Implications of blood glucose, insulin resistance and beta-cell function in impaired glucose tolerance.
Insulin secretion is stimulated by ingestion of food. The combination of hyperinsulinaemia plus hyperglycaemia effectively promotes glucose uptake by the liver and by peripheral tissues, such as muscle and fat cells, and suppresses hepatic glucose output. These simultaneous processes maintain normal glucose homeostasis in a co-ordinated fashion. Type 2 diabetes mellitus is associated with impaired insulin in target tissues due to insulin resistance and/or insulin deficiency. At first, increased insulin secretion overcomes insulin resistance, but ultimately this fails, leading progressively to increased blood glucose levels. Individuals pass through a phase of impaired glucose tolerance (IGT) and increased fasting plasma glucose levels (IFG) before developing overt type 2 diabetes. Therefore, IGT/IFG is a dysglycaemic state that is intermediate between normal glucose tolerance and diabetes. In this article, we discuss the relative importance of hyperglycaemia, insulin resistance and beta-cell function in the development of glucose intolerance, taking the new diagnostic criteria into consideration. New recommendations from the Expert Committee on the Diagnosis and Classification of Diabetes Mellitus are discussed where appropriate.
Göke
B
B
Gastrointestinal Unit, Inselspital, University Hospital, Bern, Switzerland.
D001786:Blood Glucose / Q000032:analysis*; D002318:Cardiovascular Diseases / Q000209:etiology; D003924:Diabetes Mellitus, Type 2 / Q000209:etiology; D018450:Disease Progression; D018149:Glucose Intolerance / Q000097:blood / Q000503:physiopathology*; D006801:Humans; D007333:Insulin Resistance / Q000502:physiology*; D007515:Islets of Langerhans / Q000503:physiopathology*; D008954:Models, Biological
D001786:Blood Glucose