Diabetes, obesity, metabolism, and SARS-CoV-2 infection: the end of the beginning

The increased prevalence of obesity, diabetes, and cardiovascular risk factors in people hospitalized with severe COVID-19 illness has engendered considerable interest in the metabolic aspects of SARS-CoV-2-induced pathophysiology. Here, I update concepts informing how metabolic disorders and their...

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Published inCell metabolism Vol. 33; no. 3; pp. 479 - 498
Main Author Drucker, Daniel J.
Format Journal Article
LanguageEnglish
Published United States Elsevier Inc 02.03.2021
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Abstract The increased prevalence of obesity, diabetes, and cardiovascular risk factors in people hospitalized with severe COVID-19 illness has engendered considerable interest in the metabolic aspects of SARS-CoV-2-induced pathophysiology. Here, I update concepts informing how metabolic disorders and their co-morbidities modify the susceptibility to, natural history, and potential treatment of SARS-CoV-2 infection, with a focus on human biology. New data informing genetic predisposition, epidemiology, immune responses, disease severity, and therapy of COVID-19 in people with obesity and diabetes are highlighted. The emerging relationships of metabolic disorders to viral-induced immune responses and viral persistence, and the putative importance of adipose and islet ACE2 expression, glycemic control, cholesterol metabolism, and glucose- and lipid-lowering drugs is reviewed, with attention to controversies and unresolved questions. Rapid progress in these areas informs our growing understanding of SARS-CoV-2 infection in people with diabetes and obesity, while refining the therapeutic strategies and research priorities in this vulnerable population. COVID-19 infection produces excess mortality in people with obesity or diabetes. Here we review the epidemiology, susceptibility to infection, pathophysiology, immunology, complications, potential therapeutic options, and response to vaccinations in people with metabolic disorders and SARS-CoV-2 infection.
AbstractList The increased prevalence of obesity, diabetes, and cardiovascular risk factors in people hospitalized with severe COVID-19 illness has engendered considerable interest in the metabolic aspects of SARS-CoV-2-induced pathophysiology. Here, I update concepts informing how metabolic disorders and their co-morbidities modify the susceptibility to, natural history, and potential treatment of SARS-CoV-2 infection, with a focus on human biology. New data informing genetic predisposition, epidemiology, immune responses, disease severity, and therapy of COVID-19 in people with obesity and diabetes are highlighted. The emerging relationships of metabolic disorders to viral-induced immune responses and viral persistence, and the putative importance of adipose and islet ACE2 expression, glycemic control, cholesterol metabolism, and glucose- and lipid-lowering drugs is reviewed, with attention to controversies and unresolved questions. Rapid progress in these areas informs our growing understanding of SARS-CoV-2 infection in people with diabetes and obesity, while refining the therapeutic strategies and research priorities in this vulnerable population. COVID-19 infection produces excess mortality in people with obesity or diabetes. Here we review the epidemiology, susceptibility to infection, pathophysiology, immunology, complications, potential therapeutic options, and response to vaccinations in people with metabolic disorders and SARS-CoV-2 infection.
The increased prevalence of obesity, diabetes, and cardiovascular risk factors in people hospitalized with severe COVID-19 illness has engendered considerable interest in the metabolic aspects of SARS-CoV-2-induced pathophysiology. Here, I update concepts informing how metabolic disorders and their co-morbidities modify the susceptibility to, natural history, and potential treatment of SARS-CoV-2 infection, with a focus on human biology. New data informing genetic predisposition, epidemiology, immune responses, disease severity, and therapy of COVID-19 in people with obesity and diabetes are highlighted. The emerging relationships of metabolic disorders to viral-induced immune responses and viral persistence, and the putative importance of adipose and islet ACE2 expression, glycemic control, cholesterol metabolism, and glucose- and lipid-lowering drugs is reviewed, with attention to controversies and unresolved questions. Rapid progress in these areas informs our growing understanding of SARS-CoV-2 infection in people with diabetes and obesity, while refining the therapeutic strategies and research priorities in this vulnerable population.
The increased prevalence of obesity, diabetes, and cardiovascular risk factors in people hospitalized with severe COVID-19 illness has engendered considerable interest in the metabolic aspects of SARS-CoV-2-induced pathophysiology. Here, I update concepts informing how metabolic disorders and their co-morbidities modify the susceptibility to, natural history, and potential treatment of SARS-CoV-2 infection, with a focus on human biology. New data informing genetic predisposition, epidemiology, immune responses, disease severity, and therapy of COVID-19 in people with obesity and diabetes are highlighted. The emerging relationships of metabolic disorders to viral-induced immune responses and viral persistence, and the putative importance of adipose and islet ACE2 expression, glycemic control, cholesterol metabolism, and glucose- and lipid-lowering drugs is reviewed, with attention to controversies and unresolved questions. Rapid progress in these areas informs our growing understanding of SARS-CoV-2 infection in people with diabetes and obesity, while refining the therapeutic strategies and research priorities in this vulnerable population.The increased prevalence of obesity, diabetes, and cardiovascular risk factors in people hospitalized with severe COVID-19 illness has engendered considerable interest in the metabolic aspects of SARS-CoV-2-induced pathophysiology. Here, I update concepts informing how metabolic disorders and their co-morbidities modify the susceptibility to, natural history, and potential treatment of SARS-CoV-2 infection, with a focus on human biology. New data informing genetic predisposition, epidemiology, immune responses, disease severity, and therapy of COVID-19 in people with obesity and diabetes are highlighted. The emerging relationships of metabolic disorders to viral-induced immune responses and viral persistence, and the putative importance of adipose and islet ACE2 expression, glycemic control, cholesterol metabolism, and glucose- and lipid-lowering drugs is reviewed, with attention to controversies and unresolved questions. Rapid progress in these areas informs our growing understanding of SARS-CoV-2 infection in people with diabetes and obesity, while refining the therapeutic strategies and research priorities in this vulnerable population.
Author Drucker, Daniel J.
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Tue Aug 05 10:20:51 EDT 2025
Mon Jul 21 06:08:57 EDT 2025
Tue Jul 01 03:58:19 EDT 2025
Thu Apr 24 23:11:18 EDT 2025
Fri Feb 23 02:46:07 EST 2024
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Issue 3
Keywords adipose tissue
glucose
immunity
islet
virus
vaccination
Language English
License Copyright © 2021 Elsevier Inc. All rights reserved.
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Snippet The increased prevalence of obesity, diabetes, and cardiovascular risk factors in people hospitalized with severe COVID-19 illness has engendered considerable...
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SubjectTerms adipose tissue
Angiotensin-Converting Enzyme 2 - metabolism
Blood Glucose - analysis
Cholesterol - metabolism
Comorbidity
COVID-19 - epidemiology
COVID-19 - pathology
COVID-19 Drug Treatment
Diabetes Mellitus - pathology
Genetic Predisposition to Disease - genetics
glucose
Glucose - metabolism
Heart Disease Risk Factors
Humans
Hyperglycemia - pathology
immunity
islet
Metabolic Diseases - pathology
Obesity - pathology
Review
SARS-CoV-2
vaccination
virus
Title Diabetes, obesity, metabolism, and SARS-CoV-2 infection: the end of the beginning
URI https://dx.doi.org/10.1016/j.cmet.2021.01.016
https://www.ncbi.nlm.nih.gov/pubmed/33529600
https://www.proquest.com/docview/2486145382
https://pubmed.ncbi.nlm.nih.gov/PMC7825982
Volume 33
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