Longitudinal multi-omics study reveals common etiology underlying association between plasma proteome and BMI trajectories in adolescent and young adult twins.

Body mass index (BMI) Changes in BMI Longitudinal twin study Metabolome Multi-omics Polygenic risk scores Proteome Transcriptome

Journal

BMC medicine
ISSN: 1741-7015
Titre abrégé: BMC Med
Pays: England
ID NLM: 101190723

Informations de publication

Date de publication:
21 Dec 2023
Historique:
received: 03 07 2023
accepted: 27 11 2023
medline: 22 12 2023
pubmed: 22 12 2023
entrez: 22 12 2023
Statut: epublish

Résumé

The influence of genetics and environment on the association of the plasma proteome with body mass index (BMI) and changes in BMI remains underexplored, and the links to other omics in these associations remain to be investigated. We characterized protein-BMI trajectory associations in adolescents and adults and how these connect to other omics layers. Our study included two cohorts of longitudinally followed twins: FinnTwin12 (N = 651) and the Netherlands Twin Register (NTR) (N = 665). Follow-up comprised 4 BMI measurements over approximately 6 (NTR: 23-27 years old) to 10 years (FinnTwin12: 12-22 years old), with omics data collected at the last BMI measurement. BMI changes were calculated in latent growth curve models. Mixed-effects models were used to quantify the associations between the abundance of 439 plasma proteins with BMI at blood sampling and changes in BMI. In FinnTwin12, the sources of genetic and environmental variation underlying the protein abundances were quantified by twin models, as were the associations of proteins with BMI and BMI changes. In NTR, we investigated the association of gene expression of genes encoding proteins identified in FinnTwin12 with BMI and changes in BMI. We linked identified proteins and their coding genes to plasma metabolites and polygenic risk scores (PRS) applying mixed-effects models and correlation networks. We identified 66 and 14 proteins associated with BMI at blood sampling and changes in BMI, respectively. The average heritability of these proteins was 35%. Of the 66 BMI-protein associations, 43 and 12 showed genetic and environmental correlations, respectively, including 8 proteins showing both. Similarly, we observed 7 and 3 genetic and environmental correlations between changes in BMI and protein abundance, respectively. S100A8 gene expression was associated with BMI at blood sampling, and the PRG4 and CFI genes were associated with BMI changes. Proteins showed strong connections with metabolites and PRSs, but we observed no multi-omics connections among gene expression and other omics layers. Associations between the proteome and BMI trajectories are characterized by shared genetic, environmental, and metabolic etiologies. We observed few gene-protein pairs associated with BMI or changes in BMI at the proteome and transcriptome levels.

Sections du résumé

BACKGROUND BACKGROUND
The influence of genetics and environment on the association of the plasma proteome with body mass index (BMI) and changes in BMI remains underexplored, and the links to other omics in these associations remain to be investigated. We characterized protein-BMI trajectory associations in adolescents and adults and how these connect to other omics layers.
METHODS METHODS
Our study included two cohorts of longitudinally followed twins: FinnTwin12 (N = 651) and the Netherlands Twin Register (NTR) (N = 665). Follow-up comprised 4 BMI measurements over approximately 6 (NTR: 23-27 years old) to 10 years (FinnTwin12: 12-22 years old), with omics data collected at the last BMI measurement. BMI changes were calculated in latent growth curve models. Mixed-effects models were used to quantify the associations between the abundance of 439 plasma proteins with BMI at blood sampling and changes in BMI. In FinnTwin12, the sources of genetic and environmental variation underlying the protein abundances were quantified by twin models, as were the associations of proteins with BMI and BMI changes. In NTR, we investigated the association of gene expression of genes encoding proteins identified in FinnTwin12 with BMI and changes in BMI. We linked identified proteins and their coding genes to plasma metabolites and polygenic risk scores (PRS) applying mixed-effects models and correlation networks.
RESULTS RESULTS
We identified 66 and 14 proteins associated with BMI at blood sampling and changes in BMI, respectively. The average heritability of these proteins was 35%. Of the 66 BMI-protein associations, 43 and 12 showed genetic and environmental correlations, respectively, including 8 proteins showing both. Similarly, we observed 7 and 3 genetic and environmental correlations between changes in BMI and protein abundance, respectively. S100A8 gene expression was associated with BMI at blood sampling, and the PRG4 and CFI genes were associated with BMI changes. Proteins showed strong connections with metabolites and PRSs, but we observed no multi-omics connections among gene expression and other omics layers.
CONCLUSIONS CONCLUSIONS
Associations between the proteome and BMI trajectories are characterized by shared genetic, environmental, and metabolic etiologies. We observed few gene-protein pairs associated with BMI or changes in BMI at the proteome and transcriptome levels.

