Background: In spite of high rates of initiating breast milk feeding (BMF) among preterm infants, a significant rate of discontinuation occurs shortly after discharge. Aim: To investigate the effect of mode (direct feeding at the breast vs. expressing) and exclusivity (breast milk combined with formula vs. breast milk only) as well as maternal perceptions on the duration of BMF among preterm infants. Methods: The study included mothers whose infants were born before 32 weeks gestation, between January 2012 and August 2015 at Sheba Medical Center (SMC). Perinatal data were collected retrospectively from infants’ computerized charts. Mothers were approached >12 months postpartum and were asked to complete a questionnaire. Those who agreed to participate were asked (during their visit to the follow-up clinic or by phone or mail) to complete a questionnaire regarding mode and duration of BMF as well as reasons for its discontinuation. Mothers were also asked about their pre-partum intentions to feed directly at the breast. Results: Out of 162 eligible mothers, 131 (80.8%) initiated BMF during their intensive care unit (ICU) hospitalization. Of these, 66 (50.3%) discontinued BMF earlier than six months postpartum. BMF ≥ 6 months was significantly associated with direct feeding at the breast, duration of exclusive BMF, and singleton birth. Regression analysis revealed that direct feeding at the breast (any or only) and duration of BMF exclusivity were the only significant variables associated with BMF duration (Odds ratio (OR) 5.5 and 95% confidence interval (CI) 2.00–15.37; OR 1.5 and 95% CI 1.25–1.88, respectively). Milk supply (inadequate or nonexistent) was the most commonly reported cause for BMF discontinuation <6 months. Direct feeding at the breast was significantly associated with BMF duration and was more common among singletons. Conclusions: Direct feeding at the breast and duration of exclusive BMF are associated with duration of BMF among infants born <32 weeks of gestational age (GA). These findings suggest that targeting these two factors may play a key role in prolonging BMF duration among preterm infants.

During pregnancy, fetal glucose production is suppressed, with rapid activation immediately postpartum. Fatty acid–binding protein 4 (FABP4) was recently demonstrated as a regulator of hepatic glucose production and systemic metabolism in animal models. Here, we studied the role of FABP4 in regulating neonatal glucose hemostasis. Serum samples were collected from pregnant women with normoglycemia or gestational diabetes at term, from the umbilical circulation, and from the newborns within 6 hours of life. The level of FABP4 was higher in the fetal versus maternal circulation, with a further rise in neonates after birth of approximately 3-fold. Neonatal FABP4 inversely correlated with blood glucose, with an approximately 10-fold increase of FABP4 in hypoglycemic neonates. When studied in mice, blood glucose of 12-hour-old WT, Fabp4 ^–/+ , and Fabp4 ^–/– littermate mice was 59 ± 13 mg/dL, 50 ± 11 mg/dL, and 43 ± 11 mg/dL, respectively. Similar to our observations in humans, FABP4 levels in WT mouse neonates were approximately 8-fold higher compared with those in adult mice. RNA sequencing of the neonatal liver suggested altered expression of multiple glucagon-regulated pathways in Fabp4 ^–/– mice. Indeed, Fabp4 ^–/– liver glycogen was inappropriately intact, despite a marked hypoglycemia, with rapid restoration of normoglycemia upon injection of recombinant FABP4. Our data suggest an important biological role for the adipokine FABP4 in the orchestrated regulation of postnatal glucose metabolism.