Adiposity and NMR-measured lipid and metabolic biomarkers among 30,000 Mexican adults.


Journal

Communications medicine
ISSN: 2730-664X
Titre abrégé: Commun Med (Lond)
Pays: England
ID NLM: 9918250414506676

Informations de publication

Date de publication:
14 Nov 2022
Historique:
received: 03 05 2022
accepted: 28 10 2022
entrez: 14 11 2022
pubmed: 15 11 2022
medline: 15 11 2022
Statut: epublish

Résumé

Adiposity is a major cause of morbidity and mortality in part due to effects on blood lipids. Nuclear magnetic resonance (NMR) spectroscopy provides direct information on >130 biomarkers mostly related to blood lipid particles. Among 28,934 Mexican adults without chronic disease and not taking lipid-lowering therapy, we examine the cross-sectional relevance of body-mass index (BMI), waist circumference (WC), waist-hip ratio (WHR), and hip circumference (HC) to NMR-measured metabolic biomarkers. Confounder-adjusted associations between each adiposity measure and NMR biomarkers are estimated before and after mutual adjustment for other adiposity measures. Markers of general (ie, BMI), abdominal (ie, WC and WHR) and gluteo-femoral (ie, HC) adiposity all display similar and strong associations across the NMR-platform of biomarkers, particularly for biomarkers that increase cardiometabolic risk. Higher adiposity associates with higher levels of Apolipoprotein-B (about 0.35, 0.30, 0.35, and 0.25 SD higher Apolipoprotein-B per 2-SD higher BMI, WHR, WC, and HC, respectively), higher levels of very low-density lipoprotein particles (and the cholesterol, triglycerides, and phospholipids within these lipoproteins), higher levels of all fatty acids (particularly mono-unsaturated fatty acids) and multiple changes in other metabolic biomarkers including higher levels of branched-chain amino acids and the inflammation biomarker glycoprotein acetyls. Associations for general and abdominal adiposity are fairly independent of each other but, given general and abdominal adiposity, higher gluteo-femoral adiposity is associated with a strongly favourable cardiometabolic lipid profile. Our results provide insight to the lipidic and metabolomic signatures of different adiposity markers in a previously understudied population where adiposity is common but lipid-lowering therapy is not. Obesity increases the risk of multiple diseases, in part due to alterations in how the body breaks down carbohydrates and fats, which is reflected in molecules that circulate in blood. In obesity, disease risk may vary depending on whether fat accumulates in the body overall (i.e. total adiposity), in the middle of the body (i.e. abdominal adiposity) or around the hips (i.e. gluteo-femoral adiposity). Here, we show that in a population of Mexican adults higher total and abdominal adiposity relate adversely, while higher gluteo-femoral adiposity relates favourably, to numerous molecules in blood that are linked to type 2 diabetes and heart disease. These findings provide insight on the processes that link the accumulation of fat across the body with disease risk in a population where obesity rates are high.

Sections du résumé

BACKGROUND BACKGROUND
Adiposity is a major cause of morbidity and mortality in part due to effects on blood lipids. Nuclear magnetic resonance (NMR) spectroscopy provides direct information on >130 biomarkers mostly related to blood lipid particles.
METHODS METHODS
Among 28,934 Mexican adults without chronic disease and not taking lipid-lowering therapy, we examine the cross-sectional relevance of body-mass index (BMI), waist circumference (WC), waist-hip ratio (WHR), and hip circumference (HC) to NMR-measured metabolic biomarkers. Confounder-adjusted associations between each adiposity measure and NMR biomarkers are estimated before and after mutual adjustment for other adiposity measures.
RESULTS RESULTS
Markers of general (ie, BMI), abdominal (ie, WC and WHR) and gluteo-femoral (ie, HC) adiposity all display similar and strong associations across the NMR-platform of biomarkers, particularly for biomarkers that increase cardiometabolic risk. Higher adiposity associates with higher levels of Apolipoprotein-B (about 0.35, 0.30, 0.35, and 0.25 SD higher Apolipoprotein-B per 2-SD higher BMI, WHR, WC, and HC, respectively), higher levels of very low-density lipoprotein particles (and the cholesterol, triglycerides, and phospholipids within these lipoproteins), higher levels of all fatty acids (particularly mono-unsaturated fatty acids) and multiple changes in other metabolic biomarkers including higher levels of branched-chain amino acids and the inflammation biomarker glycoprotein acetyls. Associations for general and abdominal adiposity are fairly independent of each other but, given general and abdominal adiposity, higher gluteo-femoral adiposity is associated with a strongly favourable cardiometabolic lipid profile.
CONCLUSIONS CONCLUSIONS
Our results provide insight to the lipidic and metabolomic signatures of different adiposity markers in a previously understudied population where adiposity is common but lipid-lowering therapy is not.
Obesity increases the risk of multiple diseases, in part due to alterations in how the body breaks down carbohydrates and fats, which is reflected in molecules that circulate in blood. In obesity, disease risk may vary depending on whether fat accumulates in the body overall (i.e. total adiposity), in the middle of the body (i.e. abdominal adiposity) or around the hips (i.e. gluteo-femoral adiposity). Here, we show that in a population of Mexican adults higher total and abdominal adiposity relate adversely, while higher gluteo-femoral adiposity relates favourably, to numerous molecules in blood that are linked to type 2 diabetes and heart disease. These findings provide insight on the processes that link the accumulation of fat across the body with disease risk in a population where obesity rates are high.

