucose tolerance test [OGTT] glucose value of 140–199 mg/dL) (1–3). The pathogenesis of fasting and postprandial hyperglycemia in subjects with IFG remains an area of active investigation. People with IFG/IGT have defects in both insulin secretion and extrahepatic insulin action (4–10). On the other hand, the situation is not as clear in people with IFG and normal glucose tolerance (NGT). These individuals have been reported to have normal or minimally decreased insulin secretion and normal or minimally decreased insulin action (4–11).