During the spring of 2020, doctors in New York City, the U.S. epicenter of the pandemic in the time, noticed a substantial number of individuals hospitalized with COVID-19 had too much sugar in their blood, a condition known as hyperglycemia that’s a signature feature of diabetes.
“[My colleagues and I] found it very challenging to control the blood glucose level of some COVID-19 patients, even those without a history of diabetes,” says stem cell biologist Shuibing Chen in Weill Cornell Medicine. More surprising,” says Chen, was that some patients who didn’t have diabetes before the infection, developed new-onset diabetes after recovering from COVID-19.
The COVID-19 virus, SARS-CoV-2, is famous for wreak havoc at the lungs and causing acute respiratory distress. But why and how a COVID-19 patient could suddenly develop a chronic disease like diabetes is a mystery, as is the number of people who need to then handle this complication.
A worldwide 2020 investigation directed by people health researcher Thirunavukkarasu Sathish in McMaster University in Canada found that nearly 15 percent of severe COVID-19 patients also developed diabetes. But, he acknowledges,”this figure is likely to be higher among high-risk individuals, prediabetes for example.” Research headed by endocrinologist Paolo Fiorina at Harvard Medical School and published in 2021 reported that of 551 patients hospitalized for COVID-19 in Italy, nearly half became hyperglycemic.
Peter Jackson, a biochemist in the Stanford University School of Medicine, quotes”as many as 30 percent of patients with severe COVID-19 may develop diabetes.”
Intrigued by the startling link between COVID-19 and diabetes, Chen and Jackson both started separate investigations to uncover how SARS-CoV-2 might trigger hyperglycemia. Both teams released their results in the May issue of Cell Metabolism.
“Their findings provide critical insights into the underlying mechanisms by which COVID-19 can lead to the development of new-onset diabetes in infected patients,” says Rita Kalyani, an associate professor of medicine at Johns Hopkins Division of Endocrinology, Diabetes, and Metabolism, that was not involved with either study.
The pancreas is another target of the COVID-19 virus
SARS-CoV-2 affects people in very different manners. A lot of men and women experience only minor symptoms, but others develop acute, life-threatening disease. As the pandemic unfolded it became apparent that this virus may spread beyond the lungs and damage other critical organs, for example, liver, heart, and kidneys. Additionally, it became evident that diabetes and obesity were frequent risk factors for severe COVID-19.
In a previous research , Chen’s group grew various types of tissues in the laboratory and tested which ones were exposed to the COVID-19 virus. “Very surprisingly, we found that beta cells of the pancreas are highly permissive to SARS-CoV-2 infection,” says Chen. The pancreas, which is located behind the stomach, is a intricate organ composed of numerous types of cells that help with digestion. It also contains beta cells which make insulin, the hormone that escorts sugar molecules in the blood into the body’s cells where it’s used for energy.
But simply because a virus can infect cells grown in a dish in the laboratory doesn’t mean it attacks the body in the same manner. To ensure the lab observations were a true reflection of what happens in living people, both the Chen and Jackson teams obtained autopsy samples from individuals who reacted to COVID-19. Both groups discovered SARS-CoV-2 in pancreatic beta cells from these types of dead patients.
But how, exactly, does one respiratory virus move from the lungs into the pancreas? After patients encounter pneumonia, the infection of the lower lung may cause tissue damage that makes it possible for the virus to leak from lung alveoli and to the blood vessels, explains Jackson. “Once in circulation, the virus can enter other highly vascularized tissues like the pancreas, brain, and kidney.” Others have theorized that the virus might get into the blood by leaking from the gut, which may occur in patients inducing healthy intestinal bacteria. (Microbes on your gut may be new recruits in the fight against viruses)
How the virus slows down insulin generation
Both research teams noted that beta cells infected with SARS-CoV-2 cease making insulin. In Jackson’s research, the infected beta cells died via apoptosis, a genetically-programmed autodestruct sequence initiated by cells that were infected.
Chen’s group found that infected beta cells failed a procedure called transdifferentiation, so they converted into another type of cell; one that no longer generates insulin. It’s possible that some infected beta cells undergo transdifferentiation while some self-destruct.
In both cases, the end result is exactly the same: if the COVID-19 virus strikes the pancreatic beta cells, insulin production decreases.
This may lead to type 1 diabetes, which is usually brought on by genetic risk factors that spur an autoimmune response that attacks and destroys cells. Type 1 diabetes is much more commonly seen early in life and requires individuals to