Diabetes Drug Metformin Anti-inflammatory Mechanism Discovered

diabetesResearchers have found that the anti-diabetic drug metformin reduces the production of inflammatory cytokines. When inflammatory cytokines are produced in excess, they cause inflammation that increases cancer risk and the incidence of other diseases.

The University of Montreal researchers reported that metformin inhibits the expression of genes that code for several inflammatory cytokines observed during cellular senescence. These inflammatory cytokines are normally secreted by the cells in response to infection. However, chronic production of them causes cell aging. This same type of effect can be created other ways, such as by smoking.

The research indicated that metformin blocks the activity of nuclear factor kappa-beta (NF-kB), a transcription factor, which is involved in inflammation. The genes that create cytokines are normal; however, in metformin treated cells, a protein that normally triggers their activation can’t reach them. They also found that metformin “does not exert its effects through a pathway commonly thought to mediate its antidiabetic effects.”

This research has implications for our understanding of how a healthy individual defends itself from cancer. It may indicate that metformin, a common and relatively safe drug, could be applied to treat certain cancers in the future. Additionally, the drug might possibly be used in the future slow the aging process, according to the researchers. They plan on researching these possibilities.

Editor’s Note: Before using a medication for any purpose, consult your doctor. The role of inflammation in the onset of type 2 diabetes has also been researched. See our list of research into diabetes. Our page about diabetes includes symptoms, causes, dietary and lifestyle recommendations, reviews and a discussion of nutrients.

Source: “Metformin inhibits the senescence-associated secretory phenotype by interfering with IKK/NF-κB activation” by O. Moiseeva1 et. al. Aging Cell, March 23, 2013. DOI: 10.1111/acel.12075