Objective: Leptin and adiponectin are two adipocytokines that play a critical role in the control of energy balance and metabolism as well as in conditions, such as insulin resistance, inflammation, and the development of the metabolic syndrome in adult life. Leptin has been associated with asymmetric intrauterine growth restriction (IUGR). The aim of this study was to investigate the perinatal implication of leptin and adiponectin in IUGR. Design: Leptin and adiponectin were measured in the plasma of 40 mothers, in the umbilical cord (UC) blood of their 20 appropriate for gestational age (AGA) and 20 IUGR singleton, full-term fetuses, and neonates on day 1 (d1) and day 4 (d4) of life postnatally. Methods: Serum leptin and adiponectin levels were measured by RIA. Serum cortisol levels were measured with an electrochemiluminescence immunoassay. Results: Leptin and adiponectin serum levels were higher and lower respectively in IUGR (meanGS.E.M., 32.5G3.8 and 5.4G0.9 mg/l respectively) compared with AGA (20.4G2.1 and 11.8G1.3 mg/l respectively) mothers (P!0.05), although body mass index did not differ between these two groups. Leptin levels positively correlated with adiponectin levels in the AGA (rZ0.547, P!0.05) but not in the IUGR mothers. UC, d1, and d4 leptin and adiponectin levels did not differ between IUGR and AGA groups. UC were significantly higher than d1 leptin levels (P!0.05) in the IUGR group but not in the AGA group. Conclusions: The increased UC leptin levels compared with d1 in IUGR fetuses might be directly and/or indirectly related to the subsequent development of insulin resistance in these neonates. This pathologic situation seems to be related to a specific profile of increased leptin and decreased adiponectin levels in IUGR mothers indicating a genetic predisposition for the development of insulin resistance.European Journal of Endocrinology 158 343-348

Leptin is an adipocyte-derived hormone/cytokine that links nutritional status with neuroendocrine and immune functions. As a hormone, leptin regulates food intake and basal metabolism, and is sexually dimorphic that is, its serum concentration is higher in females than in males with a similar body fat mass. As a cytokine, leptin can affect thymic homeostasis and the secretion of acute-phase reactants such as interleukin-1 and tumour-necrosis factor. Similar to other pro-inflammatory cytokines, leptin promotes Thelper1 (TH1)-cell differentiation and can modulate the onset and progression of autoimmune responses in several animal models. Many studies in animals have demonstrated that leptin levels increase acutely during infection and inflammation. We studied the leptin response to infections in 27 children with bacterial infections mainly respiratory and urinary tract. Serum Amyloid A protein (SAA) and C-reactive protein (CRP) in serum were measured by particle-enhanced immunonephelometric assays (BNProSpec Dade Behring), procalcitonin (PCT) levels were determined by chemiluminescence (Brahms), while leptin levels were measured by an enzymatically amplified two-step sandwich-type immunoassay (DSL). The main results of the study are summarized in the table:Leptin levels increased in all patients independently of their BMI, at diagnosis of the infection and returned to normal levels after treatment. This is an indication of normal expression of leptin genes and leptin receptor and this suggests that leptin is also an inflammatory marker. Similar results have been described in patients with sepsis, whereas the non-increase of leptin levels was associated with increased mortality. The secretion of leptin in the first hours of inflammation in children is stimulated by the endotoxins of bacteria as it has been shown in animal models. Leptin seems to play an important role being part of the cytokine network and modulating the inflammatory-immune response and the host defense mechanisms. MORTALITY OF VERY PRETERM BIRTHS: ASSOCIATIONS WITH TER-MINATIONS OF PREGNANCY AND CONGENITAL ANOMALIES IN THE MOSAIC COHORT.E PAPIERNIK 1 1 THE MOSAIC RESEARCH GROUP (FRANCE) Context: Practices related to screening and termination of pregnancy (TOP) for congenital anomalies (CA) vary within Europe countries and could explain some of the variability in mortality among very preterm births.Methods: The MOSAIC study (1) collected data on all stillbirths and live births between 22 and 31 weeks of gestation in 10 European regions in 2003. Babies transferred to NICU were followed to discharge from hospital. Data were extracted from medical records in the maternity and neonatal wards, including information on reasons for TOP and the presence of a lethal congenital anomaly for stillbirths and live births.Results: There were significant differences in the proportion of termination of pregnancies among stillbirths, ranging from about 50% in the regions in France and Italy to lows in the regions in Poland (9%) and in Germany (17%). In most regions,...

ABSTRACT:The gut hormone peptide YY 3-36 ] has been suggested to posses anorexigenic actions in animals and human adults. However, its circulating concentrations and function have not been studied in neonates. Serum concentrations of PYY (3-36) were determined by RIA (RIA) in 62 healthy preterm infants [mean(SD) gestational age, 32.0(2.1) weeks; postnatal age, 40.9(14.8 d)] and 15 healthy fullterm infants of comparable postnatal age and gender. The correlations between PYY (3-36) levels and anthropometric characteristics, food intake, growth rates and circulating concentrations of total PYY, ghrelin, leptin, insulin and adiponectin were examined. Mean (SD) PYY (3-36) concentrations were higher in preterm [543.7(157.6) ng/L) than full term infants [350.9(114.1) ng/L; p Ͻ 0.001) and accounted for 48% and 42% of total PYY basal plasma immunoreactivity in preterm and full term infants, respectively. In multiple regression analysis, concentrations correlated negatively with the infants' BMI and positively with serum ghrelin concentrations, but not with caloric intake, weight gain or concentrations of any other hormone studied. In conclusion, PYY (3-36) represents almost half of total PYY immunoreactivity in neonates. It's correlations with ghrelin and BMI suggest a role of this peptide in the regulation of energy homeostasis; however, its specific functions and physiologic significance in neonates remain to be elucidated. ] is one of the two major molecular forms of the gut peptide YY, the other isoform being PYY (1-36) (1). Both isoforms, in addition to exerting secretory and motor activities throughout the gut (2,3), are involved in the central regulation of food intake and energy balance. Both peptides have an anorexigenic effect through a Y2 receptor-mediated mechanism at the level of hypothalamus, whereas PYY (1-36) also possesses orexigenic action by acting at central Y1 receptors (3,4). PYY (3-36) is more potent than PYY (1-36) in several effects, such as decrease of food intake and inhibition of gastric emptying (3).In adults, PYY (3-36) accounts for 37% and 54% of total PYY immunoreactivity in basal and postprandial plasma, respectively (1). However, circulating levels of PYY (3-36)have not been measured in neonates so far. The aim of the present study was to determine the circulating concentrations of PYY (3-36) in preterm and full term infants and to examine their possible associations with the infants' size, caloric intake, weight gain and the serum concentrations of total PYY or other hormones implicated in the regulation of metabolism, such as ghrelin, leptin, insulin and adiponectin (5,6). METHODSStudy population and protocol. Sixty-two preterm [mean (SD) gestational age, 32.0 (2.1) weeks; birth weight, 1542 (275) g; males, 28] and 15 healthy full term infants [gestational age, 39.0 (1.0) weeks; birth weight, 3200 (498) g; males, 6] who served as the reference group were studied. Full term infants had similar gender distribution to that of preterm infants. Gestational age was estimated from the last ...