1257-P: Impact of Parental Smoking on Adipokine Profiles and Cardiometabolic Risk Factors in Chinese Children: The Beijing Child and Adolescent Metabolic Syndrome Cohort Study

Abstract

Exposure to secondhand smoke has relatively recently been recognized to be an important modifiable risk factor for obesity and cardiovascular disease, along with unhealthy diet, sedentary lifestyle and insufficient sleep. The mechanism(s) by which passive smoking imparts this risk and the tissues involved still require elucidation. We aimed to evaluate the association between parental smoking exposure (PSE), secretion of adipokines and cardiometabolic risk in Chinese children. A total of 3150 children (6-18ys) from the Beijing Child and Adolescent Metabolic Syndrome (MetS) study with data on PSE and potential confounders (pubertal stage, physical activity, diet and socioeconomic factors plus family history) were included. Six adipokines related to insulin resistance and MetS (leptin, adiponectin, retinol binding protein 4 (RBP4), fibroblast growth factor 21 (FGF-21), resistin and osteonectin) were measured. Of those children studied, nearly 65% reported PSE, defined as smoking in either parent. After adjusting for covariates, including pubertal stage, lifestyle factors, and family history, PSE was independently associated with increases of 39.2% in leptin and 3.9% in RBP-4 and decreases of 11.4% in FGF-21 and 4.6% in adiponectin levels (P < 0.05 for all). The risks of central obesity (OR 1.59, 95% CI 1.33-1.90, P < 0.001), hyperglycemia (OR 1.30, 95%CI 1.02-1.66, P<0.05), hypertension (1.22, 1.02-1.46, P = 0.001) and MetS (1.43, 1.11-1.85, P < 0.001) were all increased with PSE. However, the associations of PSE with hypertension and MetS were abolished after adjusting for adiposity parameters or the above-mentioned adipokines. In contrast, PSE was still associated with increased risk of hyperglycemia after adjusting for BMI in boys (OR 1.42, 95%CI: 1.01-2.00, P<0.05). Our findings suggest that PSE was associated with dysregulation of adipokine levels, which may mediate the development of MetS in early life. Disclosure M. Li: None. Q. Zhang: None. S. Gao: None. S.M. Willi: Advisory Panel; Self; Boehringer Ingelheim International GmbH. Research Support; Self; Eli Lilly and Company, Janssen Pharmaceuticals, Inc., Tolerion, Inc. Other Relationship; Self; Caladrius Biosciences, Inc. Funding National Natural Science Foundation of China (81970732); National Key Research and Development Program of China (2016YFC1304801); Key Program of Beijing Municipal Science and Technology Commission (D111100000611001, D111100000611002); Beijing Natural Science Foundation (7172169); Beijing Science and Technology Star Program (2004A027); Novo Nordisk Union Diabetes Research Talent Fund (2011A002); National Key Program of Clinical Science (WBYZ2011-873); Central Research Institute Fund of Chinese Academy of Medical Sciences (2017PT32020, 2018PT32001)