A recent Um-Madison study reveals that if a gene from insulin-producing cells is removed mice do not develop Type-1 diabetes. This gene induces the autoimmune responses on the body cells so by removing the gene body cells are protected from the attack of their own immune system.
The study suggests the ways to prevent the individuals from Type-1 diabetes who are at high risk, Also, it protects the body from other diseases in which the body cells are targeted by the body’s own immune system.
The study is published today in journal Cell Metabolism. No insulin hormone is produced in the Type-1 diabetic patients. This type of diabetes also called Juvenile diabetes. Insulin is a hormone released from the beta cells of pancreases which converts the blood sugar into energy that is required to maintain different cellular or life activities.
During the early stages of the disease, the solider like cells of the immune system called T-cells detect the insulin-producing beta cell as a foreign agent and kill them. Hence it leads to a complete deficiency of insulin in the body.
There is no proper cure available for the disease, but several medications are present in the market to slow down its progression. The disease in the patients can be managed through proper diet, by measuring the blood sugar level at regular intervals and through giving insulin shots. 20 million people across the whole world are having type-1 diabetes. This disease further leads to neuropathy, retinopathy, and high blood pressure. Diabetics patients have a poor quality of life and from the last decade, life expectancy is reduced in the United States.
Feyza Engin who is a lead author of the study and a biomolecular chemistry professor at the University of Wisconsin-Madison said that the individuals at high risk can be screened because the blood serum of these patients contain autoantibodies and hence through detecting the level of autoantibodies, the doctors can easily detect the person who will be going to develop Type-1 diabetes in near future.
During the experimental studies in the lab, Engin altered the genetic makeup of mice to intentionally develop Type-1 diabetes. Before the immune system starts to kill their own body cells, scientists removed a gene named IRE1-alpha from the beta-cell.
Engin expected that removal of this gene in insulin-producing cells would lead to accelerated diabetes. But the gene removal made a striking and unexpected difference in the mice.
Engine believed that if this gene is removed then insulin is not produced, and it accelerated the process of diabetes in mice. But the results were found totally opposite and striking. He added that researchers expected that by removing this gene, beta cells would not able to survive but they observed that the sugar level of blood first increases for a couple of weeks and then becomes normal. This is totally unexpected and unbelievable.
The beta cells were producing the normal insulin level just like the healthy beta cells, but before becoming the normal insulin producer they took a step back into immaturity.
If the gene is removed from the beta cells, they look like to undergo a disguise. After the gene, removal cells lose their maturity and they de-differentiate again into immature cells that exhibit the features of antecedent cells. Hence these cells express all other hormones including insulin.
He further explained that when the beta cells undergo de-differentiation then they don’t act like normal beta cells as they lessen the expression of many genes which activates the autoimmune response and signals the T- cells to come and kill them. These signals get reduced and hence T-cells do not sense the beta cells as a foreign or problematic agent in the body, so they don’t kill them.
After de-differentiation, the immature beta cells again differentiate into mature and functional beta cells.
National Institute of Health and the Juvenile Diabetes Research foundation support the Engin’s lab for this research.
This research has discovered a very vital point that “the de-differentiation greatly lessens the diabetogenic activity of immune cells.” Through determining the cells that are targeted by the autoimmune response it becomes easy to induce changes in these cells and make them less mature, less functional at the start of the process. This may reduce the progression of other diseases that are related to an autoimmune disorder.