New research suggests that targeting glucagon may be a better approach in the treatment for type 2 diabetes, according to a new study published in Cell Metabolism.
As diabetics will understand, insulin is the hormone responsible for lowering blood sugar levels while glucagon is the hormone which raises your blood glucose. The research shows that rather than targeting insulin, preventing glucagon from increasing your glucose levels may be a better approach.
Ira Tabas, MD, PhD, Richard J. Stock Professor and Vice Chair of Research in the Department of Medicine and professor of Anatomy & Cell Biology, led the study alongside Lale Ozcan, PhD, associate research scientist.
In a press release, Dr.Tabas said:
"What we’ve found is a way to reduce glucagon’s influence on blood sugar without the side effects of global glucagon repression."
Drugs that target glucagon have been tested previously but it was found that they also disrupted the other important roles that glucagon plays in the body. This new study looked at the role that the enzyme CaMKII plays. The researchers found that if they blocked this enzyme in diabetic mice, their blood sugars went down with no ill effects. They also discovered that cholesterol levels went down, the liver wasn't so fatty and insulin sensitivity was improved.
Dr. Tabas said:
"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."
“Until now, it has been difficult to block glucagon’s effect on blood sugar without interfering with glucagon’s other function but we think CaMKII is different.”
Dr. Tabas is now working on CaMKII inhibitor which could treat type 2 diabetes.
As diabetics will understand, insulin is the hormone responsible for lowering blood sugar levels while glucagon is the hormone which raises your blood glucose. The research shows that rather than targeting insulin, preventing glucagon from increasing your glucose levels may be a better approach.
Ira Tabas, MD, PhD, Richard J. Stock Professor and Vice Chair of Research in the Department of Medicine and professor of Anatomy & Cell Biology, led the study alongside Lale Ozcan, PhD, associate research scientist.
In a press release, Dr.Tabas said:
"What we’ve found is a way to reduce glucagon’s influence on blood sugar without the side effects of global glucagon repression."
Drugs that target glucagon have been tested previously but it was found that they also disrupted the other important roles that glucagon plays in the body. This new study looked at the role that the enzyme CaMKII plays. The researchers found that if they blocked this enzyme in diabetic mice, their blood sugars went down with no ill effects. They also discovered that cholesterol levels went down, the liver wasn't so fatty and insulin sensitivity was improved.
Dr. Tabas said:
"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."
“Until now, it has been difficult to block glucagon’s effect on blood sugar without interfering with glucagon’s other function but we think CaMKII is different.”
Dr. Tabas is now working on CaMKII inhibitor which could treat type 2 diabetes.
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