New Study Results In On Metformin

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New Study Results In On Metformin

New Study Results In On Metformin

According to a study performed by Morris J. Birnbaum, MD, PhD, the Willard and Rhoda Ware professor of Medicine, with the Institute for Diabetes, Obesity, and Metabolism, Perelman School of Medicine, University of Pennsylvania and a team of researchers, the diabetes drug metformin works much differently than what researchers once understood it to work.

Studies performed on mice found that metformin represses the liver hormone glucagon’s capacity to produce a central signaling molecule.

When it comes to decreasing the overactive glucose production that is associated with diabetes, for fifty years, biguanides have been used as therapeutics, which includes metformin.

Bimbaum says, “Overall, metformin lowers blood glucose by decreasing liver production of glucose. But we didn’t really know how the drug accomplished that.”

A little more than a decade ago, researchers found that Metformin reduces glucose synthesis by activating the enzyme AMPK. However, in 2010 this theory was disputed by genetic experiments by collaborators on the current study.  It was found that the livers of mice who were without AMPK were still responding to metformin. This meant that blood glucose levels were being controlled outside the AMPK trail.

Researchers had to look closer at how glucose it regulated normally in the body. It is known that when no food is taken in, glucose starts to decrease. Glucagon is then released from the pancreas that will in turn tell the liver that it needs to produce glucose. Researchers wanted to find out if metformin stops this release of glucagon.

Metformin provokes the action of glucagon which decreases fasting glucose levels. It was shown in the study that metformin leads to the buildup of AMP in mice. This restrains an enzyme called cyclase, which reduces levels of cyclic AMP and protein kinase activity. Eventually, this process blocks glucagon-dependent glucose production from liver cells.

Based off this evidence, Bimbaum suggests that adenylate cyclase will possibly be a new target drug because it imitates the action repressed by metformin. It is also something that could lead to patients feeling fewer side effects, which is always a great goal to strive for.

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