Impact of parental smoking on adipokine profiles and cardiometabolic risk factors in Chinese children

Yu Li; Dongmei Wang; Yuhan Wang; Yanglu Zhao; Lanwen Han; Ling Zhong; Qian Zhang; John R Speakman; Ming Li; Shan Gao

doi:10.1016/j.atherosclerosis.2020.03.023

Impact of parental smoking on adipokine profiles and cardiometabolic risk factors in Chinese children

Yu Li, Dongmei Wang, Yuhan Wang, Yanglu Zhao, Lanwen Han, Ling Zhong, Qian Zhang, John R Speakman, Ming Li^* (Corresponding Author), Shan Gao^* (Corresponding Author)

^*Corresponding author for this work

Research output: Contribution to journal › Article › peer-review

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Abstract

BACKGROUND AND AIMS: The mechanisms by which passive smoking leads to cardiometabolic risks, and the tissues involved still require elucidation. We aimed to evaluate the association of parental smoking exposure (PSE) with the secretion of adipocyte-derived hormones and cardiometabolic risk factors in Chinese children.

METHODS: We included 3150 school children aged 6-18 years from the Beijing Child and Adolescent Metabolic Syndrome (BCAMS) study. Data on PSE and potential confounders were collected. Six adipokines related to insulin resistance and metabolic syndrome (MetS) were measured.

RESULTS: PSE was reported in nearly two-thirds of the children. After adjusting for covariates, including age, sex, pubertal stages, lifestyle factors, and family history, PSE was independently associated with increases of 39.2% in leptin and 3.9% in retinol binding protein-4 and decreases of 11.4% in fibroblast growth factor 21 and 4.6% in adiponectin levels (p < 0.05 for all), plus risks for central obesity (OR 1.59, 95% CI 1.33-1.90), elevated blood pressure (1.22, 1.02-1.46) and MetS (1.43, 1.11-1.85). However, the associations of PSE with hypertension and MetS were abolished when adjusted for adiposity parameters or the above-mentioned adipokine profiles.

CONCLUSIONS: PSE was associated with dysregulation of adipokine levels, which might mediate the development of MetS in early life.

Original language	English
Pages (from-to)	23-29
Number of pages	7
Journal	Atherosclerosis
Volume	301
Early online date	5 Apr 2020
DOIs	https://doi.org/10.1016/j.atherosclerosis.2020.03.023
Publication status	Published - 1 May 2020

Bibliographical note

Acknowledgments
We thank Prof. Jie Miandall, the BCAMS study members,and all participants for their continuing support with this research effort.

Financial support
This work was supported by National Key Research program of China (2016YFC1304801),key program of Beijing Municipal Science & Technology Commission (D111100000611001, D111100000611002), Beijing Natural Science Foundation (7172169), Beijing Science & Technology Star Program (2004A027), Novo Nordisk Union Diabetes Research Talent Fund (2011A002), National Key Program of Clinical Science (WBYZ2011-873), the Non-profit Central Research Institute Fund of Chinese Academy of Medical Sciences (2017PT32020, 2018PT32001) and Jingxi Scientific Program of Beijing Chaoyang Hospital (JXPY201606).

Keywords

Parental smoking
Cardiometabolic factors
Adiposity
Adipokines
Children

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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Li_ImpactOfParentalSmoking_VOR
© 2020 The Authors. Published by Elsevier B.V. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/BY-NC-ND/4.0/)
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Cite this

@article{74a30cd0cbc24efc8844b9e8cd77a3aa,

title = "Impact of parental smoking on adipokine profiles and cardiometabolic risk factors in Chinese children",

abstract = "BACKGROUND AND AIMS: The mechanisms by which passive smoking leads to cardiometabolic risks, and the tissues involved still require elucidation. We aimed to evaluate the association of parental smoking exposure (PSE) with the secretion of adipocyte-derived hormones and cardiometabolic risk factors in Chinese children.METHODS: We included 3150 school children aged 6-18 years from the Beijing Child and Adolescent Metabolic Syndrome (BCAMS) study. Data on PSE and potential confounders were collected. Six adipokines related to insulin resistance and metabolic syndrome (MetS) were measured.RESULTS: PSE was reported in nearly two-thirds of the children. After adjusting for covariates, including age, sex, pubertal stages, lifestyle factors, and family history, PSE was independently associated with increases of 39.2% in leptin and 3.9% in retinol binding protein-4 and decreases of 11.4% in fibroblast growth factor 21 and 4.6% in adiponectin levels (p < 0.05 for all), plus risks for central obesity (OR 1.59, 95% CI 1.33-1.90), elevated blood pressure (1.22, 1.02-1.46) and MetS (1.43, 1.11-1.85). However, the associations of PSE with hypertension and MetS were abolished when adjusted for adiposity parameters or the above-mentioned adipokine profiles.CONCLUSIONS: PSE was associated with dysregulation of adipokine levels, which might mediate the development of MetS in early life.",

keywords = "Parental smoking, Cardiometabolic factors, Adiposity, Adipokines, Children",

author = "Yu Li and Dongmei Wang and Yuhan Wang and Yanglu Zhao and Lanwen Han and Ling Zhong and Qian Zhang and Speakman, {John R} and Ming Li and Shan Gao",

note = "Acknowledgments We thank Prof. Jie Miandall, the BCAMS study members,and all participants for their continuing support with this research effort. Financial support This work was supported by National Key Research program of China (2016YFC1304801),key program of Beijing Municipal Science & Technology Commission (D111100000611001, D111100000611002), Beijing Natural Science Foundation (7172169), Beijing Science & Technology Star Program (2004A027), Novo Nordisk Union Diabetes Research Talent Fund (2011A002), National Key Program of Clinical Science (WBYZ2011-873), the Non-profit Central Research Institute Fund of Chinese Academy of Medical Sciences (2017PT32020, 2018PT32001) and Jingxi Scientific Program of Beijing Chaoyang Hospital (JXPY201606).",

