Introduction:
Metformin (1, 1 Dimethylbiguanide hydrochloride ®Glucophage) is a semisynthetic biguanide derived from the alkaloide substance galegine of a herbaceous plant Galega officinalis (gout rue). It is the only member of beguanide class of oral hypoglycemic drug, [1] generally accepted as a first line treatment for type 2 non-insulin dependent diabetes mellitus (NIDDM).[2]
Metformin exist as a hydrophilic cation, reduces the blood glucose levels by overwhelming hepatic gluconeogenesis and increasing glucose uptake by skeletal muscle and adipose tissues[3]. It decreases blood insulin levels, upsurges insulin sensitivity,[4] suppresses synthesis of proteins, fatty acids and cholesterol,[5] and increases free fatty acid utilization.[6]
The molecular mechanisms by which metformin achieves these effects are still largely debated. However, principal evidence is that due to its positive charge, metformin accumulates within the cellular mitochondrial matrix and inhibits complex I of the mitochondrial respiratory chain, which results in excess of AMP production [7-9]. This in turn, leads to the activation of the energy sensing enzyme AMP-activated protein kinase (AMPK), which inhibits energy consuming processes and switches cellular metabolism towards energy production to restore energy homeostasis [10]. Indeed, metformin-mediated AMPK activation results in modulation of ensuing goals that enhance glucose uptake into skeletal muscle [11] and inhibit genes that …show more content…
In particular, data have emerged to suggest that metformin may have precise utility for cancer treatment in combination with radiation therapy. These evidence, as well as proposals for future, is the platform on which the review is