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Insulin is a hormone that keeps the blood glucose level in check.

PHOTOGRAPH BY KLAUS OHLENSCHLAEGER, ALAMY STOCK PHOTO

SCIENCE C O R O N AV I R U S C O V E R A G E

Can COVID-19 lead to diabetes?

Here’s what you need to know
New studies show that the COVID-19 virus can attack the pancreas,
destroy cells that make insulin, and cause some cases of diabetes.

B Y B I L L S U L L I VA N

PUBLISHED JUNE 11, 2021 • 8 MIN READ

During the spring of 2020, physicians in New York City, the U.S. epicenter
of the pandemic at the time, noticed a considerable number of people
hospitalized with COVID-19 had too much sugar in their blood, a condition
called hyperglycemia that is 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 at Weill Cornell
Medicine. More surprising, says Chen, was that some patients who did not
have diabetes prior to the infection, developed new-onset diabetes after
recovering from COVID-19.

The COVID-19 virus, SARS-CoV-2, is best known for wreaking havoc in the
lungs and causing acute respiratory distress. But how and why a COVID-19
patient would suddenly develop a chronic disease like diabetes is a
mystery, as is the number of people who must then deal with this
complication.

A global 2020 analysis led by population health researcher

Thirunavukkarasu Sathish at McMaster University in Canada found that
nearly 15 percent of severe COVID-19 patients also developed diabetes.
But, he admits, “this figure is likely to be higher among high-risk
individuals, prediabetes for example.”Research led 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 at the Stanford University School of Medicine,

estimates “as many as 30 percent of patients with severe COVID-19 may
develop diabetes.”

Intrigued by the startling connection between COVID-19 and diabetes,

Chen and Jackson both launched independent investigations to uncover
how SARS-CoV-2 might trigger hyperglycemia. Both groups published
their results in the May issue of Cell Metabolism.

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“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, who
was not involved with either study.

The pancreas is another target of the COVID-19 virus

SARS-CoV-2 affects people in very different ways. Many people experience
only minor symptoms, but others develop severe, life-threatening disease.
As the pandemic unfolded it became apparent that this virus could spread
beyond the lungs and damage other critical organs, including the liver,
heart, and kidneys. It also became clear that diabetes and obesity were
common risk factors for severe COVID-19.

In an earlier study, Chen’s group grew various types of tissues in the lab
and tested which ones were vulnerable 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 lies behind the
stomach, is a complex organ composed of numerous types of cells that
assist with digestion. It also contains beta cells that make insulin, the
hormone that escorts sugar molecules from the blood into the body’s cells
where it is used for energy.

But just because a virus can infect cells grown in a dish in the lab doesn’t
mean it attacks the body in the same way. To ensure the laboratory
observations were a true reflection of what happens in living humans, both
the Chen and Jackson teams acquired autopsy samples from patients who
succumbed to COVID-19. Both groups detected SARS-CoV-2 in pancreatic
beta cells from these deceased patients.

But how, exactly, does a respiratory virus move from the lungs to the
pancreas? After patients experience pneumonia, the infection of the lower
lung may cause tissue damage that allows the virus to leak from lung
alveoli and into the blood vessels, explains Jackson. “Once in circulation,
the virus can enter other highly vascularized tissues like the pancreas,
brain, and kidney.” Others have speculated that the virus could get into the
bloodstream by leaking out of the gut, which may occur in patients lacking
healthy intestinal bacteria. (Microbes in your gut may be new recruits in
the fight against viruses)

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How the virus shuts down insulin production

Both research teams noted that beta cells infected with SARS-CoV-2 stop

5
making insulin. In Jackson’s study, the infected beta cells died via
apoptosis, a genetically-programmed autodestruct sequence initiated by
injured cells.
]
Chen’s group found that infected beta cells underwent a process called
transdifferentiation, which means they converted into another type of cell;
one that no longer manufactures insulin. It is possible that some infected
beta cells undergo transdifferentiation while others self-destruct.

In both cases, the end result is the same: when the COVID-19 virus attacks
the pancreatic beta cells, insulin production decreases.

This can lead to type 1 diabetes, which is usually caused by genetic risk
factors that spur an autoimmune reaction that attacks and destroys beta
cells. Type 1 diabetes is more commonly seen early in life and requires
patients to inject insulin every day since their body no longer makes the
hormone. Type 1 diabetes also involves an environmental trigger, such as
an infection, to initiate the autoimmune reaction.

In contrast, the far more common type 2 diabetes occurs when the body
becomes resistant to the insulin it makes. Type 2 diabetes can be managed
with changes in diet and exercise, although sometimes medications that
enhance insulin sensitivity are needed. Collectively, 34.2 million
Americans have diabetes according to a 2020 report issued by the Centers
for Disease Control.

The fate of the infected beta cells is important to study further as there
may be a way to prevent their destruction in patients with severe COVID-
19. Chen’s team surveyed a large panel of chemicals in hopes of finding one
that could prevent the transdifferentiation process.

Possible therapies
The survey identified a compound called trans-ISRIB that helped beta cells
maintain their identity and their ability to produce insulin when infected
with SARS-CoV-2. Trans-ISRIB, which stands for Integrated Stress
Response InhiBitor, is a compound discovered in 2013 that is able to
prevent a cell’s normal response to stress. Such compounds are being
explored as potential therapeutics to prevent widespread apoptosis and
damage.

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Chen cautions, “Trans-ISRIB is not an FDA-approved drug, so it cannot be

used in patients yet. But our studies support the idea that a new drug could
be developed to prevent COVID-19 from causing diabetes.” Jackson’s
=
group found that a cellular protein receptor called neuropilin-1 was critical
for SARS-CoV-2 to invade beta cells; blocking this receptor keeps them
from being infected.
There is also great interest among the broader research community to
develop drugs that stop cells from destroying themselves by apoptosis.
Experimental compounds called caspase inhibitors, which prevent cell
suicide, are being studied by others as potential therapies to ameliorate or
prevent severe COVID-19. Unfortunately, caspase inhibitors have not
proved a complete success in the clinic despite great promise and interest.
Nonetheless, “they might work for short term exposure to limit viral
damage,” Jackson says.

Chen adds that SARS-CoV-2 is not the only virus that threatens the
pancreas. “Coxsackievirus B, rotavirus, mumps virus, and cytomegalovirus
have been shown to infect and damage beta cells. Whether they are a direct
cause of type 1 diabetes has been controversial.” More research is needed
to determine if it is possible to neutralize the viral attacks on the pancreas,
either by blocking infection or preventing the virus from reaching the
organ in the first place.

Kalyani stresses that these studies “further underscore the importance of

getting vaccinated for COVID-19. Individuals who contract COVID-19,
particularly those with prediabetes or other risk factors for diabetes,
should let their health care providers know if they develop symptoms of
hyperglycemia such as frequent urination, excessive thirst, blurry vision,
or unexplained weight loss."

These new findings emphasize that there is much to learn about COVID-19
and its aftereffects. It seems clear that for some unlucky people, defeating
the virus is only the beginning. Additional complications may arise
depending on which systems in the body have been damaged in the wake
of the viral infection.

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