The Type 2 diabetes drug metformin works differently than previously thought, EurekAlert reports. Metformin, marketed first by Bristol-Myers Squibb as Glucophage, 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 and increases sensitivity to insulin—a hormone that converts sugar and other foods into energy within the body.
Until now, researchers believed metformin disabled the mTOR (mammalian target of rapamycin) complex by first activating the tuberous sclerosis complex (TSC) proteins through the enzyme AMPK. But the results of this new study, led by George Thomas, PhD, scientific director of UC’s Metabolic Diseases Institute, show 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.
These findings may lead to wider use of metformin.
Until now, researchers believed metformin disabled the mTOR (mammalian target of rapamycin) complex by first activating the tuberous sclerosis complex (TSC) proteins through the enzyme AMPK. But the results of this new study, led by George Thomas, PhD, scientific director of UC’s Metabolic Diseases Institute, show 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.
These findings may lead to wider use of metformin.
