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Oral antidiabetic drugs
Many types of oral antidiabetic drugs are approved for use in the United States. Types of available oral antidiabetic drugs include:
· first-generation sulfonylureas, which include acetohexamide, chlorpropamide, tolazamide, and tolbutamide
· second-generation sulfonylureas, which include gliclazide, glip-izide, glimepiride, and glyburide.
· thiazolidinediones, which include pioglitazone and rosiglitazone
· a biguanide drug, metformin
· alpha-glucosidase inhibitors, which include acarbose and miglitol
· a meglitinide drug, repaglinide
· an amino acid derivative, nateglinide
· combination therapies, which include glipizide and metformin, glyburide and metformin, and rosiglitazone and metformin.
Oral antidiabetic drugs are well absorbed from the GI tract and distributed via the bloodstream throughout the body. Because repaglinide has a short duration of action, it’s given before meals.
Oral antidiabetic drugs are metabolized primarily in the liver and are excreted mostly in urine, with some excreted in bile. Gly-buride is excreted equally in urine and stool; rosiglitazone and pi-oglitazone are largely excreted in both.
It’s believed that oral antidiabetic drugs produce actions both within and outside the pancreas (extrapancreatic) to regulate blood glucose.
Oral antidiabetic drugs probably stimulate pancreatic beta cells to release insulin in a patient with a minimally functioning pancreas. Within a few weeks to a few months of starting sulfonylureas, pan-creatic insulin secretion drops to pretreatment levels, but blood glucose levels remain normal or near-normal. Most likely, it’s the actions of the oral antidiabetic agents outside of the pancreas that maintain this glucose control.
Oral antidiabetic drugs provide several extrapancreatic actions to decrease and control blood glucose. They can go to work in the liver and decrease glucose production (gluconeogenesis) there. Also, by increasing the number of insulin receptors in the periph-eral tissues, they provide more opportunities for the cells to bind sufficiently with insulin, initiating the process of glucose metabolism.
Other oral antidiabetic agents produce specific ac-tions:
§ Pioglitazone and rosiglitazone improve insulin sensitivity and lower glucose production by the liver.
§ Metformin decreases liver production and intestinal absorption of glucose and improves insulin sensitivity.
§ Acarbose and miglitol inhibit enzymes, delaying glucose absorp-tion.
§ Repaglinide and nateglinide increase insulin secretion.
Oral antidiabetic drugs are indicated for patients with type 2 dia-betes if diet and exercise can’t control blood glucose levels. These drugs aren’t effective in patients with type 1 diabetes because the patients’ pancreatic beta cells aren’t functioning at a minimal level.
Combinations of multiple oral antidiabetic drugs or an oral anti-diabetic drug with insulin therapy may be indicated for some pa-tients who don’t respond to either therapy alone. (See Cautionarytales.)
Hypoglycemia and hyperglycemia are the main risks when oral an-tidiabetic drugs interact with other drugs.
Hypoglycemia may occur when sulfonylureas are combined with alcohol, anabolic steroids, chloramphenicol, cimetidine, clofi-brate, coumadin, fluconazole, gemfibrozil, MAOIs, phenylbuta-zone, ranitidine, salicylates, or sulfonamides. It may also occur when metformin is combined with cimetidine, nifedipine, pro-cainamide, ranitidine, or vancomycin. Hypoglycemia is less likely to occur when metformin is used as a single agent.
Hyperglycemia may occur when sulfonylureas are taken with cor-ticosteroids, dextrothyroxine, rifampin, sympathomimetics, and thiazide diuretics.
Because metformin given with iodinated contrast dyes can cause acute renal failure, metformin doses should be withheld in patients undergoing procedures that require I.V. contrast dye and not restarted for at least 48 hours after the procedure. (See Adverse reactions to oral antidiabetic drugs.)
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