Along with the pneumonia, blood clots, and other serious health concerns caused by SARS-CoV-2, the COVID-19 virus, some studies have also identified another troubling connection. Some people can develop diabetes after an acute COVID-19 infection.
Pre-proofs in the journal Cell Metabolism help to answer this important question, confirming that SARS-CoV-2 can target and impair the body’s insulin-producing cells.
Type 1 diabetes occurs when beta cells in the pancreas don’t secrete enough insulin to allow the body to metabolize food optimally after a meal. As a result of this insulin insufficiency, blood glucose levels go up, the hallmark of diabetes.
Earlier lab studies had suggested that SARS-CoV-2 can infect human beta cells. They also showed that this dangerous virus can replicate in these insulin-producing beta cells, to make more copies of it and spread to other cells.
NIH (National Institute Of Health) studies confirmed infection of pancreatic beta cells in autopsy samples from people who died of COVID-19. Additional studies suggest that the coronavirus may preferentially infect the insulin-producing beta cells.
This also makes biological sense. Beta cells and other cell types in the pancreas express the ACE2 receptor protein, the TMPRSS2 enzyme protein, and neuropilin 1 (NRP1), all of which SARS-CoV-2 depends upon to enter and infect human cells. Indeed, Research teams saw signs of the coronavirus in both insulin-producing beta cells and several other pancreatic cell types in the studies of autopsied pancreatic tissue.
The new findings also show that the coronavirus infection changes the function of islets—the pancreatic tissue that contains beta cells. In addition, research reports evidence that infection with SARS-CoV-2 leads to reduced production and release of insulin from pancreatic islet tissue. The infection leads directly to the death of some of those all-important beta cell.
In addition to the loss of beta cells, the infection also appears to change the fate of the surviving cells following SARS-CoV-2 infection. These studies showed that beta cells go through a process of transdifferentiation, in which they appeared to get reprogrammed.
In this process, the cells begin producing less insulin and more glucagon, a hormone that encourages glycogen in the liver to be broken down into glucose. They also began producing higher levels of a digestive enzyme trypsin. Importantly, they also showed that this transdifferentiation process could be reversed by a chemical (called trans-ISRIB) known to reduce an important cellular response to stress.
The consequences of this transdifferentiation of beta cells aren’t yet clear, but would be predicted to worsen insulin deficiency and raise blood glucose levels. More study is needed to understand how SARS-CoV-2 reaches the pancreas and what role the immune system might play in the resulting damage.
All that as explained above is what causes Diabetes.
This work provides yet another reminder of the importance of protecting yourself, your family members, and your community from COVID-19 by getting vaccinated if you haven’t already—and encouraging your loved ones to do the same.
Dr. Ian Kansiime Focus Medical Centre-Ntinda, Kisaasi Road