Popular Diabetes Medication Supposed to Work Differently than Expected
Metformin, as popular diabetes medication, may work in different way than currently accepted. New elements could lead to wider use of this drug, particularly in treatment of cancer and some diseases related to TSC deficiency, such as tuberous sclerosis and LAM (lymphangioleiomyomatosis).
This surprising information has been published in the May 5th edition of Cell Metabolism as a result of a study led by PhD George Thomas, scientific director of UC’s Metabolic Diseases Institute.
Metformin, first marketed as Glucophage by Bristol-Myers Squibb, now available in generic form, as well as in a number of combinations, is frequently prescribed to patients with type 2 diabetes and could also be used as a treatment against certain forms of cancer. The drug has an important effect in blocking the production of glucose and determines increased sensitivity to insulin, a hormone that has the role of converting sugar and other foods into energy necessary to the body.
Researchers have believed that metformin, which is an energy-deprivation agent, has effect on disabling the mTOR (mammalian target of rapamycin) complex by activating, in the first instance, the TSC (tuberous sclerosis complex) proteins through an enzyme named AMPK.
The scientific team concluded that mTOR could be disabled without AMPK and even without TSC. The research determined that metformin annihilates mTOR by means of another enzyme, RAG GTPase.
Thomas opinion is that scientists have to reconsider things already labeled as classified. Professor Thomas thinks that latest researches have revealed the possibility of using metformin in new directions.
An extended use of metformin, a drug already prescribed to 100 million patients worldwide, is perfectly possible, according to the professor.
Such a drug, which increases insulin sensitivity, could be a viable alternative to medication that targets mTOR, but may present long-term injurious effects on insulin production. Type 2 diabetes originates in the body’s impossibility of using insulin properly. If not treated, diabetes has harmful effects on vision, leading to vision loss, heart attack, kidney failure, stroke and serious damages of nerves or blood vessels.
Study co-authors are, in alphabetical order, Nabeel Bardeesy, Sophie Brûlé, Patrick Dennis, Pawan Gulati, Adem Kalender, Bruce Kemp, So Young Kim, Sara Kozma, André Marette, John Schlager, Anand Selvaraj and Benoit Viollet.
George Thomas and Sara Kozma are supported by the National Institutes of Health (NIH) Mouse Models for Human Cancer Consortium, and the NIH’s National Institute of Diabetes and Digestive and Kidney Diseases. Adem Kalender and Anand Selvaraj receive support by appointments to the Research Participation Program at the Air Force Research Laboratory, Human Effectiveness Directorate, Bioscience and Protection, Wright Patterson Air Force Base, administered by the Oak Ridge Institute for Science and Education.
