Abstract
BackgroundHypoadiponectinemia has been associated with various cardiometabolic disease states. Previous studies in adults have shown that adiponectin levels were regulated by specific genetic and behavioral or lifestyle factors. However, little is known about the influence of these factors on adiponectin levels in children, particularly as mitigated by pubertal development.MethodsWe performed a cross-sectional analysis of data from 3,402 children aged 6-18 years from the Beijing Child and Adolescent Metabolic Syndrome (BCAMS) study. Pubertal progress was classified as prepubertal, midpuberty, and postpuberty. Six relevant single nucleotide polymorphisms (SNPs) were selected from previous genome-wide association studies of adiponectin in East Asians. Individual SNPs and two weighted genetic predisposition scores, as well as their interactions with 14 lifestyle factors, were analyzed to investigate their influence on adiponectin levels across puberty. The effect of these factors on adiponectin was analyzed using general linear models adjusted for age, sex, and BMI.ResultsAfter adjustment for age, sex, and BMI, the associations between adiponectin levels and diet items, and diet score were significant at prepuberty or postpuberty, while the effect of exercise on adiponectin levels was more prominent at mid- and postpuberty. Walking to school was found to be associated with increased adiponectin levels throughout puberty. Meanwhile, the effect of WDR11-FGFR2-rs3943077 was stronger at midpuberty (P = 0.002), and ADIPOQ-rs6773957 was more effective at postpuberty (P = 0.005), while CDH13-rs4783244 showed the strongest association with adiponectin levels at all pubertal stages (all P < 3.24 × 10-15). We further found that effects of diet score (P interaction = 0.022) and exercise (P interaction = 0.049) were stronger in children with higher genetic risk of hypoadiponectinemia, while higher diet score and exercise frequency attenuated the differences in adiponectin levels among children with different genetic risks.ConclusionsOur study confirmed puberty modulates the associations between adiponectin, and genetic variants, lifestyle factors, and gene-by-lifestyle interactions. These findings provide new insight into puberty-specific lifestyle suggestions, especially in genetically susceptible individuals.
Highlights
Childhood obesity has emerged as a global public health problem, in part due to its association with cardiometabolic disease [1]
Adiponectin levels significantly decreased after the onset of puberty, and adiponectin levels were higher in girls after adjusting for age
In line with Genome-wide association study (GWAS) conducted in adults, we found that ADIPOQ-rs10937273, ADIPOQ-rs6773957, CDH13rs4783244, WDR11-FGFR2-rs3943077, and PEPD-rs889140 were associated with adiponectin levels among school children
Summary
Childhood obesity has emerged as a global public health problem, in part due to its association with cardiometabolic disease [1]. The mechanisms responsible for obesity’s contribution to cardiometabolic risk, like adipocyte metabolic dysregulation, remain unclear [4]. Known as hypoadiponectinemia, and a marker of adipose tissue dysfunction, and the condition that is common in obesity [7], have been robustly associated with an increased risk of insulin resistance, diabetes, cardiovascular diseases, and certain kinds of cancer [8, 9]. Adiponectin is regarded as a protective molecule and a potentially novel therapeutic target for diabetes and related diseases [10]. Some diabetes drugs, such as rosiglitazone, operate partially by increasing circulating adiponectin levels [11]. Little is known about the influence of these factors on adiponectin levels in children, as mitigated by pubertal development
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