Ochoa-Rosales Carolina, Mardones Lorena, Villagrán Marcelo, Aguayo Claudio, Martorell Miquel, Celis-Morales Carlos, Ulloa Natalia
Latin American Brain Health Institute (BrainLat), Universidad Adolfo Ibáñez, Santiago 7941169, Chile.
Centro de Vida Saludable, Universidad de Concepción, Concepción 4070374, Chile.
Children (Basel). 2023 Feb 22;10(3):426. doi: 10.3390/children10030426.
Children carrying the minor allele 'A' at the fat mass and obesity-associated protein ( gene have higher obesity prevalence. We examined the link between rs9939609 polymorphism and plasma adiponectin and the mediating role of body adiposity, in a cross-sectional study comprising 323 children aged 6-11 years. Adiponectin and genotypes were assessed using a commercial kit and a real-time polymerase chain reaction with high-resolution melting analysis, respectively. Body adiposity included body mass index z-score, body fat percentage and waist-to-hip ratio. To investigate adiponectin (outcome) associations with and adiposity, linear regressions were implemented in additive models and across genotype categories, adjusting for sex, age and Tanner's stage. Using mediation analysis, we determined the proportion of the association adiponectin- mediated by body adiposity. Lower adiponectin concentrations were associated with one additional risk allele (β = -0.075 log-μg/mL [-0.124; -0.025]), a homozygous risk genotype (β = -0.150 [-0.253; -0.048]) and a higher body mass index z-score (β = -0.130 [-0.176; -0.085]). Similar results were obtained for body fat percentage and waist-to-hip ratio. Body adiposity may mediate up to 29.8% of the -adiponectin association. In conclusion, rs9939609-related differences in body adiposity may partially explain lower adiponectin concentrations. Further studies need to disentangle the biological pathways independent from body adiposity.
携带脂肪量和肥胖相关蛋白（基因）次要等位基因“A”的儿童肥胖患病率更高。在一项包含323名6至11岁儿童的横断面研究中，我们研究了rs9939609多态性与血浆脂联素之间的联系以及身体肥胖的中介作用。分别使用商业试剂盒和带有高分辨率熔解分析的实时聚合酶链反应评估脂联素和基因型。身体肥胖包括体重指数z评分、体脂百分比和腰臀比。为了研究脂联素（结果）与和肥胖的关联，在加性模型中并跨基因型类别进行线性回归，同时调整性别、年龄和坦纳分期。使用中介分析，我们确定了由身体肥胖介导的脂联素关联的比例。较低的脂联素浓度与一个额外的风险等位基因（β = -0.075 log-μg/mL [-0.124; -0.025]）、纯合风险基因型（β = -0.150 [-0.253; -0.048]）以及较高的体重指数z评分（β = -0.130 [-0.176; -0.085]）相关。体脂百分比和腰臀比也得到了类似结果。身体肥胖可能介导高达29.8%的脂联素关联。总之，rs9939609相关的身体肥胖差异可能部分解释了较低的脂联素浓度。需要进一步研究理清独立于身体肥胖的生物学途径。
