Ted security interventions in the general Bev Lkerung, and five co t of the intervention in terms not only of therapies, as well as laboratory tests, adverse events and diagnostic procedures should be in relation to the benefits to be considered therapy in reducing the incidence of illness, disability and cause-specific mortality t. proteasome inhibitors Is currently the only drug Se treatment, the insulin resistance or glucose in the blood, which modifies these properties in a big en asymptomatic Bev Lkerung just too high risk for type 2 diabetes with metformin. Metformin was approved as a drug Glucophage in 1995. It was for the treatment of PCOS in women before menopause by reducing the Ausma It uses the severe insulin resistance.
In the UKPDS, in ADIP These patients with T2DM, metformin has been entered Born in overall mortality reduction of t and complications, both micro-and macro-complications in patients with newly diagnosed diabetics. Many other studies have shown the benefits Amonafide Topoisomerase inhibitor of metformin therapy in reducing kardiovaskul Rer disease in patients with T2DM documented. Metformin reduces the risk, at least for a short time, type 2 diabetes in the DPP. The effect of metformin Similar to that of non-pharmacological interventions, was au He Older age groups. Metformin reduced HbA1c by 1% to 1.5%. Long term monitoring in the DPP documented that nearly 40% to 50% of treated patients with metformin, k can To convert the IFG from diabetes. Thus, it is probably too late t to treatment with metformin, when individuals have IFG or IGT or start near 6.5% HbA1c. Metformin is rare with premiums hypoglycaemia Associated.
There seems to be a certain weight loss with metformin. Some studies have reported decreased levels of triglycerides and increased Hte HDL-cholesterol. Metformin decreases hepatic glucose production, increases peripheral glucose utilization and ht the limited Dimensions, erh Ht peripheral glucose utilization in muscle. It obtains Ht not insulin secretion. Numerous case-control studies and some long-term studies show that metformin m for may have the risk of cancer, in particular to reduce the gastrointestinal and pancreatic cancer. Pr Prevention of cancer, pancreatic cancer is in particular an extremely important advantage of the drug. However, there are no clinical studies on the time that metformin reduces the risk of cancer.
There is also an experimental animal data showing that metformin increased life expectancy, but no experimental study of man Ht. Metformin inhibits oxidative phosphorylation by one Change adenosine monophosphate to adenosine 5 rate. AMP-activated kinase activation involved in the transcription blunting TORC2 nuclear genes in gluconeogenesis. The tumor suppressor LKB1 is necessary for the AMPK activity t. Experimental studies show that metformin has an effect on the neoplastic transformation of cells. The dose of metformin in these studies is much h Higher than the recommended dose or drug that is currently in the treatment of insulin resistance or type 2 diabetes. To assess a test of whether metformin would reduce the risk of cancer is a very big s sampling and another advanced age, perhaps too late T, due to the low incidence of cancer site-specific. Potentially serious side effect of metformin use is a small risk of lactic acidosis, particularly in patients with kidney disease. The risk
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