The popular diabetes medication metformin does not work the way researchers previously thought.
And the discovery could open the door to using metformin to treat cancer, tuberous sclerosis complex and other diseases.
The results of this study, led by George Thomas, PhD, scientific director of UC's Metabolic Diseases Institute, are published in the May 5 edition of Cell Metabolism.
Metformin is widely prescribed to people with type 2 diabetes and may be extended to the treatment of certain cancers.
The drug blocks the production of glucose (sugar) and increases sensitivity to insulin-a hormone that converts sugar and other foods into energy within the body.
Researchers have thought that metformin, an energy-deprivation agent, disables the mTOR (mammalian target of rapamycin) complex by first activating the tuberous sclerosis complex (TSC) proteins through the enzyme AMPK.
Thomas' team determined that mTOR could actually be disabled without AMPK, and even without TSC. The team was able to determine that metformin works to knock out mTOR through another enzyme, RAG GTPase.
"We've poked a hole in dogma," says Thomas, a professor in the cancer and cell biology department. "Scientists can and should go back and ask about things they had crossed off their list."
The importance of this finding, says Thomas, is the possibility it holds for broader use of metformin.
"Metformin is already prescribed to 100 million people worldwide, and our study raises the question, 'Could this drug be used even more widely?'"