Background. Maternal obesity and physical inactivity have been identified as correlates of overweight and obesity and physical inactivity in older preadolescents; however, no study has explored this relationship in Hispanic preadolescents. Furthermore, the relation between maternal physical activity (PA) and blood pressure (BP) in Hispanic preadolescents has not been examined. Purpose. This study aimed to assess the associations between Hispanic mothers’ PA and body mass index (BMI) and their preadolescents’ PA, screen time, BP, and BMI. Methods. Data of 118 mother-child (aged 2–10 years) dyads enrolled in a crosssectional study of metabolic syndrome in Hispanic preadolescents at a community health center in Johnson City, TN were used. Parent and child questionnaires were used to ascertain mothers’ BMI and PA and preadolescents’ PA and screen time.

Obesity develops early in childhood and is accompanied by early signs of adipose tissue (AT) dysfunction and metabolic disease in children. In order to analyse the molecular processes during obesity-related AT accumulation in children, we investigated genome-wide expression profiles in AT samples, isolated adipocytes, and stromal vascular fraction (SVF) cells and assessed their relation to obesity as well as biological and functional AT parameters. We detected alterations in gene expression associated with obesity and related parameters, i.e., BMI SDS, adipocyte size, macrophage infiltration, adiponectin, and/or leptin. While differential gene expression in AT and adipocytes shared an enrichment in metabolic pathways and pathways related to extracellular structural organisation, SVF cells showed an overrepresentation in inflammatory pathways. In adipocytes, we found the strongest positive association for epidermal growth factor-like protein 6 (EGFL6) with adipocyte hypertrophy. EGFL6 was also upregulated during in vitro adipocyte differentiation. In children, EGFL6 expression was positively correlated to parameters of AT dysfunction and metabolic disease such as macrophage infiltration into AT, hs-CRP, leptin levels, and HOMA-IR. In conclusion, we provide evidence for early alterations in AT gene expression related to AT dysfunction in children and identified EGFL6 as potentially being involved in processes underlying the pathogenesis of metabolic disease.