COVID-19 and Diabetes: What You Need to Know
The rise in diabetes cases during the pandemic has been a subject of concern, but new research shows that the COVID-19 virus may be associated with the disease.
In their article published in the New England Journal of Medicine, coauthors Rüdiger Groß and Alexander Kleger discuss three areas of interest:
- Clinical and epidemiological evidence,
- SARS-Cov-2 infect pancreatic B cells, and
- SARS-CoV-2 triggers diabetes through mechanisms beyond the pancreas.
1) Clinical and epidemiological evidence
Diabetes mellitus (DM) type -1 and type -2 have spiked following a peak of Sars-Cov-2 numbers. Scottish and German registries, in particular, have found increased Type 1 DM cases in children. Nevertheless, studies in Canada have not corroborated this. The pandemic-associated delay could have resulted in this effect. Data supporting DM-type 2 induction, however, is more robust.
There is an increased risk of new-onset diabetes up to 12 months after infection. In one study, glucose control improved in 63–79% of patients 6 months after recovery. In another study, glucose control improved in 41–79% of patients 10 months after recovery.
2. Sars- Cov-2 infects pancreatic Beta cells
Sars-Cov-2 has a genuine capacity to infect the crucial Beta cells of the pancreas and make them less functional.
In a healthy pancreatic B cell, many insulin granules are ready to be released in response to glucose concentration outside the cells. Once the glucose around the cell increases, the granules are discharged to lower glucose concentration.
The ACE-2 and TMPRSS-2, which enable viral entry, are said to have increased expression in Beta-cells. Besides these, ACE-2 potentiating factor Neurolipin -1 expression also ensures an additional entry mechanism into B cells.
Once the virus infects the Beta- cells, they can lose their endocrine nature (hormonal character). The virus is said to interfere with the transcription of genes responsible for insulin synthesis, production, and release (the whole events). Degranulation is also said to occur.
It will also be intriguing to look into what the primate studies indicate. Such studies showed a typical DM phenotype + B cells atrophy+lower granularity. Not all animals had hyperglycemia — only 50% displayed this. This is similar to humans; only a few develop it, most likely due to individual vulnerability.
Once hyperglycemia has evolved, less insulin is available to reduce it. It induces a vicious cycle of hyperglycemia.
This direct evidence offers a sound basis for how Covid-19 triggers DM.
3. Mechanisms beyond the pancreas
Infection of beta cells is not significant, and humans have a high insulin reserve. The virus also shows tropism (affinity) to adipose (fat) and hepatic tissues. This means hyperglycemia could potentially emerge from outside the pancreas.
In postmortem studies, Sars-Cov-2 proteins were found in the fatty tissue of 56% of those who died from covid.
Following infection, fat cells secrete less adiponectin (than usual). As adiponectin has an insulin-sensitizing effect, its reduction triggers generalized insulin resistance.
This seems to be the primary mechanism in obese individuals who develop hyperglycemia following covid. Intriguingly only males display this mechanism.
Another mechanism of increased glucose levels is — the infection of hepatic tissues. The hepatocytes secrete GP73 following infection, which promotes gluconeogenesis (conversion of non-carbohydrate substrates into glucose).
Adiponectin and GP73 form the two mechanistic explanations for how glucose levels increase after infection of non-pancreatic tissues.
Final thoughts
How can we block the Diabetogenic (diabetes-causing) effect of Sars-Cov-2? The researcher’s job is to find out. In the meantime, we can still take charge of other diabetes contributors. Simple decisions, like choosing the type of food, the amount of food, reducing junk food, and increasing physical activity, can go a long way.
It is in times like these we should make sure we act wisely!
