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Background: Lipocalin-2 (LCN-2) has been identified as an osteoblast-secreted hormone regulating immunity, inflammation and metabolic homeostasis and has emerged as a diagnostic and prognostic biomarker for acute kidney injury in neonates. We investigated the impact of fetal growth on antepartum maternal serum, cord serum and breast milk LCN-2 concentrations and the associations of the latter with perinatal parameters., Methods: Maternal serum, cord serum and breast milk LCN-2 concentrations were measured by ELISA in samples from 80 mothers who delivered 40 appropriate (AGA), 20 large for gestational age (LGA) and 20 intrauterine growth restricted (IUGR) neonates, classified by customized weight centiles. LCN-2 concentrations were associated with birth weight, customized centile, gender, maternal age and delivery mode., Results: Antepartum maternal serum LCN-2 concentrations were significantly higher in women delivering AGA infants compared to the other two groups. Cord blood LCN-2 concentrations were significantly higher compared to maternal ones; furthermore, they were significantly elevated in the IUGR group compared to the LGA one ( p = .019). Lowest concentrations were detected in breast milk, which did not differ between the three growth groups. A negative correlation was documented between cord blood LCN-2 concentrations and customized centiles ( r : -0.304, p = .007)., Conclusions: The higher cord serum LCN-2 concentrations, compared to maternal ones, may point to its fetal origin and potential role in intrauterine growth. The negative correlation of cord LCN-2 concentrations with customized centiles, possibly implies reduced nephron endowment/subclinical kidney damage in IUGR neonates. The extremely low LCN-2 breast milk concentrations could imply that the secretion of LCN-2 from maternal circulation to breast milk is not influenced by factors leading to intrauterine growth pathology.

Background/objective: To study the concentrations of preadipocyte factor-1 (Pref-1) -an inhibitor of adipocyte differentiation, implicated in adipose tissue metabolism, late metabolic disorders and fetal growth- in maternal and umbilical cord serum, as well as maternal milk and correlate above concentrations with intrauterine growth and other perinatal parameters., Material and Methods: Pref-1 concentrations were determined by ELISA in antepartum maternal and umbilical cord serum, as well as day 3 to 4 postpartum breast milk, deriving from 80 women, who delivered 40 appropriate (AGA), 20 large for gestational age (LGA) and 20 intrauterine growth restricted (IUGR) neonates, classified by the use of customized birth-weight standards adjusted for significant determinants of fetal growth., Results: Umbilical cord serum Pref-1 concentrations were significantly higher than antepartum maternal ones (p < 0.001), while breast milk concentrations were the lowest (p < 0.001 concerning umbilical serum, p < 0.001 concerning maternal serum). Umbilical cord serum Pref-1 concentrations were significantly lower in the LGA group than in the AGA one (p = 0.044). Breast milk and maternal serum Pref-1 concentrations did not differ between the three intrauterine growth groups. Maternal serum and breast milk Pref-1 concentrations did not correlate with maternal age, body mass index before and after gestation, birth weight, body length, and customized centile. A positive weak correlation was recorded between maternal serum and milk Pref-1 concentrations (r = 0.238, p = 0.034)., Conclusions: Pref-1 concentrations in umbilical cord serum are higher than in antepartum maternal serum, probably pointing to its fetal origin and role in intrauterine growth. Breast milk concentrations, being extremely low, and possibly implying infant protection from metabolic disorders, positively correlate with maternal serum ones, conceivably suggesting a transfer of the substance from the circulation to the breast. Umbilical cord serum Pref-1 concentrations were lower in LGA fetuses/neonates, as compared to respective AGA ones., (Copyright © 2018 Elsevier Ltd. All rights reserved.)

Objective: To prospectively investigate maternal concentrations of the myokine irisin in large for gestational age (LGA) and intrauterine growth restricted (IUGR) versus appropriate for gestational age (AGA) normal pregnancies and associate them with various perinatal parameters., Methods: Plasma irisin and insulin concentrations were measured by enzyme-linked immunosorbent assay (ELISA) and immunoradiometric assay (IRMA), respectively, in a cohort of 80 mothers delivering LGA (n = 30), IUGR (n = 30) and AGA (n = 20) singleton full-term infants., Results: Maternal irisin concentrations were similar among LGA, IUGR and AGA groups and did not correlate with respective insulin ones or maternal body mass index. In a combined group, maternal irisin concentrations decreased with advancing gestational age (p < 0.001) and were lower in multi-, compared to nulliparous women (p = 0.004). In the IUGR group, maternal irisin concentrations were higher in cases of smoking (p = 0.006)., Conclusions: Irisin may not be differentially regulated in insulin resistance-associated pregnancy disorders resulting in fetal macrosomia and IUGR. Maternal irisin down-regulation with advancing gestation could possibly contribute to the observed maternal fat accumulation and progressive insulin resistance towards term. Similarly, lower maternal irisin concentrations in multiparous women may reflect the documented positive association between parity and fat deposition. Irisin up-regulation in cases of smoking may indicate the need for enhanced oxygen consumption to maintain energy production under conditions of hypoxia.

