Metformin is a biguanide antihyperglycemic agent used for treating non-insulin-dependent diabetes mellitus (NIDDM). It improves glycemic control by decreasing hepatic glucose production, as well as decreasing glucose absorption and increasing insulin-mediated glucose uptake.
Another well-known benefit of this drug is modest weight loss. Metformin is the drug of choice for obese NIDDM (non-insulin dependent diabetes mellitus) patients.
Metformin was approved in Canada initially in 1972, the 1970s in Europe, and in 1995 in the USA.
For use as an adjunct to diet and exercise in adult patients (18 years and older) with non-insulin dependent diabetes mellitus. Metformin may also be used for the management of metabolic and reproductive abnormalities associated with polycystic ovary syndrome (PCOS). Metformin may be used concomitantly with a sulfonylurea or insulin to improve glycemic control in adults.
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Metformin decreases hepatic glucose production, decreases intestinal absorption of glucose, and improves insulin sensitivity by increasing peripheral glucose uptake and utilization.
Unlike sulfonylureas, metformin does not produce hypoglycemia in either patients with type 2 diabetes or normal subjects (except in special circumstances) 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.
Mechanism of action
Metformin’s mechanisms of action are unique from other classes of oral antihyperglycemic drugs. Metformin decreases blood glucose levels by decreasing hepatic glucose production (gluconeogenesis), decreasing the intestinal absorption of glucose, and increasing insulin sensitivity by increasing peripheral glucose uptake and utilization.
Findings of recent studies however, show that metformin, at clinically relevant plasma concentrations, inhibits hepatic gluconeogenesis in a redox-dependent manner independently of reduction in citrate synthase flux, liver nucleotide concentrations, acetyl-CoA carboxylase enzyme activity, or gluconeogenic enzyme protein expression.
Previous studies indicate that the glucose-lowering effects of metformin are mediated by the activation by metformin of AMP-activated protein kinase (AMPK), a liver enzyme which plays an important role in insulin signaling, energy balance, and the metabolism of both glucose and lipids. The activation of AMPK is thought to be necessary for metformin’s inhibitory effect on the production of glucose by liver cells. Increased peripheral utilization of glucose may be due to improved insulin binding to insulin receptors. Metformin administration also increases AMPK activity in skeletal muscle.
The mechanism of action of metformin has been under extensive study in recent years, and research is ongoing…
All medicines may cause side effects, but many people have no, or minor, side effects.Some medical conditions may interact with Metformin.
Tell your doctor or pharmacist if you have any medical conditions.
Common adverse effects: The most common adverse effects of metformin include: epigastric discomfort, nausea, flatulence, and vomiting. Diarrhea, drowsiness, weakness, dizziness, malaise, and headache may also occur.
A note on lactic acidosis: Metformin decreases liver uptake of lactate, thereby increasing lactate blood levels which may increase the risk of lactic acidosis.
A note on renal function: In patients with decreased renal function, the plasma and blood half-life of metformin is prolonged and the renal clearance is decreased.
A note on hypoglycemia: When used alone, metformin does not cause hypoglycemia, however, it may potentiate the hypoglycemic effects of sulfonylureas and insulin when they are used concomitantly.
This is not a complete list of all side effects that may occur. If you have questions about side effects, contact your health care provider.
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