Abstract
Metformin is the leading drug for treating type 2 diabetics, but the mechanism of action of metformin, despite some suggested mechanisms such as the activation of the AMP-kinase, is largely unknown. Among its many positive effects are the reduction of blood glucose levels, the inhibition of cyclic AMP synthesis, gluconeogenesis and an increase in sensitivity to insulin. Recent studies have described the natural antagonist of cyclic AMP, prostaglandylinositol cyclic phosphate. Synthesis of cyclic PIP is stimulated in all organs by hormones such as insulin and also by drugs such as metformin. Its primary action is to trigger the dephosphorylation of proteins/enzymes, phosphorylated on serine/threonine residues. Cyclic PIP triggers many of the regulations requested by insulin. The parallels between the beneficial effects of metformin and the regulations triggered by cyclic PIP suggest that the mechanism of action of this key drug may well be explained by its stimulation of the synthesis of cyclic PIP.
Highlights
Type 1 diabetes results from the destruction of pancreatic β-cells by an autoimmune reaction leading to the inability to synthesize the hormone insulin
This causes a decrease in the activation of blood glucose uptake by muscle and other cells and a decrease in the ability of pancreatic β-cells to switch off insulin secretion
PIP synthesis in the liver of rodents [10]. This raises the question of whether this activation of cyclic PIP synthase can explain the mechanism of action of the biguanide metformin, a common therapeutic for humans with type 2 diabetes
Summary
Type 1 diabetes results from the destruction of pancreatic β-cells by an autoimmune reaction leading to the inability to synthesize the hormone insulin. The dose-response curves of most other cell types, e.g., muscle, liver and fat cells, are shifted less far and respond better to secreted insulin. This results in a reasonable uptake of glucose into various cell types and can lead to decreases in blood glucose levels below basal values, making a patient feel hungry shortly after having eaten. PIP synthesis in the liver of rodents [10] This raises the question of whether this activation of cyclic PIP synthase can explain the mechanism of action of the biguanide metformin, a common therapeutic for humans with type 2 diabetes
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