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Source: Diabetes and COVID-19  Jul 02, 2020  10 months ago
BREAKING! Diabetes And COVID-19: German Case Study Confirms That SARS-CoV-2 Can Trigger Diabetes In Young Adults Otherwise Healthy
BREAKING! Diabetes And COVID-19: German Case Study Confirms That SARS-CoV-2 Can Trigger Diabetes In Young Adults Otherwise Healthy
Source: Diabetes and COVID-19  Jul 02, 2020  10 months ago
Diabetes And COVID-19: A case study by German researchers from University of Kiel have confirmed that the Sars-CoV-2 coronavirus can trigger diabetes and insulin dependency in young adults who have otherwise been healthy with any prior history of sickness or diabetes. It is assumed that the diabetes is triggered by the SARS-CoV-2 coronavirus attacking the pancreas thru the ACE-2 receptors present there, hence destroying the functionality of the organ in certain aspects.

The case study is presented on the preprint server: researchsquare.
Thailand Medical News had already reported on this phenomena earlier in June but this represents the first clinically detailed documented case.
The researchers reported the manifestation of insulin dependent diabetes after a COVID-19 infection in the absence of typical autoantibodies for type 1 diabetes.
The patient, a 19-year-old Caucasian male subject presented to the University of Kiel’s hospital at the emergency department with diabetic ketoacidosis (DKA). C-peptide levels accounted to 0.62µg/L in the presence of blood glucose concentrations of 30.6 mmol/L (552 mg/dL). The patient´s case history revealed a COVID-19 disease 6-8 weeks prior to admission.
This is of interest, since COVID-19 internalization into host cells is mediated via Angiotensin-converting enzyme 2 (ACE2), a transmembrane glycoprotein which amongst others is crucial for β-cell homeostasis and function.
Detailed laboratory testing was performed, revealing no serum-antibodies against islet-cells (ICA), glutamic acid decarboxylase (GAD65-AA), tyrosine phosphatase (IA-2-AA), insulin (IAA) and zinc-transport-8 (ZnT8-AA), but against COVID-19.
This is a presentation of an insulin-dependent diabetes mellitus in the absence of markers of autoimmunity, which might suggest direct cytolytic effects of COVID-19 on pancreatic β-cells presumably mediated via ACE2.
ACE2 is widely expressed in eukaryotic cells membranes including those of pancreatic β-cells.
The hallmark in the pathology of classical type 1 diabetes is the β-cell destruction caused by a complex autoimmune process.
Environmental factors are suspected to be responsible, i.e. activating the immune system by reduction in gut microbiota, by early introduction to fruit or cow milk during childhood, by gluten, by toxins and especially by viruses. Interestingly, besides inducing autoimmunity, some viruses like Enteroviruses might also exert direct cytolyti c effects on pancreatic β-cell.
The young male patient reported here presented several weeks after a viral infection with a severe DKA with a profound loss of β-cell function. However, in contrast to the general idea that viral infections indirectly affect pancreatic β-cells by triggering autoimmunity, the absence of five typical antibodies in the patient might argue against classical autoimmune type 1 diabetes.
Since ACE2 is expressed on pancreatic β-cells and ACE2 is the main receptor for COVID-19 (Sars-CoV-2) internalization the researchers propose a direct cytolytic β-cell damage due to COVID-19 (Sars-CoV-2) resulting in an insulin-depended diabetes without a classical autoimmune pathology in the patient. This assumption is supported by a recent mechanistic study demonstrating that adult human pancreatic alpha and beta cells are permissive to Sars-CoV-2 pseudo-entry virus and Sars-CoV-2 virus infection.
Furthermore, Sars-CoV-2 infection of pancreatic endocrine cells resulted in robust chemokine induction as seen in Covid-19 patients and upregulation of markers of cell death.
To date, the complex immunopathology of type 1 diabetes is still not elusively understood. A detailed understanding in the induction and progression of pancreatic β-cell failure, however, is crucial to develop novel innovative therapies to prevent and/or cure this important metabolic disease. In that regard, the detailed examination of patients developing β-cell failure and insulin-dependent diabetes after a COVID-19 infection in the future might yield novel insight into the yet unknown role of ACE2 in β-cell function and also possible virus induced cytolytic processes in type 1 diabetes development.
A global registry has been launched to provide a systematic platform for collecting and analyzing such patients. It will be critical to explore the frequency, severity and duration of these complications and to explore more deeply the mechanisms in primary human tissue. However, giving the fact that five different antibodies were tested negative the research findings clearly suggest that diabetologists need to be aware of the possibility of an insulin dependent diabetes as an acute complication in COVID-19 (Sars-CoV-2) infected patients.
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