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Review
. 2020 Jul-Aug;14(4):469-471.
doi: 10.1016/j.dsx.2020.04.033. Epub 2020 Apr 29.

SARS-CoV-2 infection and obesity: Common inflammatory and metabolic aspects

Konstantinos Michalakis  1 , Ioannis Ilias  2
Affiliations
Review

SARS-CoV-2 infection and obesity: Common inflammatory and metabolic aspects

Konstantinos Michalakis et al. Diabetes Metab Syndr. 2020 Jul-Aug.

Abstract

Backround and aims: According to the World Obesity Federation, "obesity-related conditions seem to worsen the effect of Covid-19 (SARS-CoV-2)"; additionally the Centres for Disease Control and Prevention reported that "people with heart disease and diabetes are at higher risk of SARS-CoV-2 complications and that severe obesity poses a higher risk for severe illness". Recent reports have shown elevated levels of cytokines due to increased inflammation in patients with SARS-CoV-2 disease. On the other hand, obesity represents a state of low-grade inflammation, with various inflammatory products directly excreted by adipose tissue. In this concise report we aimed to assess common elements of obesity and SARS-CoV-2 infection.

Methods: Pubmed search on obesity and SARS-CoV-2 infection.

Results: We present "mechanistic" obesity-related problems that aggravate SARS-CoV-2 infection as well as tentative inflammatory/metabolic links between these diseases.

Conclusion: Obesity and SARS-CoV-2 share common elements of the inflammatory process (and possibly also metabolic disturbances), exacerbating SARS-CoV-2 infection in the obese.

Keywords: Coronavirus; Glucose; Human; Infection; Inflammation; Obesity.

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Conflict of interest statement

Declaration of competing interest The authors do not have any conflicts of interest and sources of funding to declare. The authors received no funding for this work.

Figures

Fig. 1
Fig. 1
Selected metabolic pathways for obesity and SARS-CoV-2 infection; their common elements are shown in grey boxes. In obesity, resistance to leptin (along with resistin) leads to insulin resistance (both in the brain and in peripheral tissues) and eventually to hyperglycemia and T2DM. Moreover, adipose tissue releases ATG, which, via ACE is converted to AT II and increases blood pressure. SARS-CoV-2 attaches to cells via ACE2 and may provoke hyperglycemia (see text for more details); FFA: free fatty acids, ATG: angiotensinogen, ACE: angiotensin converting enzyme, AT II: angiotensin II, AT 1–7: angiotensin 1-7 (vasodilatory), NO: Nitric Oxide, T2DM: type 2 diabetes mellitus, ACE2: angiotensin converting enzyme 2, ∗: is usually upregulated in subjects with hypertension on ACE-inhibitors and AT receptor blockers (ARB), ∗∗hyperglycemia has been reported in patients with SARS-CoV-2 infection – the specific mechanisms have not been elucidated.
See this image and copyright information in PMC

References

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