CRISPR/Cas9 Editing of HAT Enzyme Gene in Pancreatic Beta Cells Reduces Cell Death & Increases Insulin Secretion

With the help of the CRISPR/Cas9 gene scissors, researchers at the Lund University Diabetes Centre in Sweden have managed to "turn off" an enzyme that proved to play a key role in the regulation of a diabetes-associated gene. The results are decreased cell death and increased insulin production in the genetically modified pancreatic beta cells. In the study, researchers conducted an investigation on a group of enzymes, histone acetyltransferases (HATs), that play a crucial role in the regulation of the TXNIP gene that, in cases of high blood sugar levels, leads to beta cell death and reduced insulin production. The researchers compared donated insulin -producing pancreatic islets from type 2 diabetes patients with those from healthy people and discovered that the gene activity of HAT enzymes is twice times higher in diabetic cells than in the healthy cells. Following this discovery, the goal was to remove the genetic function of the enzyme to study its effect on diabetes. And this effort proved to be successful. Using CRISPR/Cas9, the researchers were able to remove a sequence in the genetic code that controls the function of the HAT enzyme in insulin-producing cells from rats. This resulted in reduced TXNIP gene activity, and thereby reduced cell death and increased insulin production. "Our research shows that HAT enzymes play a key role in the regulation of TXNIP gene and that by targeting at this mechanism, we improved insulin secretion and prevent cell death,” says researcher Dr. Yang De Marinis who led the study. She adds: "CRISPR/Cas9 is one of the most important discoveries in molecular genetics made in recent years, and we are very happy to have managed to establish this cutting-edge technology in our research team. It opens up new possibilities to study the function of an endless number of genes related to diabetes.
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