Metformin is the first line medical therapy for patients with type 2 diabetes mellitus (T2DM) because unlike other antidiabetic agents, it does not cause hypoglycemia.
Metformin can be used in PCOS particularly in women with co-morbid insulin resistance, as evidenced by the presence of type 2 diabetes or lab measures of insulin resistance. It can also assist with weight loss.
Metformin has multiple mechanisms of action. Metformin decreases hepatic gluconeogenesis via inhibition of mitochondrial glycerophosphate dehydrogenase (mGPD), an enzyme which normally facilitates the conversion of glycerol to glucose.
Metformin also increases insulin sensitivity, which is the primary affliction in patients with T2DM. Metformin helps increase peripheral glucose uptake, helping to lower the blood sugar.
Metformin can cause elevations in lactate levels due to its inhibition of gluconeogenesis and prevention of lactate being converted to glucose. Therefore a side effect can be lactic acidosis, seen especially in cases of overdose or concurrent renal failure.
Metformin use can cause GI distress. It is associated with diarrhea, nausea and vomiting.
This drug promotes weight loss, which is actually a favorable side effect for most patients.
Another side effect of metformin is inhibition of vitamin B12 and/or folate absorption from the gastrointestinal tract.
Due to the increased risk of lactic acidosis, metformin is contraindicated in patients with a GFR < 30 ml/min. Patients whose GFR is greater than 45ml/min are generally considered to be candidates for a full dose of metformin. Patients whose GFR is 30-45 should be closely monitored and prescribed metformin judiciously. For patients receiving intravenous contrast for radiologic studies, metformin may be stopped for a period of time since contrast increases the risk of acute kidney injury.
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