New York Study Shows Almost 50 Percent Of COVID-19 Patients Will Develop Hyperglycemia As A Result Of SARS-CoV-2 Triggering Adipose Tissue Dysfunction!

COVID-19 Hypoglycemia: Researchers from Weill Cornell Medicine - New York City in a new study have found that the SARS-Cov-2 coronavirus is able to triggers adipose tissue dysfunction, driving insulin resistance and causing hyperglycemia in infected individuals. In the study involving more than 3,800 COVID-19 patients, almost 50% developed high blood sugar levels.


 
Should further studies also corroborate the same study findings, the implications are clear that the world will also be or is already facing a Diabetes crisis!

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It has been found that individuals infected with SARS-CoV-2 who also display hyperglycemia suffer from longer hospital stays, higher risk of developing acute respiratory distress syndrome (ARDS), and increased mortality.
 
However, to date, the pathophysiological mechanism of hyperglycemia in COVID-19 remains poorly characterized.
 
The COVID-19 Hypoglycemia study team in this new research showed that hyperglycemia is similarly prevalent among patients with ARDS independent of COVID-19 status. Yet among patients with ARDS and COVID-19, insulin resistance is the prevalent cause of hyperglycemia, independent of glucocorticoid treatment, which is unlike patients with ARDS but without COVID-19, where pancreatic beta cell failure predominates.
 
Importantly a screen of glucoregulatory hormones revealed lower levels of adiponectin in patients with COVID-19.
 
In further research involving hamsters infected with SARS-CoV-2, it was found a strong antiviral gene expression program in the adipose tissue and diminished expression of adiponectin.
 
The study findings show that SARS-CoV-2 can infect adipocytes. Together these data suggest that SARS-CoV-2 may trigger adipose tissue dysfunction to drive insulin resistance and adverse outcomes in acute COVID-19.
 
The study findings were published in the peer reviewed journal: Cell Metabolism.
 https://www.cell.com/cell-metabolism/fulltext/S1550-4131(21)00428-9
 
Alarmingly in the study involving more than 3,800 COVID-19 patients, almost 50 % developed high blood sugar levels especially many who were not previously diabetic.
 
The study also found that about 91 percent of the intubated COVID-19 patients had high blood sugar, as did almost 73 percent of people who died of the disease.
 
Thailand Medical News had since mid-2020, been reporting on the ability of S ARS-CoV-2 infections to trigger hyperglycemia and diabetes in otherwise previously healthy individuals with no prior diagnosis of diabetes or even pre-diabetes.
 
https://www.thailandmedical.news/news/breaking-medical-experts-warn-that-covid-19-could-trigger-diabetes-in-otherwise-healthy-individuals-who-never-had-the-condition-before-
 
https://www.thailandmedical.news/news/breaking-diabetes-and-covid-19-german-case-study--confirms-that-sars-cov-2-can-trigger-diabetes-in-young--adults-otherwise-healthy
 
https://www.thailandmedical.news/news/covid-19-news-doctors-worldwide-are-reporting-increases-of-new-onset-diabetes-cases-most-probably-triggered-by-covid-19
 
https://www.thailandmedical.news/news/breaking-covid-19-latest-study-shows-patients-not-previously-diagnosed-with-diabetes-exhibiting-hyperglycemia-and-increased-mortality
 
https://www.thailandmedical.news/news/study-warns-of-an-emerging-surge-in-diabetes-in-otherwise-healthy-individuals-as-a-result-of-covid-19
 
https://www.thailandmedical.news/news/scientists-at-odds-on-what-s-causing-diabetes-in-covid-19-patients-as-two-studies-show-that-ace-2-is-not-expressed-in-pancreatic-beta-cells
 
https://www.thailandmedical.news/news/breaking-covid-19-and-children-uk-researchers-warn-that-covid-19-could-be-linked-to-onset-of-type-one-diabetes-and-diabetic-ketoacidosis-in-children
 
https://www.thailandmedical.news/news/covid-19-research-cases-of-covid-19-patients-developing-diabetes-for-first-time-can-be-due-to-high-ace2-expression-in-pancreatic-islet-cells-during-in
 
The study team focused on identifying what was causing high blood sugar in COVID-19 patients and what to do about it.
 
Corresponding author, Dr James C. Lo from the Weill Center for Metabolic Health, Cardiovascular Research Institute, Division of Cardiology, Department of Medicine, Weill Cornell Medicine noticed that many of the COVID-19 patients in his hospital’s intensive care unit had high blood sugar. Preexisting diabetes is a risk factor for poor outcomes from COVID-19.
 
However, many of the patients Dr Lo and his colleagues were seeing did not have diabetes before they got ill. People sometimes develop diabetes as they age, but Lo’s patients with high blood sugar were often “youngish, in their 30s and 40s,” he says. And levels of glucose in their blood were incredibly high, sometimes more than twice the level that indicates diabetes.
 
The study team found that such sky-high levels of blood sugar were associated with a 15 times higher risk of intubation and 3.6 times higher risk of death compared with people with the disease who had normal blood sugar levels.”
 