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doi = "10.1016/j.atherosclerosis.2020.03.023",

language = "English",

volume = "301",

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T1 - Impact of parental smoking on adipokine profiles and cardiometabolic risk factors in Chinese children

AU - Li, Yu

AU - Wang, Dongmei

AU - Wang, Yuhan

AU - Zhao, Yanglu

AU - Han, Lanwen

AU - Zhong, Ling

AU - Zhang, Qian

AU - Speakman, John R

AU - Li, Ming

AU - Gao, Shan

N1 - Acknowledgments We thank Prof. Jie Miandall, the BCAMS study members,and all participants for their continuing support with this research effort. Financial support This work was supported by National Key Research program of China (2016YFC1304801),key program of Beijing Municipal Science & Technology Commission (D111100000611001, D111100000611002), Beijing Natural Science Foundation (7172169), Beijing Science & Technology Star Program (2004A027), Novo Nordisk Union Diabetes Research Talent Fund (2011A002), National Key Program of Clinical Science (WBYZ2011-873), the Non-profit Central Research Institute Fund of Chinese Academy of Medical Sciences (2017PT32020, 2018PT32001) and Jingxi Scientific Program of Beijing Chaoyang Hospital (JXPY201606).

PY - 2020/5/1

Y1 - 2020/5/1

N2 - BACKGROUND AND AIMS: The mechanisms by which passive smoking leads to cardiometabolic risks, and the tissues involved still require elucidation. We aimed to evaluate the association of parental smoking exposure (PSE) with the secretion of adipocyte-derived hormones and cardiometabolic risk factors in Chinese children.METHODS: We included 3150 school children aged 6-18 years from the Beijing Child and Adolescent Metabolic Syndrome (BCAMS) study. Data on PSE and potential confounders were collected. Six adipokines related to insulin resistance and metabolic syndrome (MetS) were measured.RESULTS: PSE was reported in nearly two-thirds of the children. After adjusting for covariates, including age, sex, pubertal stages, lifestyle factors, and family history, PSE was independently associated with increases of 39.2% in leptin and 3.9% in retinol binding protein-4 and decreases of 11.4% in fibroblast growth factor 21 and 4.6% in adiponectin levels (p < 0.05 for all), plus risks for central obesity (OR 1.59, 95% CI 1.33-1.90), elevated blood pressure (1.22, 1.02-1.46) and MetS (1.43, 1.11-1.85). However, the associations of PSE with hypertension and MetS were abolished when adjusted for adiposity parameters or the above-mentioned adipokine profiles.CONCLUSIONS: PSE was associated with dysregulation of adipokine levels, which might mediate the development of MetS in early life.

AB - BACKGROUND AND AIMS: The mechanisms by which passive smoking leads to cardiometabolic risks, and the tissues involved still require elucidation. We aimed to evaluate the association of parental smoking exposure (PSE) with the secretion of adipocyte-derived hormones and cardiometabolic risk factors in Chinese children.METHODS: We included 3150 school children aged 6-18 years from the Beijing Child and Adolescent Metabolic Syndrome (BCAMS) study. Data on PSE and potential confounders were collected. Six adipokines related to insulin resistance and metabolic syndrome (MetS) were measured.RESULTS: PSE was reported in nearly two-thirds of the children. After adjusting for covariates, including age, sex, pubertal stages, lifestyle factors, and family history, PSE was independently associated with increases of 39.2% in leptin and 3.9% in retinol binding protein-4 and decreases of 11.4% in fibroblast growth factor 21 and 4.6% in adiponectin levels (p < 0.05 for all), plus risks for central obesity (OR 1.59, 95% CI 1.33-1.90), elevated blood pressure (1.22, 1.02-1.46) and MetS (1.43, 1.11-1.85). However, the associations of PSE with hypertension and MetS were abolished when adjusted for adiposity parameters or the above-mentioned adipokine profiles.CONCLUSIONS: PSE was associated with dysregulation of adipokine levels, which might mediate the development of MetS in early life.

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KW - Cardiometabolic factors

KW - Adiposity

KW - Adipokines

KW - Children

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DO - 10.1016/j.atherosclerosis.2020.03.023

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SN - 0021-9150

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SP - 23

EP - 29

JO - Atherosclerosis

JF - Atherosclerosis

ER -

Impact of parental smoking on adipokine profiles and cardiometabolic risk factors in Chinese children

Abstract

Bibliographical note

Keywords

UN SDGs

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