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The Interesting Link Between Diabetes and COVID-19

Article by: Elad Goren

Covid-19 is a rapidly spreading, infectious disease caused by a newly discovered coronavirus.
Scientific evidence shows that older individuals as well as patients with preexsisting and underlying metabolic disorders caused by diabetes mellitus, hypertension and even hyperlipidemia are a significant higher risk of morbidity and mortality.

There is a reciprocal relationship between diabetes and Covid-10.
We know that diabetes is linked with an increased risk of a serious Covid-19 infection.

On the other hand, we know that metabolic complications of preexsisting diabetes, such as: hypertension, ketoacidosis, persistent oxidative stress, hyperosmolarity and hyperglycemia for which high levels of insulin are necessitated - have also been reported in patients with Covid-19.(1,2)

These complications and manifestations of diabetes present immense clinical challenges in managing the disease and also suggest complex pathophysiology of Covid-19 related diabetes.


The virus that causes Covid-19, is SARS-CoV-2 (Severe Acute Respiratory Syndrome Coronavirus 2)

Interestingly, the virus binds to angiotensin converting enzyme 2 (ACE-2) receptors which are expressed in several key metabolic tissues and sites in the body including: pancreatic betta cells, adipose tissue, the small intestine and even the kidneys (9)

that is why it is tenable to presume that SARS-CoV-2 may lead to alterations in glucose metabolism that could complicate the pathophysiology of preexisting diabetes and even lead to the discovery of novel mechanisms of the disease.

SARS-CoV-2 and ACE-2 interaction schematic representation. (3)

Spike proteins primed by tissue serene protease, allow this interaction.

The virus uses the ACE-2 protein to enter the alveolar cells in the lungs.

The renin angiotensin system consists of renin which catalyzes the conversion of angiotensinogen to angiotensin , the subsequent axis depends of the balance between ACE and ACE-2 enzymes.

Generally, ACE is an enzyme that converts Angiotensin 1 to Angiotensin 2 and this acts in the angiotensin receptor.


In the respiratory system activation of ACE leads to a proinflammatory mechanism of fibrotic and proinflammatory response. (3,4)

However, ACE-2 converts Angiotensin 1 to Angiotensin 1-7, which acts on the Mas receptor.

The activation of ACE-2-Angiotensin 1-7-Mas, induces a protective mechanism of anti-inflammatory, antifibrotic and antihyperesponsiveness.


In diabetes and hypertension the ACE related pathway is activated with downregulation of the ACE-2 pathway which may often result in multi organ complications that can be seen in metabolic diseases with increased:cardiac fibrosis, diabetec nephropathy, hyperactivity of adrenal gland and it can also decrease insulin release and increase insulin resistance.


According to the scientific data detailed above, it is very tempting to speculate that the blocking of the ACE-Angiotensin-2-Angiotensin-1 receptor axis along with Angiotensin 1 blockers that very commonly used to treat hypertension, may assist to tilt the balance in favor of the ACE-2 Angiotensin-1-7-Mas axis which, theoretically  may help to accelerate respiratory recovery in patients suffering from Covid-19.

However, there is insufficient data to indicate such intervention, as expression of ACE-2 is not clinically and statistically associated with higher susceptibility to infection with SARS-CoV.

Additionally, is very intriguing finding is that patients who were treated with ACE and Angiotensin 1 blockers have been shown to have poorest results and prognosis in Covid-19.(5,6,7)

There is no up to date clinical data to support one or the other direction, which is why the American Heart Association and the American College of Cardiology have both issued statements to suggest that there no evidence of harm or benefit with the use to ACE- inhibitors or Angiotensin 1 receptor blockers and that patients should continue to take their medications as usual. (8)


The Diabetogenic Effect of Coronavirus:

There also several cases that set a new precedent for viral cause of ketosis-prone diabetes, including other coronavirus that bind to ACE-2 receptors. (10)

It seems that greater incidences of high fasting glycemia levels in the blood plasma as well as acute - onset diabetes have been reported among patients with SARS coronavirus 1 pneumonia than among those with non - SARS pneumonia. (11) 


In the aggregate, these findings may provide the support for the hypothesis of a potential diabetogenic effect of Covid-19, beyond the well recognized stress response that is associated with the severe illness.

