4.7 Article

Human Milk Adiponectin and Leptin and Infant Body Composition over the First 12 Months of Lactation

Journal

NUTRIENTS
Volume 10, Issue 8, Pages -

Publisher

MDPI
DOI: 10.3390/nu10081125

Keywords

adipokines; adiponectin; leptin; breastfeeding; infant; body composition; bioelectrical impedance spectroscopy; ultrasound skinfolds; human milk; lactation

Funding

  1. Medela AG (Switzerland)
  2. Australian Postgraduate Award from University of Western Australia (Australia)
  3. Margaret Lomann-Hall Scholarship from School of Human Sciences, The University of Western Australia (Australia)

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Human milk (HM) adipokines may influence infant feeding patterns, appetite regulation, and body composition (BC). The associations between concentrations/calculated daily intakes (CDI) of HM adipokines in the first 12 months postpartum and maternal/term infant BC, and infant breastfeeding parameters were investigated. BC of breastfeeding dyads (n = 20) was measured at 2, 5, 9, and/or 12 months postpartum with ultrasound skinfolds (infants) and bioimpedance spectroscopy (infants/mothers). 24-h milk intake and feeding frequency were measured along with whole milk adiponectin and skim and whole milk leptin (SML and WML) and CDI were calculated. Statistical analysis used linear regression/mixed effects models; results were adjusted for multiple comparisons. Adipokine concentrations did not associate with infant BC. Higher CDI of adiponectin were associated with lower infant fat-free mass (FFM; p = 0.005) and FFM index (FFMI; p = 0.009) and higher fat mass (FM; p < 0.001), FM index (FMI; p < 0.001), and %FM (p < 0.001). Higher CDI of SML were associated with higher infant FM (p < 0.001), FMI (p < 0.001), and %FM (p = 0.002). At 12 months, higher CDI of WML were associated with larger increases in infant adiposity (2-12 month: FM, p = 0.0006; %FM, p = 0.0004); higher CDI of SML were associated with a larger decrease in FFMI (5-12 months: p = 0.0004). Intakes of HM adipokines differentially influence development of infant BC in the first year of life, which is a critical window of infant programming and may potentially influence risk of later disease via modulation of BC.

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