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Conventional and genetic associations of adiposity with 1463 proteins in relatively lean Chinese adults

Abstract:
Adiposity is associated with multiple diseases and traits, but little is known about the causal relevance and mechanisms underlying these associations. Large-scale proteomic profiling, especially when integrated with genetic data, can clarify mechanisms linking adiposity with disease outcomes. We examined the associations of adiposity with plasma levels of 1463 proteins in 3977 Chinese adults, using measured and genetically-instrumented BMI. We further used two-sample bi-directional MR analyses to assess if certain proteins influenced adiposity, along with other (e.g. enrichment) analyses to clarify possible mechanisms underlying the observed associations. Overall, the mean (SD) baseline BMI was 23.9 (3.3) kg/m2, with only 6% being obese (i.e. BMI ≥ 30 kg/m2). Measured and genetically-instrumented BMI was significantly associated at FDR < 0.05 with levels of 1096 (positive/inverse: 826/270) and 307 (positive/inverse: 270/37) proteins, respectively, with FABP4, LEP, IL1RN, LSP1, GOLM2, TNFRSF6B, and ADAMTS15 showing the strongest positive and PON3, NCAN, LEPR, IGFBP2 and MOG showing the strongest inverse genetic associations. These associations were largely linear, in adiposity-to-protein direction, and replicated (> 90%) in Europeans of UKB (mean BMI 27.4 kg/m2). Enrichment analyses of the top > 50 BMI-associated proteins demonstrated their involvement in atherosclerosis, lipid metabolism, tumour progression and inflammation. Two-sample bi-directional MR analyses using cis-pQTLs identified in CKB GWAS found eight proteins (ITIH3, LRP11, SCAMP3, NUDT5, OGN, EFEMP1, TXNDC15, PRDX6) significantly affect levels of BMI, with NUDT5 also showing bi-directional association. The findings among relatively lean Chinese adults identified novel pathways by which adiposity may increase disease risks and novel potential targets for treatment of obesity and obesity-related diseases.
Publication status:
Published
Peer review status:
Peer reviewed

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Files:
Publisher copy:
10.1007/s10654-023-01038-9

Authors


More by this author
Institution:
University of Oxford
Division:
MSD
Department:
Nuffield Department of Population Health
Sub department:
Clinical Trial Service Unit
Role:
Author
More by this author
Institution:
University of Oxford
Division:
MSD
Department:
Nuffield Department of Population Health
Sub department:
Clinical Trial Service Unit
Role:
Author
More by this author
Institution:
University of Oxford
Division:
MSD
Department:
Nuffield Department of Population Health
Sub department:
Clinical Trial Service Unit
Role:
Author
ORCID:
0000-0002-3981-3418
More by this author
Institution:
University of Oxford
Division:
MSD
Department:
Nuffield Department of Population Health
Sub department:
Clinical Trial Service Unit
Role:
Author
More by this author
Institution:
University of Oxford
Division:
MSD
Department:
Nuffield Department of Population Health
Sub department:
Clinical Trial Service Unit
Role:
Author
ORCID:
0000-0002-3946-1870

Contributors


More from this funder
Grant:
CH/1996001/9454
FS/18/23/33512
More from this funder
Grant:
104085/Z/14/Z
212946/Z/18/Z
088158/Z/09/Z
202922/Z/16/Z
More from this funder
Grant:
MC_U137686851
MC_UU_12026/2
MC_UU_00017/1


Publisher:
Springer
Journal:
European Journal of Epidemiology More from this journal
Volume:
38
Issue:
10
Pages:
1089–1103
Place of publication:
Netherlands
Publication date:
2023-09-07
Acceptance date:
2023-07-28
DOI:
EISSN:
1573-7284
ISSN:
0393-2990
Pmid:
37676424


Language:
English
Keywords:
Pubs id:
1522649
Local pid:
pubs:1522649
Deposit date:
2024-03-05

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