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Metformin is a member of the biguanide class, improves glucose tolerance in patients with type 2 diabetes, lowering both basal and postprandial plasma glucose. Metformin decreases hepatic glucose production, decreases intestinal absorption of glucose and improves insulin sensitivity by increasing peripheral glucose uptake and utilization.
The most important and serious side effect is lactic acidosis, therefore metformin is contraindicated in advanced chronic kidney disease. Kidney function should be assessed before starting metformin. Phenformin and buformin are more prone to cause acidosis than metformin; therefore they have been practically replaced by it.
Common adverse effects include diarrhea, nausea, and abdominal pain. [16] It has a small risk of causing low blood sugar. [16] High blood lactic acid level is a concern if the medication is used in overly large doses or prescribed in people with severe kidney problems. [23] [24] Metformin is a biguanide anti-hyperglycemic agent. [16]
The most common side effects are gastrointestinal (everyone’s favs: diarrhea, bloating, stomach pain, gas, indigestion and constipation). These affect up to 30 percent of metformin users.
As noted, timing your metformin dosage is crucial for mitigating the risk — and overall severity — of side effects. But what are those side effects exactly? The most common side effects of ...
The side effects encountered are anorexia, nausea, diarrhea, metallic taste, and weight loss. Its use is contraindicated in diabetic coma, ketoacidosis, severe infection, trauma, other conditions where buformin is unlikely to control the hyperglycemia, renal or hepatic impairment, heart failure, recent myocardial infarct, dehydration ...
Vildagliptin/metformin is indicated in the treatment of type-2 diabetes mellitus: [4] [6] [7] it is indicated in the treatment of adults who are unable to achieve sufficient glycaemic control at their maximally tolerated dose of oral metformin alone or who are already treated with the combination of vildagliptin and metformin as separate tablets.
Thiazolidinedione ligand dependent transactivation is responsible for the majority of anti-diabetic effects. The activated PPAR/RXR heterodimer binds to peroxisome proliferator hormone response elements upstream of target genes in complex with a number of coactivators such as nuclear receptor coactivator 1 and CREB binding protein, this causes upregulation of genes (for a full list see PPARγ):
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