Identifiants

pubmed: 38129841
doi: 10.1186/s12916-023-03198-7
pii: 10.1186/s12916-023-03198-7
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

508

Informations de copyright

© 2023. The Author(s).

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Auteurs

Gabin Drouard (G)

Institute for Molecular Medicine Finland (FIMM), HiLIFE, University of Helsinki, Helsinki, Finland. gabin.drouard@helsinki.fi.

Fiona A Hagenbeek (FA)

Institute for Molecular Medicine Finland (FIMM), HiLIFE, University of Helsinki, Helsinki, Finland.
Department of Biological Psychology, Vrije Universiteit Amsterdam, Amsterdam, The Netherlands.
Amsterdam Public Health Research Institute, Amsterdam, The Netherlands.

Alyce M Whipp (AM)

Institute for Molecular Medicine Finland (FIMM), HiLIFE, University of Helsinki, Helsinki, Finland.

René Pool (R)

Department of Biological Psychology, Vrije Universiteit Amsterdam, Amsterdam, The Netherlands.
Amsterdam Public Health Research Institute, Amsterdam, The Netherlands.

Jouke Jan Hottenga (JJ)

Department of Biological Psychology, Vrije Universiteit Amsterdam, Amsterdam, The Netherlands.
Amsterdam Public Health Research Institute, Amsterdam, The Netherlands.

Rick Jansen (R)

Department of Psychiatry, Amsterdam UMC Location Vrije Universiteit Amsterdam, Amsterdam, the Netherlands.
Amsterdam Neuroscience, Mood, Anxiety, Psychosis, Sleep & Stress Program, Amsterdam, The Netherlands.

Nikki Hubers (N)

Department of Biological Psychology, Vrije Universiteit Amsterdam, Amsterdam, The Netherlands.
Amsterdam Public Health Research Institute, Amsterdam, The Netherlands.
Amsterdam Reproduction & Development (AR&D) Research Institute, Amsterdam, The Netherlands.

Aleksei Afonin (A)

A.I. Virtanen Institute for Molecular Sciences, University of Eastern Finland, Kuopio, Finland.

Gonneke Willemsen (G)

Department of Biological Psychology, Vrije Universiteit Amsterdam, Amsterdam, The Netherlands.
Amsterdam Public Health Research Institute, Amsterdam, The Netherlands.

Eco J C de Geus (EJC)

Department of Biological Psychology, Vrije Universiteit Amsterdam, Amsterdam, The Netherlands.
Amsterdam Public Health Research Institute, Amsterdam, The Netherlands.

Samuli Ripatti (S)

Institute for Molecular Medicine Finland (FIMM), HiLIFE, University of Helsinki, Helsinki, Finland.
Department of Public Health, Faculty of Medicine, University of Helsinki, Helsinki, Finland.
Broad Institute of MIT and Harvard, Cambridge, MA, USA.

Matti Pirinen (M)

Institute for Molecular Medicine Finland (FIMM), HiLIFE, University of Helsinki, Helsinki, Finland.
Department of Public Health, Faculty of Medicine, University of Helsinki, Helsinki, Finland.
Department of Mathematics and Statistics, University of Helsinki, Helsinki, Finland.

Katja M Kanninen (KM)

A.I. Virtanen Institute for Molecular Sciences, University of Eastern Finland, Kuopio, Finland.

Dorret I Boomsma (DI)

Department of Biological Psychology, Vrije Universiteit Amsterdam, Amsterdam, The Netherlands.
Amsterdam Public Health Research Institute, Amsterdam, The Netherlands.
Amsterdam Reproduction & Development (AR&D) Research Institute, Amsterdam, The Netherlands.

Jenny van Dongen (J)

Department of Biological Psychology, Vrije Universiteit Amsterdam, Amsterdam, The Netherlands.
Amsterdam Public Health Research Institute, Amsterdam, The Netherlands.
Amsterdam Reproduction & Development (AR&D) Research Institute, Amsterdam, The Netherlands.

Jaakko Kaprio (J)

Institute for Molecular Medicine Finland (FIMM), HiLIFE, University of Helsinki, Helsinki, Finland. jaakko.kaprio@helsinki.fi.

Classifications MeSH