Chapter 1 • Drugs Used in Diabetes
Chapter Summary
•Type 1 (IDDM) and type 2 (NIDDM) diabetes mellitus are defined at the beginning ofthe chapter.
•The times ofactivity onset, peak activity, and duration of activity for lispro, regular, lente, and ultralente insulins are summarized in Table Vlll-1-1.
•The oral antidiabetic drugs are the sulfonylureas, metformin, acarbose, thiazolidinediones, and repaglinide.
•By blocking K+ channels in the pancreatic cells, the sulfonylureas stimulate insulin release. The extra insulin in turn inhibits glucagon release from the cells and increases peripheral tissue sensitivity to insulin (Figure Vlll-1-1).
The firstand second-generation drugs are listed. The adverse effects include weight gain and potential hypoglycemia.
•Metformin enhances tissue sensitivity to insulin and inhibits liver gluconeogenesis. The potential side effect is lactic acidosis.
•Acarbose inhibits intestinal-glucosidase, thereby slowing glucose absorption and decreasing insulin demand. The side effect is gastrointestinal distress.
•The thiazolidinediones (glitazones) act via peroxisome proliferation activating receptors that control insulin-responsive genes. They are less hypoglycemic than the sulfonylureas, but they still induce weight gain and edema and have potential liver toxicity.
•Repaglinide, like the sulfonylureas, stimulates-cell secretion of insulin. Figure Vlll-1-2 summarizes the modes of action of these drugs.
•Both exenatide and sitagliptin increase glucose-dependent insulin secretion.
