RESUMO
WHAT IS ALREADY KNOWN ABOUT THIS SUBJECT: Mexican-American children are at particularly high risk of obesity. Features of the perinatal environment, including maternal nutrition, anthropometry, glucose tolerance and growth rate during infancy are implicated in programming of obesity in the offspring. WHAT THIS STUDY ADDS: Greater rate of weight or length gain in the first 6 months of life is associated with lower 9-year child adiponectin levels, adjusting for 9-year child BMI. Nine-year-old child adipokine levels are strongly related to those of their mothers'. OBJECTIVES: To (i) determine whether perinatal factors (including maternal anthropometry and nutrition and early life growth measures) are associated with adiponectin and leptin levels in 9-year-old children, and (ii) assess relationships between adiponectin, leptin and concurrent lipid profile in these children. METHODS: We measured plasma adiponectin and leptin for 146 mothers-9-year-old child pairs from the ongoing longitudinal birth cohort followed by the Center for the Health Assessment of Mothers and Children of Salinas. Data on perinatal factors, including sociodemographics, maternal anthropometry and nutrition, and early life child growth were collected during pregnancy, birth and 6-month visits. RESULTS: Greater rate of weight and length gain during the first 6 months of life were associated with lower adiponectin in 9-year-olds (ß = -2.0, P = 0.04; ß = -8.2, P = 0.02, respectively) adjusting for child body mass index (BMI). We found no associations between child adipokine levels and either maternal calorie, protein, total fat, saturated fat, fibre, sugar-sweetened beverage consumption during pregnancy or children's concurrent sugar-sweetened beverage and fast food intake. Lipid profile in 9-year-old children closely reflected adiponectin but not leptin levels after adjustment for child BMI. Additionally, we report that child adipokine levels were closely related to their mothers' levels at the 9-year visit. CONCLUSION: Overall, our results support the hypothesis that early life factors may contribute to altered adipokine levels in children.