Diabetes: new player
Protein Found to Play a Big Role in Diabetes
Tatiana Matveeva, "Scientific Russia"
According to a new study by Japanese scientists, a key role in regulating glucose levels is played by a protein called CNOT3. It silences a set of genes that would otherwise cause disruption of insulin-producing cells, which is associated with the development of diabetes, the press service of the Institute of Science and Technology at the University of Okinawa reports. The results of the study are published in the journal Communications Biology (Mostafa et al., Loss of β-cell identity and diabetic phenotype in mice caused by disruption of CNOT3-dependent mRNA deadenylation).
Diabetes is a common disease in which the level of glucose in the blood is greatly increased. If left untreated, diabetes can lead to serious health problems such as kidney failure, heart disease and vision loss. This disorder occurs when there is not enough insulin in the body or when insulin-induced reactions are weakened. Insulin usually passes glucose into cells to release energy, so without it, glucose accumulates in the blood. Lack of insulin often occurs due to the fact that the beta cells of the pancreas, which normally secrete insulin, cease to function properly.
In the new work, scientists have found that the normal functioning of beta cells is supported by the CNOT3 protein. CNOT3 is a jack of all trades. It is expressed by many organs throughout the body, and it regulates different genes in different tissues. But its activity has a common basis – it helps to keep cells alive, healthy, and helps them function without failures.
The researchers studied the function of this protein in the islets of Langerhans of the pancreatic tissue of mice. Beta cells are located in these formations, which make up from one to two percent of the pancreatic tissue. First, they found out whether the expression of CNOT3 in mice with diabetes differs from mice without diabetes. By studying islet cells, scientists have found that diabetic mice have much less CNOT3 in the "islets" than healthy mice.
Further, the authors of the work blocked its production in beta cells of healthy mice. For four weeks, the animals' metabolism functioned normally, but by the eighth week, they developed glucose intolerance, and by the 12th week, diabetes.
The researchers found that without CNOT3, some genes that are normally disabled in beta cells turn on and start producing proteins. Under normal conditions, these genes are silenced, because otherwise they cause all sorts of problems for beta cells, for example, they do not allow them to produce insulin in response to glucose.
In addition, scientists have discovered a link between CNOT3 and the informational RNA of genes that are usually turned off. Informational RNA (mRNA) is a single-stranded molecule that corresponds to the genetic sequence of a gene and is necessary for protein synthesis.
Under normal conditions, the mRNA of these genes is practically not expressed. But once CNOT3 was removed, the researchers found that the mRNA became much more stable. In fact, the protein was produced from stabilized mRNA, which has an adverse effect on normal tissue function. This suggests that at least one way to turn off these genes is to destabilize their CNOT3–driven mRNA.
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