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How Diabetes Is Emerging In Patients With COVID-19

COVID-19 has a plethora of underlying effects. However, researchers may have just identified the most dangerous long-term impact.

3D medical animation still of Type One Diabetes

While researchers have been studying COVID-19 for the past two years, pharmacy technician Nola Sullivan of Kellogg, Idaho, has uncovered the virus’s extending underlying conditions. Sullivan faced an additional struggle as a result of being infected with COVID-19 last year, despite the virus’s long-term effects, which included a loss of taste and smell, nausea, and diarrhea. Many COVID-19 patients too are grappling with an additional struggle: the onset of diabetes. In a research involving nearly 3,800 patients infected with the virus, cardiologist James Lo and colleagues discovered that just under half of the patients acquired elevated blood sugar levels that were not previously present. How is it conceivable for COVID-19 patients to develop diabetes? Many researchers have been tackling this exact issue for a long time.

WHO EN Be SAFE from CORONAVIRUS COVID-19 9Mar2020COVID-19 biểu trưng

When a patient develops diabetes, he or she must learn to control the illness and live an active life due to an insulin shortage. Because diabetes is incurable, the prospect that it is a long-term side effect of COVID-19 is very troubling. Insulin is essential in the human body because it lowers triglycerides by boosting lipoprotein lipase activity, which degrades triglycerides into glycerol and fatty acids. A lack of pancreatic B-cells, which release proper quantities of insulin, has a direct impact on mitochondria and the glycolysis process which is utilized for energy synthesis by all cells in the human body, eventually prompting the pyruvate product to join the Krebs cycle for ongoing energy production. Both processes are required for continual energy generation. Glucose is broken down into pyruvate and energy during glycolysis. The process can take place in the absence of oxygen, making it anaerobic. Insulin promotes glycolysis by raising the rate of glucose transport across the cell membrane and the rate of glycolysis by boosting the activities of hexokinase and 6-phosphofructokinase.

Glycolysis metabolic pathway 3

Nonetheless, people with COVID-19 have experienced sugar surges. The elevated blood sugar levels were new after infection for the majority of the patients, suggesting that many of them had not been diagnosed with diabetes prior to contracting the virus. According to Lo and other experts, the mechanism by which COVID-19 causes diabetes is currently being investigated. Patients with ARDS caused by COVID-19 and a high blood sugar level were in the hospital three times longer than those with normal blood sugar levels. While the exact cause of diabetes is unknown, researchers have discovered evidence that the coronavirus attacks pancreatic B-cells, which produce insulin. This does not yet address the question because patients who received COVID-19 continued to generate significant amounts of C-peptide, indicating that pancreatic cells were still generating insulin. Despite this, their blood sugar levels remained elevated, suggesting that something else was at fault. The virus-infected fat cells must be stimulating other cells in a detrimental way, resulting in diabetes. As a result, Lo and colleagues observed that individuals with COVID-19 had low amounts of adiponectin, a hormone generated by fat cells that helps other cells respond to insulin’s urge to take up sugar. COVID-19 can clearly infect fat cells. The virus may also cause replication in human fat, which provides another indication as to how fat is implicated in the virus and, as a result, diabetes. While obesity has a significant impact on the onset of diabetes as a result of the virus, this is not always the case. The miscommunication of fat cells is to blame. 

How may fat cell miscommunication be controlled, and who is directly affected? This is the next question that has to be addressed in order to develop a deep understanding of the long term effects of the virus.

An Antidepressant Is The Next “Weapon” Against COVID-19

Is the COVID-19 vaccine the only way to lower death rates and hospitalization rates? While more individuals are becoming vaccinated against COVID-19, researchers have looked at how a low-cost antidepressant prescription could potentially tackle the virus. Fluvoxamine (Luvox), an antidepressant medication, has the capacity to reduce hospitalization and morality rates after patients receive COVID-19 within a few days. Although fluvoxamine is licensed by the FDA for the treatment of obsessive-compulsive disorder (OCD) and other disorders such as depression, it is not approved for the treatment of COVID-19. In a study, conducted in Brazil, 1,500 newly diagnosed COVID-19 patients were assessed. 741 of the participants received a 100 mg pill of fluvoxamine twice a day for 10 days and the remaining 756 participants received a placebo twice a day. 16 percent of those who took the placebo twice a day got ill enough to necessitate a lengthy hospital stay compared to 11 percent of those who took fluvoxamine. Researchers discovered that participants who took at least 80% of the fluvoxamine administered to them had a two-thirds lower chance of hospitalization! Furthermore, there was only one fatality among individuals that took fluvoxamine, compared to 12 fatalities in the placebo group. According to The Lancet Global Health, this research has shown that the drug has reduced morality rates by roughly 91 percent. The antidepressant drug can be easily prescribed by doctors for COVID-19 using their clinical judgement.


