Biological plausibility for interactions between dietary fat, resveratrol, ACE2 and SARS-CoV illness severity.
Identifieur interne : 000965 ( 2020/Analysis ); précédent : 000964; suivant : 000966Biological plausibility for interactions between dietary fat, resveratrol, ACE2 and SARS-CoV illness severity.
Auteurs : Justine R. Horne [Canada] ; Marie-Claude Vohl [Canada]Source :
- American journal of physiology. Endocrinology and metabolism [ 1522-1555 ] ; 2020.
Abstract
The ACE2 cellular receptor is responsible for the pathogenesis of SARS-CoV, thus impacting the entrance and clearance of the virus. Studies demonstrate that upregulation of ACE2 has a protective effect on SARS-CoV-2 illness severity. Moreover, animal studies demonstrate that dietary intake can modulate ACE2 gene expression and function. A high intake of resveratrol may have a protective role, upregulating ACE2, whereas a high intake of dietary fat may have a detrimental role, downregulating ACE2. As such, we postulate on the biological plausibility of interactions between dietary fat and/or resveratrol and ACE2 gene variations in the modulation of SARS-CoV-2 illness severity. We call to action the research community to test this plausible interaction in a sample of human subjects.
DOI: 10.1152/ajpendo.00150.2020
PubMed: 32310688
Affiliations:
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pubmed:32310688Le document en format XML
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<front><div type="abstract" xml:lang="en">The ACE2 cellular receptor is responsible for the pathogenesis of SARS-CoV, thus impacting the entrance and clearance of the virus. Studies demonstrate that upregulation of ACE2 has a protective effect on SARS-CoV-2 illness severity. Moreover, animal studies demonstrate that dietary intake can modulate ACE2 gene expression and function. A high intake of resveratrol may have a protective role, upregulating ACE2, whereas a high intake of dietary fat may have a detrimental role, downregulating ACE2. As such, we postulate on the biological plausibility of interactions between dietary fat and/or resveratrol and ACE2 gene variations in the modulation of SARS-CoV-2 illness severity. We call to action the research community to test this plausible interaction in a sample of human subjects.</div>
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