Autres résumés

Type: plain-language-summary (eng)
Obesity increases the risk of multiple diseases, in part due to alterations in how the body breaks down carbohydrates and fats, which is reflected in molecules that circulate in blood. In obesity, disease risk may vary depending on whether fat accumulates in the body overall (i.e. total adiposity), in the middle of the body (i.e. abdominal adiposity) or around the hips (i.e. gluteo-femoral adiposity). Here, we show that in a population of Mexican adults higher total and abdominal adiposity relate adversely, while higher gluteo-femoral adiposity relates favourably, to numerous molecules in blood that are linked to type 2 diabetes and heart disease. These findings provide insight on the processes that link the accumulation of fat across the body with disease risk in a population where obesity rates are high.

Identifiants

pubmed: 36376486
doi: 10.1038/s43856-022-00208-2
pii: 10.1038/s43856-022-00208-2
pmc: PMC9663185
doi:

Types de publication

Journal Article

Langues

eng

Pagination

143

Subventions

Organisme : Medical Research Council
ID : MC_PC_12028
Pays : United Kingdom
Organisme : Medical Research Council
ID : G0300622
Pays : United Kingdom
Organisme : Medical Research Council
ID : MC_UU_00017/3
Pays : United Kingdom
Organisme : Medical Research Council
ID : MC_PC_12027
Pays : United Kingdom
Organisme : Wellcome Trust (Wellcome)
ID : 058299/Z/99
Organisme : British Heart Foundation (BHF)
ID : RE/13/1/30181
Organisme : British Heart Foundation
ID : CH/1996001/9454
Pays : United Kingdom
Organisme : Medical Research Council
ID : MC_PC_12029
Pays : United Kingdom
Organisme : Medical Research Council
ID : MC_U137686854
Pays : United Kingdom
Organisme : Medical Research Council
ID : MC_EX_G0801669
Pays : United Kingdom
Organisme : RCUK | Medical Research Council (MRC)
ID : MC_UU_00017/2
Organisme : Medical Research Council
ID : MC_U137686857
Pays : United Kingdom
Organisme : British Heart Foundation
ID : RE/13/1/30181
Pays : United Kingdom
Organisme : Medical Research Council
ID : MC_UU_12026/3
Pays : United Kingdom

Informations de copyright

© 2022. The Author(s).

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Auteurs

Diego Aguilar-Ramirez (D)

Clinical Trial Service Unit & Epidemiological Studies Unit, Nuffield Department of Population Health, University of Oxford, Oxford, UK.

William G Herrington (WG)

Clinical Trial Service Unit & Epidemiological Studies Unit, Nuffield Department of Population Health, University of Oxford, Oxford, UK.

Jesus Alegre-Díaz (J)

Faculty of Medicine, National Autonomous University of Mexico, Mexico City, Mexico.

Natalie Staplin (N)

Clinical Trial Service Unit & Epidemiological Studies Unit, Nuffield Department of Population Health, University of Oxford, Oxford, UK.
MRC Population Health Research Unit, Nuffield Department of Population Health, University of Oxford, Oxford, UK.

Raúl Ramírez-Reyes (R)

Faculty of Medicine, National Autonomous University of Mexico, Mexico City, Mexico.

Louisa Friedrichs Gnatiuc (LF)

Clinical Trial Service Unit & Epidemiological Studies Unit, Nuffield Department of Population Health, University of Oxford, Oxford, UK.
MRC Population Health Research Unit, Nuffield Department of Population Health, University of Oxford, Oxford, UK.

Michael Hill (M)

Clinical Trial Service Unit & Epidemiological Studies Unit, Nuffield Department of Population Health, University of Oxford, Oxford, UK.
MRC Population Health Research Unit, Nuffield Department of Population Health, University of Oxford, Oxford, UK.

Frederik Romer (F)

Clinical Trial Service Unit & Epidemiological Studies Unit, Nuffield Department of Population Health, University of Oxford, Oxford, UK.

Eirini Trichia (E)

Clinical Trial Service Unit & Epidemiological Studies Unit, Nuffield Department of Population Health, University of Oxford, Oxford, UK.
MRC Population Health Research Unit, Nuffield Department of Population Health, University of Oxford, Oxford, UK.

Fiona Bragg (F)

Clinical Trial Service Unit & Epidemiological Studies Unit, Nuffield Department of Population Health, University of Oxford, Oxford, UK.
MRC Population Health Research Unit, Nuffield Department of Population Health, University of Oxford, Oxford, UK.

Rachel Wade (R)

Clinical Trial Service Unit & Epidemiological Studies Unit, Nuffield Department of Population Health, University of Oxford, Oxford, UK.
MRC Population Health Research Unit, Nuffield Department of Population Health, University of Oxford, Oxford, UK.

Sarah Lewington (S)

Clinical Trial Service Unit & Epidemiological Studies Unit, Nuffield Department of Population Health, University of Oxford, Oxford, UK.

Rory Collins (R)

Clinical Trial Service Unit & Epidemiological Studies Unit, Nuffield Department of Population Health, University of Oxford, Oxford, UK.

Jonathan R Emberson (JR)

Clinical Trial Service Unit & Epidemiological Studies Unit, Nuffield Department of Population Health, University of Oxford, Oxford, UK. jonathan.emberson@ndph.ox.ac.uk.
MRC Population Health Research Unit, Nuffield Department of Population Health, University of Oxford, Oxford, UK. jonathan.emberson@ndph.ox.ac.uk.

Pablo Kuri-Morales (P)

Faculty of Medicine, National Autonomous University of Mexico, Mexico City, Mexico.

Roberto Tapia-Conyer (R)

Faculty of Medicine, National Autonomous University of Mexico, Mexico City, Mexico. tapiaconyer@gmail.com.

Classifications MeSH