Atherosclerosis · 2020
Impact of parental smoking on adipokine profiles and cardiometabolic risk factors in Chinese children.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод пока не подготовлен
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Li Yu, Wang Dongmei, Wang Yuhan, Zhao Yanglu, Han Lanwen, Zhong Ling, Zhang Qian, Speakman John R, Li Ming, Gao Shan
Аннотация
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.
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.