When the COVID-19 virus enters the body through the eyes, nose, or mouth and travels to the lungs, the immune system strives to protect itself from the invading pathogens by producing antibodies that, on occasion, eliminate invading infections. If the invading pathogen is unfamiliar to the body, B-memory cells will be unable to detect it, and B-plasma cells (antibody secreting cells) will be unable to manufacture antibodies, allowing the virus to enter the cell and flourish in the body.


Fluvoxamine is a 2-aminoethyl oxime ether of aralkylketones. The antidepressant medication, if taken promptly after receiving COVID-19, may be an additional method of minimizing viral transmission and accompanying medical concerns. Fluvoxamine is easy to get and inexpensive to manufacture, particularly as a generic drug. COVID-19 treatments, in general, serve as both a cure for severe sickness and a treatment for the beginning of illness. Fluvoxamine, as an SSRI (selective serotonin reuptake inhibitor), attaches to a cell’s receptor that governs cellular stress response and the generation of cytokines, proteins that alert the body of a problem and lead to extreme inflammation. Nevertheless, fluvoxamine has been shown to minimize inflammation. When people get COVID-19, it’s theorized that the damaged cells produce a slew of cytokines that generate inflammation in the lungs, making it difficult to breathe. Patients would be able to breathe better and require fewer hospitalizations if fluvoxamine was taken to help decrease inflammation.


Who knew that an antidepressant that inhibits the serotonin reuptake pump at the presynaptic neuronal membrane might reduce inflammation and allow you to breathe? Because fluvoxamine works by boosting serotonin levels between nerve cells in the brain, it is impressive that the medicine might be used for purposes other than treating depression or OCD. The lingering question is whether someone with COVID-19 who has been taking these antidepressants for a previous disorder has an edge.

The Potential End To COVID-19: How An Antiviral Pill Could Decrease Death Rates

When will the world return back to normal? In recent years, people have questioned the longevity of the COVID-19 outbreak. While concentrating on vaccine delivery and vaccination capabilities, a pill has been developed in the hopes of preventing future COVID variations. Hopefully, the pill will eventually be administered to patients; this would make it the first oral treatment for the virus.

A current study on molnupiravir, an antiviral pill, has published data demonstrating that the medicine has the ability to lower hospitalization and fatality rates as a result of COVID-19. The study dealt with two groups of people. One group of 377 people were given a placebo, and the other group of 385 people were given molnupiravir to examine how the antiviral affected patients with COVID-19. The findings were substantial. Within 29 days of starting the trial, 14.1 percent of the group given the placebo were hospitalized. Fortunately, of the individuals who were given molnupiravir, only 7.3 percent of them were hospitalized.

Molnupiravir is a prodrug of N4-hydroxycytidine (NHC), a nucleoside analog (meaning that it contains a sugar and a nitrogenous base). Molnupiravir metabolism

Molnupiravir is similar to the genetic coding of the coronavirus’s RNA, as is remdesivir (a FDA-approved medication). By interfering with the polymerase enzyme, the “fake” basic elements impair the coronavirus’s RNA synthesis, preventing the virus from replicating. Despite the fact that the two medications serve the same goal, they serve different actions. Remdesivir penetrates a growing RNA strand, slowing and ultimately blocking the polymerase enzyme. Unlike the COVID-19 vaccine, the structure of molnupiravir gives it the ability to target the polymerase enzyme instead of the virus’s spike protein. Molnupiravir enters the cell and is transformed into RNA-like building components. The active medication binds to the genome of RNA viruses, setting off a chain of mutations; this process is known as viral error catastrophe. In simpler terms, it disrupts how the virus replicates RNA.

Molnupiravir could theoretically be administered as soon as a patient receives a positive COVID-19 test, thereby preventing floods of COVID-19 patients from overburdening medical systems while the highly infectious delta variant continues to spread. Although the side effects of the drug remain unknown, it has been reported that the side effects of COVID-19 are much worse than those of molnupiravir. The antiviral drug has the potential to save lives, but the primary concern is about the long-term repercussions. When contemplating molnupiravir, the fear of birth abnormalities or cancer comes into play because it is a mutagenic medication. In response, the drug’s creator, Merck, stated that there is no indication of the possibility for mutagenicity. Although the manufacturer is confident in the treatment and believes that the long-term consequences are insignificant, it is logical that parents might have concerns about molnupiravir.

Ultimately, if patients receive the vaccination that targets the spike protein and are also able to take molnupiravir, hospitalization and mortality rates may dramatically reduce.

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