The Influence of Leptin, Adiponectin and Insulin in Human Milk on the Growth of Children Exposed to Adverse Intrauterine Environments: A Prospective Cohort Study

Background: Human milk (HM) acts as a metabolic signaling pathway between mother and infant, influencing appetite regulation and child growth. This function is partly determined by the hormones leptin, adiponectin, and insulin, present in HM. This study aimed to evaluate the relationship between these hormones and somatic growth from birth to preschool age, considering pre-pregnancy maternal body mass index (BMI) and fetal exposure to different adverse intrauterine environments. Methods: This cohort study recruited postpartum women and their newborns from three hospitals in southern Brazil. Mother–child dyads were allocated into five groups according to intrauterine environment: diabetes mellitus (DM), systemic arterial hypertension, smoking, intrauterine growth restriction (IUGR), and a control group. From birth to preschool age, seven assessments were conducted, during which BMI-for-age Z-scores were recorded. Pre-pregnancy BMI was also recorded. HM samples were collected within 48 hours postpartum and at 30 days for hormone analysis. Interactions between hormone concentrations over time and between groups were analyzed using generalized estimating equations and Spearman’s correlation (ρ). Results: The number of HM samples ranged from 5 to 60, depending on group and collection time. Adiponectin concentrations differed between groups (p = 0.007), while insulin levels varied across collection periods (p < 0.001). In the smoking group, pre-pregnancy maternal BMI correlated with changes in leptin (ρ = 0.574; p = 0.032) and adiponectin concentrations (ρ = 0.732; p = 0.002). In the DM group, early postpartum HM leptin correlated with neonatal BMI-for-age Z-scores at 7 (ρ = 0.886; p = 0.019) and 15 days (ρ = 0.900; p = 0.037), while leptin at 30 days correlated with BMI-for-age Z-score at six months (ρ = 0.811; p = 0.004). In the IUGR group, this latter correlation was negative (ρ = −0.709; p = 0.015). In the early postpartum period, HM adiponectin concentration correlated with neonatal BMI-for-age Z-score at 7 days in the control group (ρ = 0.783; p = 0.003), while HM insulin concentration at 30 days correlated with infant BMI-for-age Z-score at six months in the smoking group (ρ = 0.697; p = 0.025). Conclusions: Variations in HM insulin and adiponectin concentrations were positively associated with pre-pregnancy maternal BMI in the smoking group, while specific correlations between HM hormones and children’s BMI-for-age Z-scores were identified across groups.