1316-P: Adiponectin-Related Genetic Variation and Dietary Pattern Associations with Metabolic Health in Children across Weight Status: From a Large Cohort Study

Abstract

Adiponectin and related genetic variants are associated with adipose tissue function and cardio-metabolic risks. Moreover, dietary patterns affect metabolic health partly through modulating secretion of adiponectin from adipose tissue. We aimed to examine interactions between adiponectin related genetic variants and dietary patterns on metabolic health in different weight status. Childhood lifestyle factors, adiponectin and six related genetic variants (loci in/near ADIPOQ, CDH13, WDR11FGF, CMIP and PEPD) from GWAS were assessed in 3,482 children aged 6-18 years from BCAMS cohort in 2004. In 2015, 352 of these individuals completed an in-depth follow-up examination. Being metabolically unhealthy was defined as having any metabolic syndrome component or a HOMA-IR≥3.0. In multiple models, rs6773957 at ADIPOQ locus (OR=1.25, 95% CI=1.08-1.46, P =0.004) and rs4783244 at adiponectin receptor CDH13 locus (OR=0.83, 95% CI =0.70-0.98, P =0.025) were significantly correlated with metabolic risks independent of adiponectin levels and life-style factors in normal weight children, and these associations were less obvious in overweight/obesity group. Moreover, we observed a significant interaction effect between rs6773957 and dietary patterns (P =0.008) for metabolic health in normal weight children. The adiponectin-decreasing allele at rs6773957 locus was associated with greater metabolic risks in response to unfavorable dietary patterns, while no significant genotype effect was found in healthy dietary patterns. Similar interaction was found in the subgroup analysis using longitudinal data (P=0.033). In conclusion, healthy dietary patterns might affect adiponectin gene expression, which may particularly improve adipose tissue function and metabolic health independently of weight change. ADIPOQ locus confers more metabolic risks in healthy dietary patterns when contrasted with adverse dietary patterns. Disclosure S. Gao: None. G. Li: None. S.M. Willi: Advisory Panel; Self; Boehringer Ingelheim Pharmaceuticals, Inc., Roche Diagnostic USA. Research Support; Self; Jaeb Center for Health Research, National Institute of Allergy and Infectious Diseases, Sanofi-Aventis. Other Relationship; Self; National Institute of Diabetes and Digestive and Kidney Diseases. M. Li: None. Funding National Key Research and Development 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 (2011A002); National Key Program of Clinical Science (WBYZ2011-873); Chinese Academy of Medical Sciences (2017PT32020, 2018PT32001); Jingxi Scientific Program of Beijing Chaoyang Hospital (JXPY201606)