- Main action is to reduce hepatic gluconeogenesis through activation of AMP-activated protein kinase.
- Importantly – this glucose lowering action does not depend on functioning pancreatic β-cells and therefore produces less hypoglycaemia.
- It is first line in treatment of T2DM because it is an insulin sparing agent and does not increase body weight or provoke hypoglycaemia.
- Because it inhibits hepatic gluconeogenesis, it therefore impairs hepatic metabolism of lactic acid.
- Major toxicity is severe lactic acidosis (dose related complication)
- Contraindications as follows:
- Renal disease
- Hepatic disease
- Any condition leading to hypoxia (e.g. CCF) due to accumulation of lactic acid.