Objective: To determine levels of adropin (implicated in insulin resistance and endothelial dysfunction) in intrauterine growth restricted (IUGR), large (LGA) and appropriate for gestational age (AGA) pregnancies., Methods: Cord-blood (UC) adropin and insulin concentrations were measured in 30 IUGR, 30 LGA and 20 AGA full-term infants and their mothers (MS)., Results: No significant differences in adropin concentrations were observed between the three groups. In the IUGR group MS adropin was significantly decreased when neonates had higher birth weights [b = -0.003, 95% CI -0.006 to 0.0, p = 0.043]. In all groups, MS adropin levels were positively correlated with UC ones (r = 0.282, p = 0.011) and were significantly increased in female neonates [b = 0.977, 95% CI 0.122-1.832, p = 0.026]. In the LGA group, MS insulin was negatively correlated with UC adropin (r =  -0.362 p = 0.049)., Conclusions: Increased maternal adropin levels in severe IUGR cases might represent a regulatory feedback mechanism against endothelial placental dysfunction. The positive correlation between maternal and umbilical cord adropin levels implies its transplacental transfer. Increased maternal adropin levels in female neonates could be attributed to interaction of adropin with fetal estrogens through vascular endothelial growth factor (VEGF). The negative correlation between maternal insulin and fetal adropin levels in the LGA group is probably attributed to their respective insulin resistance.

Background/aims: Irisin, a novel myokine with antiobesity properties, drives brown-fat-like conversion of white adipose tissue, thus increasing energy expenditure and improving glucose tolerance. We aimed to investigate circulating irisin concentrations in large-for-gestational-age (LGA) and intrauterine-growth-restricted (IUGR) fetuses, both associated with metabolic dysregulation and long-term susceptibility to obesity and metabolic syndrome development., Methods: Plasma irisin and insulin concentrations were determined by ELISA and IRMA, respectively, in 80 mixed arteriovenous cord blood samples from LGA (n=30), IUGR (n=30) and appropriate-for-gestational-age (AGA, n=20) singleton full-term pregnancies. Fetuses were classified as LGA, IUGR or AGA, based on customized birth-weight standards adjusted for significant determinants of fetal growth., Results: Fetal irisin concentrations were lower in IUGR cases than AGA controls (p=0.031). Cord blood irisin concentrations were similar in LGA and AGA groups and positively correlated with birth-weight, as well as customized centiles (r=0.245, p=0.029 and r=0.247, p=0.027, respectively). Insulin concentrations were higher in LGA, compared to AGA fetuses (p=0.036). In the LGA group, fetal irisin concentrations positively correlated with fetal insulin concentrations (r=0.374, p=0.042)., Conclusions: Impaired skeletal muscle metabolism in IUGR fetuses may account for their irisin deficiency, which may be part of the fetal programming process, leading to increased susceptibility to later metabolic syndrome development. Furthermore, irisin down-regulation may predispose IUGR infants to hypothermia at birth, by inducing less "browning" of their adipose tissue and consequently less non-shivering thermogenesis. Irisin upregulation with increasing birth-weight may contribute to a slower fat gain during early infancy ("catch-down"), by promoting higher total energy expenditure. The positive correlation between irisin and insulin in the LGA group may reflect a counterbalance of the documented hyperinsulinemia, which is partly responsible for the excessive fat deposition in the LGA fetus., (Copyright © 2015 Elsevier Inc. All rights reserved.)

Objective: IGF-I and insulin are the main regulators of intrauterine and postnatal growth. Adipose tissue secreted cytokines are implicated in intrauterine growth. The relevant function of the adipocytokine visfatin is unknown., Materials and Methods: Serum visfatin, IGF-I and insulin levels were measured by enzyme immunoassays in 40 singleton full-term fetuses and neonates on postnatal days 1(N1) and 4 (N4)., Results: No significant correlations exist between visfatin and IGF-I or insulin. N1 and N4 visfatin positively correlated with customized (adjusted) birth weight centiles (r=0.511, P=0.021, and r=0.597, P=0.005, respectively). Fetal and N1 IGF-I positively correlated with customized centiles (r=0.608, P<0.001 and r=0.485, P=0.006, respectively). Fetal insulin positively correlated with customized centiles (r=0.654, P=0.021)., Conclusions: Potential implication of visfatin in fetal growth is probably not mediated by IGF-I or insulin. Although a more active role cannot be excluded, visfatin may simply represent a marker of fat accumulation.