Neonatal Leptin Research Articles

Maternal and neonatal serum leptin levels in normal and diabetic pregnant egyptian women

International Journal of Gynecology & ObstetricsVolume 70, Issue S4 p. D84-D84 Poster Antenatal care and diagnosis Maternal and neonatal serum leptin levels in normal and diabetic pregnant egyptian women A. El-Adawy, A. El-AdawySearch for more papers by this authorM. Ibrahim, M. IbrahimSearch for more papers by this authorO. Gohar, O. GoharSearch for more papers by this authorKasr El-Aini, Kasr El-AiniSearch for more papers by this author A. El-Adawy, A. El-AdawySearch for more papers by this authorM. Ibrahim, M. IbrahimSearch for more papers by this authorO. Gohar, O. GoharSearch for more papers by this authorKasr El-Aini, Kasr El-AiniSearch for more papers by this author First published: 11 December 2003 https://doi.org/10.1016/S0020-7292(00)84410-0AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat No abstract is available for this article. Volume70, IssueS42000Pages D84-D84 RelatedInformation

Effect of Intracerebroventricular Leptin Administration on Body Weight Gain in Neonatal Rats † 1581

Leptin, the secreted and translated product of the ob gene, acts upon the adult hypothalamus and decreases appetite and body weight gain. While neonatal rat and mouse adipocytic leptin mRNA and circulating peptide have been detected (FASB J 11:382-387, 1997; BBRC 238:44-47, 1997), and neonatal rat hypothalamic leptin receptors characterized (Ped Res 1998), the biological significance of leptin in the newborn remains unknown. To address this issue, 2 to 8 day old rats received intracerebroventricularly 0.5 μg (n=3) and 1μg (n=3) of murine leptin or vehicle (n=6) on a daily basis. In comparison to the vehicle group, a ≈27% body weight loss was noted in the 0.5 μg and 1 μg leptin groups by day 7 (leptin=8±0.5g vs vehicle=10.9±0.7g; p < 0.05). This weight loss persisted through day 9 (leptin=11.1±0.1g vs vehicle=15.5±0.3g; p < 0.05), declined to ≈11% by day 16 (leptin= 30.1±3g vs vehicle=36.9±0.7g; p< 0.05), and was no different at day 24. Though no change in plasma leptin or glucose concentrations was noted throughout, an increase in plasma insulin was observed only at day 3 in the 1μg leptin group (4.9±0.1 vs the vehicle group= 2.9±0.8 ng/ml; p < 0.05). In an attempt to determine the central mechanism(s) by which leptin induced this neonatal body weight loss, semi-quantitation of paraventricular neuropeptide Y immunoreactivity(NPY; aerence in NPY amounts was detected at 3d which is 24 hours following initiation of leptin administration. This is in contrast to our previous investigations where intracerebroventricular NPY led to biological changes within 24 hours (Varma et al Ped Res 41:1441, 1997). Studies assessing hypothalamic NPY levels between 7 to 24 days are in progress. We conclude that 1] exogenous intracerebroventricular leptin administration reduces body weight during the suckling phase, and 2] the anorexic/catabolic effect is observed 5 days after initiation of intracerebroventricular leptin injections. We speculate that the hypothalamic mechanism(s) for this biological response may include reduction in NPY synthesis/levels at later ages (7 to 24 d), or even perturbations in other anorexic neuro peptides(corticotropin-releasing hormone, proopiomelanocortin).

Ontogeny of leptin in human fetuses and newborns: effect of intrauterine growth retardation on serum leptin concentrations.

The aim of this study was to investigate the ontogeny of serum leptin concentrations during the second half of gestation and at birth in small for gestational age and normal fetuses and newborns. Serum leptin concentrations were measured in arterial cord blood of fetuses (n = 79) and newborns (n = 132), with or without intrauterine growth retardation, at 18-42 weeks gestation. Serum leptin was detectable in fetal cord blood in all subjects as early as 18 weeks gestation. Leptin levels dramatically increased after 34 weeks gestation. In newborns, serum leptin concentrations were positively correlated with body weight (P < 0.001) and body mass index (P < 0.001). Newborns with intrauterine growth retardation had significantly lower serum leptin values (P < 0.001) than those with normal growth, and leptin levels were only positively correlated with body mass index (P < 0.001). These results suggest that the development of adipose tissue and the accumulation of fat mass are the major determinants of fetal and neonatal serum leptin levels. In addition, a gender difference, with higher leptin concentrations in female fetuses, was observed during the last weeks of gestation and was confirmed at birth regardless of growth status, suggesting that a sexual dimorphism already exists in utero.

Neonatal cord blood leptin: its relationship to birth weight, body mass index, maternal diabetes, and steroids.

Leptin is a 16-kD protein encoded by the ob/ob (obesity) gene. In rodents it plays a role in obesity, diabetes, fertility, and neuroendocrine function. In humans serum concentrations of leptin correlate with total body fat in both adults and children. We measured cord blood leptin in 186 neonates that included 82 appropriate for gestational age (AGA), 47 large for gestational age (LGA), 20 infants of diabetic mothers, 52 preterm infants, and 15 intrauterine growth-retarded (IUGR) infants. There were 16 pairs of twins. The mothers of 17 preterm infants were treated with steroids before delivery. Leptin (mean +/- SD) concentration in term, AGA infants (39.4 +/- 1.1 wk) with birth weight (BW) of 3.2 +/- 0.3 kg, body mass index (BMI) of 12.6 +/- 1.1 was 4.01 +/- 3.5 ng/mL. BW correlated with cord leptin (p = 0.002) in a multivariate analysis controlling for potential confounders. Both LGA infants and infants of diabetic mothers had higher cord leptin concentration 7.3 +/- 3.8 and 6.1 +/- 4.8 ng/mL, respectively, compared with AGA infants (p < 0.05). Preterm infants had a mean leptin level of 1.8 +/- 0.97 ng/mL and a 3-fold elevation was seen if mothers received steroids antenatally (p = 0.006). IUGR infants had increased leptin (6.5 +/- 3.9 ng/mL, p = 0.03). Concerning the twin pairs, the smaller had a higher leptin level compared with larger twin (4.1 +/- 9.51 versus 2.8 +/- 5.14, p = NS). Neonatal cord leptin concentrations correlate well with BW and BMI. No gender differences were found in cord blood leptin. Maternal obesity had no effect on cord leptin, whereas exogenous maternal steroids increased neonatal leptin concentrations.