Non-insulin-dependent diabetes mellitus: a clinical strategy.
In non-insulin-dependent diabetes mellitus (NIDDM), there are defects in both islet beta cell function (insulin secretion) and in insulin action. It is proposed that these may be two manifestations of a common defect involving glucose metabolism. These may be a consequence of some aspect of the insulin-deficient state, e.g., insulin deficiency or hyperglycemia. This implies that the defects of NIDDM are both "feed-forward" (i.e., they lessen with improvement of the metabolic state) and "fail-backward" (i.e., emerging defects in islet beta cell function and insulin action aggravate each other). A subclassification of NIDDM is proposed, based on presumed pathophysiologic defects. This subclassification divides patients, on the basis of fasting (basal) plasma glucose and postprandial glucose response to meals, into four categories: mild, moderate, severe, and very severe. The therapeutic strategies for these four categories are slightly different. Diet and exercise are always a component of therapy. Sulfonylureas are used, as needed, in patients with mild or moderate NIDDM. Basal insulin therapy may be used in moderate NIDDM. Some form of around-the-clock insulin therapy is used for patients with severe NIDDM. Very severe NIDDM is treated by more intensive insulin therapy.
D003131:Combined Modality Therapy; D003920:Diabetes Mellitus / Q000503:physiopathology; D003924:Diabetes Mellitus, Type 2 / Q000145:classification / Q000178:diet therapy / Q000188:drug therapy / Q000503:physiopathology / Q000628:therapy*; D004032:Diet; D005081:Exercise Therapy; D006801:Humans; D007004:Hypoglycemic Agents / Q000627:therapeutic use; D007328:Insulin / Q000627:therapeutic use; D007333:Insulin Resistance; D007515:Islets of Langerhans / Q000502:physiology; D009765:Obesity; D011972:Receptor, Insulin / Q000187:drug effects
D007004:Hypoglycemic Agents; D007328:Insulin; D011972:Receptor, Insulin