Actually, Metformin lowers fasting blood glucose without inducing hypoglycaemia. Metformin (Glucophage, Glycomet, ect.) supposedly do not lower fasting blood glucose to a great extent as insulin does, so the risk of fasting hypoglycaemia or lactic acidosis is minimal with its use (contrary to phenformin). Previously, it was assumed that Metformin do not affect lactate metabolism and so does not induce lactic acidosis, but in fact, it may cause minimal lactic acidosis1 which is however, not a great concern. Glycomet also stimulates peripheral uptake and utilization of glucose.
Also, metformin strongly interacts with alcohol which can precipitate severe lactic acidosis if taken together. Nevertheless, its effect on controlling the Dawn phenomenon is debated although as a matter of fact metformin supresses hepatic gluconeogenesis (its primary mechanism of action).
Ref: A simple analysis of metformin's actions are discussed at this site.
Glucophage or Metformin has a good effect of fasting blood glucose. Its mode of action is inhibition of gluconeogenasis, increase glucose uptake by tissues,and decease the absorption of carbohydrates in intestine. Its advantage is there is no possibility of hypoglycemia.
Thanks for the link. As far as the effects of metformin on fasting blood glucose levels are concerned, most standard textbooks and journal articles indicate that the effect of metformin on fasting blood glucose level is minimal (in both diabetic and non-diabetic subjects). Episodes of hypoglycaemia due to metformin is rare since they do not stimulate pancreatic beta cells. Furthermore, Metformin do not cause glucose output from the liver. However, as I agree with you, patients should be cautious since the precise mechanism by which metformin actually works is still unclear.
Views expressed in discussion boards are views of individuals which can't be validated or substantiated. Nevertheless, Metformin is not a "magic pill", and it acts by an entirely different mechanism contrary to most other anti-diabetic agents (Sulfonylureas, thiazolidinediones, alpha-glucosidase inhibitors, etc.). You may search for relevant literature in PubMed on similar topics.
Furthermore, blood glucose levels are moderated by innumerable physiological factors, and due to interplay of several biochemical/metabolic pathways, substrates, diet, overnight fasting, Dawn effect etc. that should be factored in.
One of the problems with metformin usage is the dose response curve. There is a tendency to under dose with this drug, and the effect on FPG my then be minimal. This is well demonstrated in the attached graph from Graber et al American Med J 1997;103:491-497.