» Articles » PMID: 19095778

Relationship of Adiposity with Arterial Stiffness As Mediated by Adiponectin in Older Men and Women: the Hoorn Study

Overview
Specialty Endocrinology
Date 2008 Dec 20
PMID 19095778
Citations 26
Authors
Affiliations
Soon will be listed here.
Abstract

Objective: To investigate whether adiponectin is associated with arterial stiffness, and whether adiponectin explains the association between body composition and arterial stiffness.

Design: Cross-sectional cohort study.

Methods: Subjects were participants (n=456, mean age 68.9+/-6.1 years; age range 60-86 years) of the third follow-up examination of the Hoorn Study. Trunk fat, leg fat, trunk lean, and leg lean mass were measured by dual-energy X-ray absorptiometry. Ultrasound was used to measure distensibility and compliance of the carotid, femoral, and brachial arteries, and carotid Young's elastic modulus (as estimates of peripheral arterial stiffness). Results Trunk fat mass was negatively associated with (ln-transformed) adiponectin (standardized beta=-0.49, P<0.001), while leg fat mass was positively associated with adiponectin (beta=0.44, P<0.001), after adjustment for each other, age, and lean mass. After adjustment for age, sex, mean arterial pressure, and estimated glomerular filtration rate, higher adiponectin was associated with decreased peripheral arterial stiffness (beta of mean Z-scores of all three arteries=0.14, P=0.001). However, the associations of trunk fat (beta=-0.26, P<0.001) and leg fat (beta=0.16, P=0.006) with peripheral arterial stiffness were only minimally explained by adiponectin levels.

Conclusion: Trunk fat and leg fat are oppositely associated with adiponectin. Although low adiponectin was a determinant of increased peripheral arterial stiffness, it only explained a small part of the association between body fat and peripheral arterial stiffness. This indicated that factors other than adiponectin may be more important in the pathophysiological mechanisms by which abdominal obesity leads to arterial stiffness.

Citing Articles

Mendelian randomization analysis reveals causal factors behind diabetic nephropathy: evidence, opportunities, and challenges.

Huang Q, An C, Tang S, Leng Y, Zhang Y, Wan B Front Endocrinol (Lausanne). 2024; 15:1444808.

PMID: 39735650 PMC: 11671268. DOI: 10.3389/fendo.2024.1444808.


Relationships between body fat distribution and metabolic syndrome traits and outcomes: A mendelian randomization study.

Huang B, DePaolo J, Judy R, Shakt G, Witschey W, Levin M PLoS One. 2023; 18(10):e0293017.

PMID: 37883456 PMC: 10602264. DOI: 10.1371/journal.pone.0293017.


Genetically predicted body fat mass and distribution with diabetic kidney disease: A two-sample Mendelian randomization study.

Wang M, Li X, Mei H, Huang Z, Liu Y, Zhu Y Front Genet. 2022; 13:872962.

PMID: 36246637 PMC: 9557077. DOI: 10.3389/fgene.2022.872962.


The negative association of lower body fat mass with cardiometabolic disease risk factors is partially mediated by adiponectin.

Gradidge P, Jaff N, Norris S, Toman M, Crowther N Endocr Connect. 2022; 11(12).

PMID: 36169024 PMC: 9641776. DOI: 10.1530/EC-22-0156.


The Combination of High Levels of Adiponectin and Insulin Resistance Are Affected by Aging in Non-Obese Old Peoples.

Muratsu J, Kamide K, Fujimoto T, Takeya Y, Sugimoto K, Taniyama Y Front Endocrinol (Lausanne). 2022; 12:805244.

PMID: 35069451 PMC: 8777034. DOI: 10.3389/fendo.2021.805244.