For the treatment of NIDDM in conjunction with diet and exercise.
Gliclazide is a second generation sulphonylurea which acts as a hypoglycemic agent. It stimulates _ cells of the islet of Langerhans in the pancreas to release insulin. It also enhances peripheral insulin sensitivity. Overall, it potentiates insulin release and improves insulin dynamics.
Mode of Action:
Gliclazide binds to the _ cell sulfonyl urea receptor (SUR1). This binding subsequently blocks the ATP sensitive potassium channels. The binding results in closure of the channels and leads to a resulting decrease in potassium efflux leads to depolarization of the _ cells. This opens voltage-dependent calcium channels in the _ cell resulting in calmodulin activation, which in turn leads to exocytosis of insulin containing secretorty granules.
Extensively metabolized in the liver. Less than 1% of the orally administered dose appears unchanged in the urine. Metabolites include oxidized and hydroxylated derivates, as well as glucuronic acid conjugates.
LD50=3000 mg/kg (orally in mice). Gliclazide and its metabolites may accumulate in those with severe hepatic and/or renal dysfunction. Symptoms of hypoglycemia include: dizziness, lack of energy, drowsiness, headache and sweating.
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