Dr Utpal Pajvani, an endocrinologist from Columbia University Medical Center in New York City who was not involved in the study but was also seeing similar occurrences among her patients commented, “we don’t know if the high blood sugar is causal of the bad outcome or reflective of the bad outcome.”
 
However, he and other doctors aren’t totally surprised by the connection between COVID-19 and high blood sugar, or hyperglycemia and diabetes.
 
Typically, high blood sugar has also been documented in people with acute respiratory distress syndrome, or ARDS, caused by injuries or infections with other viruses or bacteria. ARDS is a condition in which the lungs can’t supply enough oxygen to the body.

The study team found that COVID-19 patients with ARDS and high blood sugar spent three times longer in the hospital than people with ARDS caused by COVID-19 who have normal blood sugar levels.
 
But strangely individuals with hyperglycemia who had ARDS caused by COVID-19 were less likely to die than hyperglycemic people with ARDS due to other causes.

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Dr Ralph DeFronzo, an endocrinologist and chief of the diabetes division at the University of Texas Health Science Center at San Antonio, who was not involved with the study added, “The outlook was still bad, just not as bad in the group with ARDS and COVID, which is surprising.”
 
To date, exactly what sends blood sugar soaring and causes diabetes in COVID-19 patients has been a mystery.
 
Past evidence has hinted at the coronavirus infecting cells in the pancreas that make insulin, a hormone that lowers blood sugar levels by signaling cells to take in sugar and burn it for fuel.
 
However, in Dr Lo’s study, it was found that COVID-19 patients with high blood sugar still made high levels of C-peptide, a naturally occurring bit of protein that links two chains of insulin and is made alongside insulin in pancreatic cells. High C-peptide levels indicate that the patients’ pancreatic cells were producing insulin.
 
It was found that these patients’ blood sugar was still high, though. So if the pancreatic cells weren’t the problem, something else must be going wrong.
 
According to the study team, that something else may be that fat cells infected with the SARS-CoV-2 coronavirus that sends the wrong message to other cells, ultimately leading to diabetes.
 
The study team discovered that COVID-19 patients had low levels of adiponectin, a hormone produced by fat cells that helps other cells heed insulin’s call to take in sugar.
 
Individuals with obesity also often make low levels of adiponectin, possibly explaining why they are at risk for poor outcomes from COVID-19. https://www.cdc.gov/mmwr/volumes/69/wr/mm6915e3.htm
 
The study team levels of several other hormones produced by fat cells were also disrupted.
 
The study findings suggest that COVID-19 patients’ high blood sugar levels result from insulin resistance ie a condition in which cells ignore insulin’s message to take in glucose brought on by a dearth of fat hormones rather than by an inability to produce insulin.
 
The SARS-CoV-2 coronavirus can infect fat cells, the study teams’ experiments with hamsters and with cells grown in lab dishes showed.
 
Damage done to fat cells directly by the SARS-CoV-2 virus, or indirectly by inflammation directed toward fighting the virus, may interfere with fat cells’ ability to make normal hormone levels and help maintain steady blood sugar levels.
 
Past studies have also indicated that SARS-CoV-2, the virus that causes COVID-19, can replicate in human fat, also known as adipose tissue. That’s yet another clue that fat is involved in severe disease.
 
In one study, autopsies revealed that the coronavirus had infected fat cells of 10 of 18 men who died of COVID-19. All 10 of the men with coronavirus in their fat were overweight or obese. The researchers also found SARS-CoV-2 in fats cells of 5 of 12 women who died of COVID-19, but those women were not all overweight or obese.
https://www.cell.com/cell-metabolism/fulltext/S1550-4131(21)00621-5
 
The German team of that autopsy study uncovered evidence that coronavirus infection also affects fat cells’ ability to metabolize some lipids, leading people with COVID-19 to develop high levels of triglycerides in their blood. That’s yet another clue that fat isn’t working properly in some COVID patients.  And these changes in fat may contribute to more severe COVID-19.
 
Often, obesity is associated with inflammation in fat and other tissues. Coronavirus infection may make that inflammation worse, tipping the scales toward messed-up hormone production and eventual diabetes.
 
Dr Lo’s study findings “lend credence to the idea that adipose is the reservoir for this low-grade inflammation that then gets triggered by COVID.”
 
Whether these SARS-CoV-2 coronavirus infections cause diabetes or simply unmask the condition in susceptible people, such as people who are overweight or obese, is not yet clear.
 
Some other scientists speculate that “a lot of these patients have an underlying state of insulin resistance, likely prediabetes, but then acute illness in the form of COVID-19 tips [them] over to diabetes.”
 
However, of significance, the study found that doctors may be able to counteract high blood sugar by giving COVID-19 patients drugs called thiazolidinediones or glitazones that make cells more sensitive to insulin’s action.
 
The study team highly recommends follow-up studies on COVID survivors and those with “long COVID” are needed to monitor for future insulin resistance (IR) and beta cell failure (BCF).
 
Already study data suggest that there may be persistent IR post-COVID-19. https://pubmed.ncbi.nlm.nih.gov/34035524/
 
It has already been seen that many COVID-19 patients who recovered from hyperglycemia prior to discharge subsequently develop diabetes.
 
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