posted on Jan, 8 2011 @ 05:57 PM
reply to post by Bhadhidar
I'm certainly no expert. I don't make the claims: These are from medical studies. If you go and read all the sources I have provided it will become
Here is a snippet from another site;
Metformin assists in lowering blood sugar levels by stimulating the pancreas, the organ that creates insulin in the body. In type 1 diabetes, the
pancreas has stopped producing insulin, so Metformin does not work for this type of diabetes. Metformin decreases the level of sugar available from
the diet. When the blood sugar level is too low, the liver produces sugar to add to the bloodstream. When the blood sugar level is out of control, the
liver loses its ability to sense the blood sugar levels and will pump sugar into the blood even when the sugar level is high. Metformin helps to
suppress the production level of sugar by the liver. By lowering the blood sugar level, Metformin helps the body respond to its own insulin
production. This promotes the burning of sugar, so the blood sugar level can stabilize at a normal level.
Read more: How Does Metformin Work? | eHow.com www.ehow.com...
I think, from my understanding, is that it works threefold. Glucophage actually stops absorption of glucose in the gut. It also makes cells more
sensitive to Insulin, please see above. Then there is another factor. Metformin induces cell death in p53-deficient HCT116 cells under nutrient
limitation. Quite a few cancers are P53 deficient.
Here is some more medical babble on it:
The biguanide metformin is the most widely used drug for treatment of type 2 diabetes (1, 2). The primary systemic effect of metformin is the lowering
of blood glucose levels. The effects of metformin on blood glucose has been explained through reduced hepatic gluconeogenesis and increased glucose
uptake in skeletal muscles (3, 4). Metformin treatment leads to activation of AMP-activated protein kinase (AMPK) in vitro and in vivo (5–7). [bT]he
molecular mechanisms by which metformin leads to AMPK activation are poorly understood. Nevertheless, through activation of AMPK, metformin
treatment decreases the expression of gluco- neogenic genes and increases fatty acid oxidation in hepatocytes (7–9). In addition, studies in mice
lacking expression of LKB1 in the liver show that the glucose-lowering effect of metformin is dependent on the LKB1/AMPK pathway (10).
Metformin induces cell death in p53-deficient HCT116 cells under nutrient limitation.