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In addition, each tablet contains the following inactive ingredients: hypromellose, magnesium stearate, polyethylene glycol and povidone.Metformin is an antihyperglycemic agent which improves glucose tolerance in patients with type 2 diabetes, lowering both basal and postprandial plasma glucose.

Metformin is negligibly bound to plasma proteins, in contrast to sulfonylureas, which are more than 90% protein bound.Food decreases the extent of and slightly delays the absorption of metformin, as shown by approximately a 40% lower mean peak plasma concentration (C) following administration of a single 850 mg tablet of metformin with food, compared to the same tablet strength administered fasting.The clinical relevance of these decreases is unknown.Its pharmacologic mechanisms of action are different from other classes of oral antihyperglycemic agents.Metformin decreases hepatic glucose production, decreases intestinal absorption of glucose, and improves insulin sensitivity by increasing peripheral glucose uptake and utilization.

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Metformin partitions into erythrocytes, most likely as a function of time.At usual clinical doses and dosing schedules of metformin, steady state plasma concentrations of metformin are reached within 24 to 48 hours and are generally ) is approximately 3.5 times greater than creatinine clearance, which indicates that tubular secretion is the major route of metformin elimination.In the presence of normal renal function, there are no differences between single- or multiple-dose pharmacokinetics of metformin between patients with type 2 diabetes and normal subjects (see ), nor is there any accumulation of metformin in either group at usual clinical doses.In patients with decreased renal function (based on measured 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 (see ).A 24-week, double-blind, placebo-controlled study of metformin plus insulin versus insulin plus placebo was conducted in patients with type 2 diabetes who failed to achieve adequate glycemic control on insulin alone (see ).

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Patients randomized to receive metformin plus insulin achieved a reduction in Hb A1c of 2.10%, compared to a 1.56% reduction in Hb A1c achieved by insulin plus placebo.

Unlike sulfonylureas, metformin does not produce hypoglycemia in either patients with type 2 diabetes or normal subjects (except in special circumstances, see ) and does not cause hyperinsulinemia.

With metformin therapy, insulin secretion remains unchanged while fasting insulin levels and day-long plasma insulin response may actually decrease.

The combination of metformin and glyburide was effective in reducing FPG, PPG, and Hb A1c levels by 63 mg/d L, 65 mg/d L, and 1.7%, respectively.

Compared to results of glyburide treatment alone, the net differences with combination treatment were - 77 mg/d L, - 68 mg/d L and -1.9%, respectively (see Not statistically significant The magnitude of the decline in fasting blood glucose concentration following the institution of metformin hydrochloride tablets therapy was proportional to the level of fasting hyperglycemia.


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