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Metaglip Information - Interactions and Warnings
METAGLIP combines glipizide and metformin hydrochloride, two antihyperglycemic agents with
complementary mechanisms of action, to improve glycemic control in patients with type 2
Glipizide appears to lower blood glucose acutely by stimulating the release of insulin from the pancreas, an effect dependent upon functioning beta cells in the pancreatic islets. Extrapancreatic effects may play a part in the mechanism of action of oral sulfonylurea hypoglycemic drugs. The mechanism by which glipizide lowers blood glucose during long-term administration has not been clearly established. In man, stimulation of insulin secretion by glipizide in response to a meal is undoubtedly of major importance. Fasting insulin levels are not elevated even on long-term glipizide administration, but the postprandial insulin response continues to be enhanced after at least 6 months of treatment.
Metformin hydrochloride is an antihyperglycemic agent that improves glucose tolerance in patients with type 2 diabetes, lowering both basal and postprandial plasma glucose. Metformin hydrochlo-ride decreases hepatic glucose production, decreases intestinal absorption of glucose, and improves insulin sensitivity by increasing peripheral glucose uptake and utilization.
The metabolism and excretion of glipizide may be slowed in patients with impaired hepatic function. No pharmacokinetic studies have been conducted in patients with hepatic insufficiency for metformin. The metabolism and excretion of glipizide may be slowed in patients with impaired renal function. In patients with decreased renal function (based on creatinine clearance), the plasma and blood half-life of metformin is prolonged and the renal clearance is decreased in proportion to the decrease in creatinine clearance.
There is no information on the pharmacokinetics of glipizide in elderly patients. Limited data from controlled pharmacokinetic studies of metformin in healthy elderly subjects sug-gest that total plasma clearance is decreased, the half-life is prolonged, and C max is increased, compared to healthy young subjects. From these data, it appears that the change in metformin pharmacokinetics with aging is primarily accounted for by a change in renal function. Metformin treatment should not be initiated in patients over 80 years of age unless measurement of creatinine clearance demonstrates that renal function is not reduced.
No data from pharmacokinetic studies in pediatric subjects are available for either glipizide or metformin.
This information is not intended to be a substitute for professional medical advice. You should not use this material to diagnose or treat a health condition or disease without consulting with your healthcare provider.
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