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- Publisher Website: 10.1186/s12916-021-01944-3
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- PMID: 33757497
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Article: Evaluation of glycemic traits in susceptibility to COVID-19 risk: a Mendelian randomization study
Title | Evaluation of glycemic traits in susceptibility to COVID-19 risk: a Mendelian randomization study |
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Authors | |
Keywords | COVID-19 Glucose Glycated hemoglobin Mendelian randomization Type 2 diabetes |
Issue Date | 2021 |
Publisher | BioMed Central Ltd. The Journal's web site is located at http://www.biomedcentral.com/bmcmed/ |
Citation | BMC Medicine, 2021, v. 19 n. 1, p. article no. 72 How to Cite? |
Abstract | Background
Observational studies suggest poorer glycemic traits and type 2 diabetes associated with coronavirus disease 2019 (COVID-19) risk although these findings could be confounded by socioeconomic position. We conducted a two-sample Mendelian randomization to clarify their role in COVID-19 risk and specific COVID-19 phenotypes (hospitalized and severe cases).
Method:
We identified genetic instruments for fasting glucose (n = 133,010), 2 h glucose (n = 42,854), glycated hemoglobin (n = 123,665), and type 2 diabetes (74,124 cases and 824,006 controls) from genome wide association studies and applied them to COVID-19 Host Genetics Initiative summary statistics (17,965 COVID-19 cases and 1,370,547 population controls). We used inverse variance weighting to obtain the causal estimates of glycemic traits and genetic predisposition to type 2 diabetes in COVID-19 risk. Sensitivity analyses included MR-Egger and weighted median method.
Results:
We found genetic predisposition to type 2 diabetes was not associated with any COVID-19 phenotype (OR: 1.00 per unit increase in log odds of having diabetes, 95%CI 0.97 to 1.04 for overall COVID-19; OR: 1.02, 95%CI 0.95 to 1.09 for hospitalized COVID-19; and OR: 1.00, 95%CI 0.93 to 1.08 for severe COVID-19). There were no strong evidence for an association of glycemic traits in COVID-19 phenotypes, apart from a potential inverse association for fasting glucose albeit with wide confidence interval.
Conclusion:
We provide some genetic evidence that poorer glycemic traits and predisposition to type 2 diabetes unlikely increase the risk of COVID-19. Although our study did not indicate glycemic traits increase severity of COVID-19, additional studies are needed to verify our findings. |
Description | key |
Persistent Identifier | http://hdl.handle.net/10722/298665 |
ISSN | 2023 Impact Factor: 7.0 2023 SCImago Journal Rankings: 2.711 |
PubMed Central ID | |
ISI Accession Number ID |
DC Field | Value | Language |
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dc.contributor.author | Au Yeung, SL | - |
dc.contributor.author | Zhao, JV | - |
dc.contributor.author | Schooling, CM | - |
dc.date.accessioned | 2021-04-12T03:01:41Z | - |
dc.date.available | 2021-04-12T03:01:41Z | - |
dc.date.issued | 2021 | - |
dc.identifier.citation | BMC Medicine, 2021, v. 19 n. 1, p. article no. 72 | - |
dc.identifier.issn | 1741-7015 | - |
dc.identifier.uri | http://hdl.handle.net/10722/298665 | - |
dc.description | key | - |
dc.description.abstract | Background Observational studies suggest poorer glycemic traits and type 2 diabetes associated with coronavirus disease 2019 (COVID-19) risk although these findings could be confounded by socioeconomic position. We conducted a two-sample Mendelian randomization to clarify their role in COVID-19 risk and specific COVID-19 phenotypes (hospitalized and severe cases). Method: We identified genetic instruments for fasting glucose (n = 133,010), 2 h glucose (n = 42,854), glycated hemoglobin (n = 123,665), and type 2 diabetes (74,124 cases and 824,006 controls) from genome wide association studies and applied them to COVID-19 Host Genetics Initiative summary statistics (17,965 COVID-19 cases and 1,370,547 population controls). We used inverse variance weighting to obtain the causal estimates of glycemic traits and genetic predisposition to type 2 diabetes in COVID-19 risk. Sensitivity analyses included MR-Egger and weighted median method. Results: We found genetic predisposition to type 2 diabetes was not associated with any COVID-19 phenotype (OR: 1.00 per unit increase in log odds of having diabetes, 95%CI 0.97 to 1.04 for overall COVID-19; OR: 1.02, 95%CI 0.95 to 1.09 for hospitalized COVID-19; and OR: 1.00, 95%CI 0.93 to 1.08 for severe COVID-19). There were no strong evidence for an association of glycemic traits in COVID-19 phenotypes, apart from a potential inverse association for fasting glucose albeit with wide confidence interval. Conclusion: We provide some genetic evidence that poorer glycemic traits and predisposition to type 2 diabetes unlikely increase the risk of COVID-19. Although our study did not indicate glycemic traits increase severity of COVID-19, additional studies are needed to verify our findings. | - |
dc.language | eng | - |
dc.publisher | BioMed Central Ltd. The Journal's web site is located at http://www.biomedcentral.com/bmcmed/ | - |
dc.relation.ispartof | BMC Medicine | - |
dc.rights | BMC Medicine. Copyright © BioMed Central Ltd. | - |
dc.rights | This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License. | - |
dc.subject | COVID-19 | - |
dc.subject | Glucose | - |
dc.subject | Glycated hemoglobin | - |
dc.subject | Mendelian randomization | - |
dc.subject | Type 2 diabetes | - |
dc.title | Evaluation of glycemic traits in susceptibility to COVID-19 risk: a Mendelian randomization study | - |
dc.type | Article | - |
dc.identifier.email | Au Yeung, SL: ayslryan@hku.hk | - |
dc.identifier.email | Zhao, JV: janezhao@hku.hk | - |
dc.identifier.email | Schooling, CM: cms1@hkucc.hku.hk | - |
dc.identifier.authority | Au Yeung, SL=rp02224 | - |
dc.identifier.authority | Zhao, JV=rp02336 | - |
dc.identifier.authority | Schooling, CM=rp00504 | - |
dc.description.nature | published_or_final_version | - |
dc.identifier.doi | 10.1186/s12916-021-01944-3 | - |
dc.identifier.pmid | 33757497 | - |
dc.identifier.pmcid | PMC7987511 | - |
dc.identifier.scopus | eid_2-s2.0-85103184655 | - |
dc.identifier.hkuros | 322139 | - |
dc.identifier.volume | 19 | - |
dc.identifier.issue | 1 | - |
dc.identifier.spage | article no. 72 | - |
dc.identifier.epage | article no. 72 | - |
dc.identifier.isi | WOS:000632864100001 | - |
dc.publisher.place | United Kingdom | - |