COVID-19 and Diabetes: A not so sweet ever after

Illustrated by Neha Adari

The connection between diabetes and SARS-CoV-2 is not unidirectional. While diabetes mellitus aggravates the body’s response to SARS-CoV-2 (COVID-19), it appears the virus may also induce the development of diabetes. Hyperglycemia, or high blood sugar, is strongly associated with diabetes and has been observed in COVID-19 patients. Unexpectedly, this condition has arisen in patients who have not been diagnosed with any form of diabetes before SARS-CoV-2 infection. This has caused researchers to express their concern about a potential increase in diabetic patients after the COVID-19 pandemic. 

Hyperglycemia is induced by insulin resistance, which occurs when an individual’s body cannot take up glucose and use it for energy. This condition is frequently associated with beta-cell hyperstimulation and eventual exhaustion in which insulin secretion by the pancreas is abnormal and insufficient. After the establishment that COVID-19 patients have an increased risk of hyperglycemia, it has been speculated that the virus demonstrates the potential to reach and impact the function of these beta cells [6]. An Italian study observed inpatients with COVID-19 and suggested such a case after uncovering that approximately half of the patients experienced altered glycol metabolic control and abnormal cytokine levels in their serum [2]. They proposed that these responses exacerbate the immune response and cause excessive inflammation. This abnormal immune response then induces a disruption in insulin signaling and results in beta cell exhaustion in the pancreas. Eventually, there is a drastic reduction in insulin being secreted and used to take up glucose, leading to excess levels of sugar in the blood. Another study also established the possibility of SARS-CoV-2 directly inducing autoimmune-immune mediated B-cell destruction [6]. The researchers in this study selectively infected human beta cells in vitro and discovered that beta-cells express the receptor of SARS-CoV-2. Once the two players are interacting, apoptosis, or cell death, of beta cells is induced. Other studies have revealed similar findings and overall, researchers have expressed their suspicion that metabolic dysregulation results from COVID-19 due to dysfunctional beta cells [4]. 

Another study conducted in New York also confirmed the strong association between hyperglycemia and adverse outcomes in COVID-19 patients [3]. While this study discussed the possibility of a dysfunctional beta cell, it also offered another mechanism for insulin resistance in COVID-19 patients. The researchers concluded that such resistance occurs by direct infection of adipose, or fat tissues. In this study, the regulatory hormones of glucose were screened, in human patients and hamsters. The researchers suggested that the virus mediates a direct infection on adipose or fat tissues. In their study, the investigators observed a reduction in adiponectin, an inducer of glucose and fatty acid metabolism, after infection. Research has found that this protein plays a role in reducing glucose levels. Insufficient levels of it are often associated with increased glucose levels and the development of Type 2 diabetes. Ultimately, many researchers have proposed that SARS-CoV-2 can directly trigger adipose tissue dysfunction, leading to insulin resistance and hyperglycemia [5]. 

Not enough time has passed to thoroughly comprehend the capacity of SARS-CoV-2 in the human body today. More studies are necessary to understand how SARS-CoV-2 can directly impact the adipose tissues, the beta cells of the pancreas, or both. Currently, researchers have found that inhibiting the excessive expressions of inflammatory cell signalers, or cytokines, such as IL-6 and TNF, can have a protective effect in COVID-19 infection [2]. As stated earlier, excessive immune responses, such as increased inflammatory cytokines, can result from infection. As a result, treatments with tocilizumab (anti-IL-6) or other cytokine inhibitors, such as ones targeting TNF, can greatly alleviate these severe responses. A European study found that patients with immune-mediated inflammatory diseases, such as arthritis, experienced a reduction in symptoms of COVID-19 after treatment with these inhibitors [1]. Although there exist discrepancies in results, it seems that these treatments have the potential to moderate viral responses. With the increasing number of patients developing hyperglycemia and the uncertainties that lie in how SARS-CoV-2 will progress, one of the greatest concerns among physicians and investigators is the potential wave of diabetic patients at the end of this long COVID-19 pandemic. 

Edited by: Isa Lee
Illustrated by: Neha Adari



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