Is This Newly-Discovered Protein To Blame For Your Diabetes?


Researchers from the Japanese island of Okinawa, have discovered that a protein in the pancreas called CNOT3 may be to blame for abnormal glucose levels that cause diabetes. 

For the more than 370 million people around the world living with diabetes, the discovery, which was announced in the journal, Communications Biology, may not mean much now. Blood sugar levels should still be closely monitored and diabetes medication instructions should be followed. However, the discovery could one day lead to targeted gene therapy that makes the pancreas better able to produce insulin. 

Beta cells in the pancreas are responsible for producing and secreting insulin, the hormone that drives glucose out of the bloodstream and into the cells. Defective beta cells are what causes insulin secretion to become insufficient. Over time, with insufficient levels of insulin to blunt the blood sugar response, blood sugar levels become chronically elevated, leading to a diagnosis of diabetes melitus. 

The newly-discovered gene, CNOT3, plays a critical role in regulating blood sugar levels. The ability of beta cells to regulate blood sugar depends on several factors, including expression of genes that drive beta-cell maturation, insulin gene expression, insulin granule formation, and how well cells can transport molecules to other cells. CNOT3, the research suggests, is involved in all these mechanisms. 

To prove their point, the researchers used so-called “knockout mice,” which are genetically modified. Researchers inactivate a certain gene by replacing it or disrupting it with an artificial piece of DNA. The researchers noticed that diabetic mice had significantly lower levels of CNOT3 in their beta cells in comparison to non-diabetic mice. Then, the researchers took the normal mice and knocked out their CNOT3 genes.

At first, the researchers didn’t notice any difference. But after two months, insulin resistance had increased, making the mice require more insulin to regulate blood sugar. And by the end of the 12th week, the knockout mice had developed diabetes. 

For those that have inadequate CNOT3 gene expression, other genes may turn on that otherwise normally wouldn’t. More troubling, according to, diseases associated with CNOT3 also include: Intellectual Developmental Disorders, including speech delay, autism and dysmorphic facies. CNOT3 abnormalities can also lead to Precursor T-Cell Acute Lymphoblastic Leukemia, an aggressive blood cancer.

Hopefully, with this discovery targeted gene therapy or medications can improve beta cell performance.

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