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

• Main Authors: Zoya Gridneva, Sambavi Kugananthan, Alethea Rea, Ching Tat Lai, Leigh C. Ward, Kevin Murray, Peter E. Hartmann, Donna T. Geddes
• Format: Article
• Language: English
• Published: MDPI AG 2018-08-01
• Series: Nutrients
• Subjects: adipokines; adiponectin; leptin; breastfeeding; infant; body composition; bioelectrical impedance spectroscopy; ultrasound skinfolds; human milk; lactation
• Online Access: http://www.mdpi.com/2072-6643/10/8/1125

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.