Description
Usually combinations are used to treat uncontrolled diabetes when the monotherapy with any of the medication fails to provide adequate control.
How these agents act on diabetic patients?
METFORMIN
Metformin belongs to the group of biguanides. Biguanides are guanidine derivatives and were introduced into clinical use for the treatment of hyperglycemia in patients with type 11 diabetes mellitus in the 1950’s. These biguanides were initially available [phenformin, Metformin, buformin]
Metformin do not lower blood sugar in normal subjects but they do so in all types of diabetes mellitus. They potentiate the hypoglycemic action of insulin and sulfonyl ureas but by themselves do not produce clinical hypoglycemia in diabetics. Metformin decreases the glycogen content of the liver. They inhibit lipogenesis but not lipolysis in the adipose tissue.
The exact mechanism of action of Metformin is not known. But the presence of either endogenous or exogenous insulin is necessary for its action. They do not stimulate insulin release from the pancreas.
They stimulate the peripheral utilization of glucose. The exact mechanism of this action is not known. Metformin inhibits aerobic glycolysis and this stimulates anaerobic glycolysis with resultant increase in glucose uptake by the cells. Metformin inhibits hepatic gluconeogenesis. They reduce glucose absorption from the intestine.
GLIMEPIRIDE
Glimepiride which is an oral antidiabetic drug belonging to the group of sulfonyl urea.
MECHANISM OF ACTION
The primary mechanism of action of glimepiride in lowering of blood glucose level appears to be dependent on stimulating the release of insulin from the functioning pancreatic beta cells. In addition, extra pancreatic effects may also play a role in the activity of glimepiride. This is supported by both clinical and preclinical studies, demonstrating that glimepiride administration can lead to increased sensitivity of peripheral tissues to insulin. However, the mechanism by which it lowers the blood glucose level during long term administration have not been clearly established. In non- fasting diabetic patients, the hypoglycemic action of single dose of glimepiride lasts for 24hrs. Glimepiride achieves and maintains good glycemic control in patients with type 2 diabetes mellitus. Glimepiride preserves myocardial preconditioning, a protective mechanism that limits damage in the event of an ischemic attack.
Glimepiride does not block the beneficial effects of mitochondrial K ATP channel opening. This also has significant effect for the treatment of type2 DM patients with ongoing ischemic heart disease. Glimepiride improves both first and second phase of insulin secretion It also increases the insulin stimulated glycogen synthesis in the skeletal muscles.
Glimepiride reduces the level of lipoprotein [a], plasminogen activator inhibitor-1 [PAI-1] and homocysteine. Thus, prevents arteriosclerosis.
INDICATIONS
Non insulin dependant diabetes mellitus [type 11]. It is used as an adjunct in diabetes along with exercise and weight reduction when these alone fails to control blood glucose levels.
Chances of developing hypoglycemia are less with Glimepiride. Body weight gain with Glimepiride treatment is less frequent in elderly patients with type2 DM. Glimepiride is ideal for treatment of obese elderly patients with type2 DM.
Glimepiride can be used safely in newly diagnosed type 2 diabetic patients.
CONTRA-INDICATIONS
– Hypersensitivity
– Severe hepatic and renal impairment
– Pregnancy and lactation
– Ketoacidosis
This should be administered strictly with the prescription and advise of medical practitioners only.
