Potential Diabetes Treatment Via Glucagon Pathway

Many diabetics have always been dependent on insulin treatment as a means to control diabetes. Insulin is a hormone that removes glucose in the bloodstream to maintain the proper levels. But researchers have recently found a potentially better approach to controlling blood sugar levels by means of the glucagon pathway.

Glucagon is a natural hormone in the body that adds glucose into the bloodstream. A recent study suggests that controlling the effects of glucagon that is associated with glucose production may provide a new approach to treating diabetes. The findings were published in the online edition of Cell Metabolism journal.

Glucagon was discovered at almost the same time as insulin. But research on the former has been quite less as more attention was given on the latter as a potential diabetes treatment. And over the last decade, a new class of drugs called incretins has been quite successful as type II diabetes treatment. This also somehow resumed the interest on glucagon research. When they were initially introduced, researchers believed that incretins were known to stimulate the production of insulin. But recent research has indicated that a significant part of the drug’s success has to do with its unsuspecting inhibiting effects on glucagon secretion.

The new discovery has renewed the interest in researchers in searching for other drugs that act against glucagon, including those that block the glucagon in the liver, the organ where the hormone acts to free glucose. There are drugs that have been tested that block the glucagon receptor in the liver. But glucagon may also have multiple roles not only connected to glucose but may also affect other functions in the body.

The recent study has shown that it is possible to block glucagon’s effect on glucose without having to disrupt its other functions in the body. This may help raise the potential of developing safer anti-glucagon treatments for diabetes in the future. Researchers Ira Tabas, MD, PhD, Richard J. Stock Professor and Vice Chair of Research in the Department of Medicine and professor of Anatomy & Cell Biology and study lead author, along with Lale Ozcan, PhD, associate research scientist, have found that when glucagon attaches to its receptor, the glucose is only released after a particular enzyme called CaMKII is activated. The enzyme then sends a protein called Fox01 into the cell nucleus where the genes needed for glucose secretion are turned on.

“Even when their disease is well controlled, most patients with type II diabetes have excess glucagon action, so blocking CaMKII could potentially be a new way to lower blood sugar and better treat the disease,” added Dr. Tabas.

When the researchers blocked the CaMKII enzyme in obese and diabetic mice, their blood sugar levels also went down. In addition, cholesterol levels declined, the body’s insulin sensitivity improved and the liver became less fatty. “Until now, it has been difficult to block glucagon’s effect on blood sugar without interfering with glucagon’s other functions. But we think CaMKII is different,” Dr. Tabas added. The researchers are currently working on the potential of a CaMKII inhibitor as a potential diabetes treatment.

Source: Medical News Today

 

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