" Metformin, introduced as frontline therapy for uncomplicated type 2 diabetes in the 1950s, up until now was believed to work by making the liver more sensitive to insulin. The Johns Hopkins study shows, however, that metformin bypasses the stumbling block in communication and works directly in the liver cells.
"Rather than an interpreter of insulin-liver communication, metformin takes over as the messenger itself," said senior investigator Fred Wondisford, who heads the Metabolism Division at Johns Hopkins Children's. "Metformin actually mimics the action of CBP, the critical signaling protein involved in the communication between the liver and the pancreas that's necessary for maintaining glucose production by the liver and its suppression by insulin."
To test their hypothesis, researchers induced insulin resistance in mice by feeding them a high- fat diet over several months. Mice on high-fat diets developed insulin resistance, and their high blood glucose levels did not drop to normal after eating. Once the mice were treated with metformin, however, CBP was activated to the levels of nondiabetic mice, and their blood glucose levels returned to normal. However, when metformin was given to diabetic mice with defective copies of CBP, it had no effect on blood glucose levels, a proof that metformin works through CBP."
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