key: cord-0900829-xu0z9pys
authors: Mukherjee, Sandip; Banerjee, Oly; Singh, Siddhartha; Maji, Bithin Kumar
title: COVID 19 could trigger global diabetes burden – A hypothesis
date: 2020-06-26
journal: Diabetes Metab Syndr
DOI: 10.1016/j.dsx.2020.06.049
sha: 720ce5308385061098d2e3e110a7c151e62ad62e
doc_id: 900829
cord_uid: xu0z9pys

nan

whether SARS-CoV-2 can enter the pancreatic islet cells. In this context, earlier studies presented evidence in favor of the entry of SARS-CoV into pancreas of infected patients [1, 5] though the comorbidities like diabetes mellitus or hypertension in these SARS infected patients were not elucidated.

Considering the structural and syndromic resemblance between SARS-CoV-2 and SARS-CoV, it is worthy to use previous knowledge of SARS-CoV infection during 2002e2003. A follow up study on SARS-CoV survivors has suggested that SARS-CoV may damage pancreatic islets and cause acute insulin dependent diabetes mellitus [1] . Further, glucose metabolic disorders including hyperglycemia, hyperinsulinemia, insulin resistance and type I or II diabetes were also reported in a large proportion of the recovered SARS patients [6] . Disturbed lipid metabolism and its associated disorders like hyperlipidemia, abnormal glucose metabolism, and cardiovascular abnormality were also reported in SARS survivors even after twelve years of infection [6] .

Moreover, accumulating evidence suggest that perturbation in intracellular signaling cascades due to metabolic dysfunction is severely affected by SARS infection [7] . For instance, infection with both viral and bacterial pathogens is known to modulate ceramide (a shpingolipid) which antagonizes insulin signaling and abrogates glucose homeostasis. More importantly, it is evident from extensive clinical dataset that both acute and chronic infection favors insulin resistance and hence a risk factor for individuals with pre-diabetes to develop type II diabetes mellitus [7] . Although epidemiological studies showcased the impact of acute or chronic infection on development of type II diabetes mellitus so far, but these molecular evidences are indicative of strong causal relationship between infection and diabetes development. Further, Ghosal et al. (2020) very recently reported that weight gain during 49 days lockdown due to COVID-19 pandemic in India may increase the risk of development of type 2 diabetes mellitus [8] .

Cytokines play pivotal role in every facet of inflammation, immunity and development of diabetes mellitus. Thus, mild or severe cytokine storms (interferons, interleukins, chemokines, colonystimulating factors and tumor necrosis factor) and virally driven hyperinflammation in COVID-19 patients [9] could be potential players directing negative impacts on the pancreatic islet cells in recovered COVID-19 patients. Also, these cytokines might have indirect effect on pancreatic islets secondary to severe lung infection in COVID-19 patients. Diabetes mellitus is one of the most important extrapulmonary comorbidities in individuals with chronic obstructive pulmonary disease, asthma, and interstitial lung diseases [10] . Thus, we presume that initial damages in lungs resulting from COVID-19 might have direct or indirect impact to cause metabolic dysfunction and diabetes mellitus in particular.

Taken together, it is noteworthy to speculate that SARS-CoV-2 might enter islets, and cause acute b-cell dysfunction followed by hyperglycemia and transient type II diabetes mellitus. Taken together, we anticipate that SARS-CoV-2 pandemic has touched off the need for follow up study to delineate the possible development of another stealthy public health crisis -diabetes mellitus in COVID-19 survivors.

Author contribution statement SM and BKM drafted the manuscript; OB and SS did literature survey. All authors were involved in manuscript editing and approved the version submitted for publication.

All authors declare no conflict of interest.

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