Nonetheless, whether the alteration of glucose metabolism that usually occurs with the sudden onset of severe cases of Covid-19 persists or remit when the infection resolves - is yet unclear.



How frequent is the phenomenon of new onset diabetes?

Is it a classic type 1 or type 2 diabetes, or is it a new type of diabetes we have not yet to discover?

Do these patients remain at higher risk after the infection is cured?

Does Covid-19 change the pathophysiology of an existing diabetes?

Answering all of these questions is of vital importance so that we can inform the immediate clinical care and it remains a top priority in the battle against Covid-19.


In an effort to find answers to some of these questions, a group of top international diabetes researchrs participating in the CoviDIAB project have established a global registry of patients with Covid-19 - related diabetes. (covidiab.e-dendrite.com)

The main goal of the registry is to establish phenotype of new - onset diabetes that is defined by hyperglycemia, confirmed cases of Covid-19, negative history of diabetes and a history of normal glycated hemoglobin levels.


The registry is planned to expand in the future so it can include patients with preexsisting diabetes who present with severe acute metabolic disturbance too.

This registry can also be used to further investigate the epidemiologic features and pathogensis of Covid-19 related diabetes, so clues regarding appropriate care for patiens during and after the course of Covid-19 can be gained.



  1.  Li J, Wang X, Chen J, Zuo X, Zhang H, Deng A. COVID-19 infection may cause ketosis and ketoacidosis. Diabetes Obes Metab 2020 April 20 (Epub ahead of print).

  2. Special Expert Group for Control of the Epidemic of Novel Coronavirus Pneumonia of the Chinese Preventive Medicine Association[An update on the epidemiological characteristics of novel coronavirus pneumonia COVID-19] Zhonghua Liu Xing Bing Xue Za Zhi 202041139–144

  3.  Korean Society of Infectious Diseases, Korean Society of Pediatric Infectious Diseases, Korean Society of Epidemiology, Korean Society for Antimicrobial Therapy, Korean Society for Healthcare-associated Infection Control and Prevention, Korea Centers for Disease Control and Prevention. Report on the Epidemiological Features of Coronavirus Disease 2019 (COVID-19) Outbreak in the Republic of Korea

  4. Guan W J, Ni Z Y, Hu Yet al.For the China Medical Treatment Expert Group for COVID-19. Clinical Characteristics of Coronavirus Disease 2019 in China N Engl J Med 202010.1056/NEJMoa2002032[Epub ahead of print

  5. Wu C, Chen X, Cai Yet al.Risk Factors Associated With Acute Respiratory Distress Syndrome and Death in Patients With Coronavirus Disease 2019 Pneumonia in Wuhan, China JAMA Intern M Ed 202010.1001/jamainternmed.2020.0994[Epub ahead of print]

  6. Dalan R, Bornstein SR, El-Armouche A, et al. The ACE-2 in COVID-19: Foe or Friend?. Horm Metab Res. 2020;52(5):257-263. doi:10.1055/a-1155-0501

  7. Bozkurt B, Kovacs R, Harrington B. HFSA/ACC/AHA statement addresses concerns re: using RAAS antagonists in COVID-19. Published and accessed on: March 17. 2020

  8. Hamming I, Timens W, Bulthuis ML, Lely AT, Navis G, van Goor H. Tissue distribution of ACE2 protein, the functional receptor for SARS coronavirus: a first step in understanding SARS pathogenesis. J Pathol 2004;203:631-637.

  9. Hamming I, Timens W, Bulthuis ML, Lely AT, Navis G, van Goor H. Tissue distribution of ACE2 protein, the functional receptor for SARS coronavirus: a first step in understanding SARS pathogenesis. J Pathol 2004;203:631-637.

  10. Yang J-K, Lin S-S, Ji X-J, Guo L-M. Binding of SARS coronavirus to its receptor damages islets and causes acute diabetes. Acta Diabetol 2010;47:193-199.
    Hamming I, Timens W, Bulthuis ML, Lely AT, Navis G, van Goor H. Tissue distribution of ACE2 protein, the functional receptor for SARS coronavirus: a first step in understanding SARS pathogenesis. J Pathol 2004;203:631-637.


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