Based on the data discussed here, it is evident that optimal metabolic control of T2DM and associated metabolic parameters in patients with COVID-19 is mandatory. This is not only relevant because of the obvious danger and increased risk of complications for patients with T2DM and a severe infectious disease, but also because this approach might help the treatment of all patients with COVID-19.

Antidiabetic medications, such as GLP1 agonists, that improve the metabolic function and induce the activity of the protective ACE2 and Mas receptor pathways might have the advantage of ameliorating glucose metabolism and blood pressure, and also preventing coronaviruses from entering cells as a result of competitive binding to ACE2. This effect might help to protect and restore pulmonary function5. Likewise, early treatment with angiotensin II receptor blockers (such as losartan or telmisartan) or, more directly, recombinant ACE2, might be useful to enhance the ACE2 and Mas system in preference to the pathways mediated by angiotensin receptors. This approach would enable the combination of an antidiabetic, anti-inflammatory and antiviral effect.

Finally, the synthetic protease inhibitor camustat, which blocks the serine protease TMPRSS2 required for ACE2-mediated coronavirus entry into the cells4, also reverses dyslipidaemia and hyperglycaemia8. The intriguing link between coronavirus infections and these endocrine and metabolic pathways will have an important effect on the general medical management of severe COVID-19. Glucocorticoids that have been helpful in the treatment of acute respiratory distress syndrome might not be indicated in patients with coronavirus infection. Glucocorticoids not only aggravate metabolic control, but also attenuate angiotensin 1–7 and Mas receptor expression9. Hence, they might have a limited role in the management of patients with COVID-19. By contrast, the anti-rheumatic drug hydroxychloroquine, which is now widely used in many centres around the world treating patients with COVID-19, has also attracted interest as a potential therapeutic intervention for patients with T2DM10. At this point, it is unclear whether hydroxychloroquine in addition to anti-inflammatory and antidiabetic drugs will also directly interfere with the coronavirus–ACE2 pathways.

In conclusion, COVID-19 is not primarily a metabolic disease, but metabolic control of glucose, lipid levels and blood pressure are key in these patients. This approach is important to address the well-established metabolic and cardiovascular complications of this primary comorbidity. Moreover, effective control of these metabolic parameters might represent a specific and mechanistic approach to prevent and ameliorate the acute effects of this virus by reducing the local inflammatory response and blocking its entry into cells.