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      Resistin in Cord Blood of Small for Gestation Age and Appropriate for Gestation Age Term Neonates

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          Abstract

          Objective

          Placental hormones such as resistin, adiponectin, ghrelin and leptin are known to have considerable role in fetal growth and there are some articles published in this area recently. Nevertheless there is a shortage of data showing association between resistin level and fetal growth; that was why we decided to conduct a study to evaluate this association.

          Methods

          This study was approved by ethic committee of pediatric health research center and research vice chancellor of Tabriz University of Medical Sciences. In this case-control study we measured the insulin, glucose and resistin in the cord blood of neonates with gestational age of 37 weeks or more in Al Zahra tertiary hospital from March 2011 to March 2012. Thirty-nine appropriate for gestation age (AGA) neonates and 41 small for gestation age (SGA) neonates were studied.

          Findings

          The umbilical cord blood resistin level was not found to have significant correlation with the type of delivery [normal vaginal delivery (NVD) or cesarean-section (C-S)], neonate’s gender, maternal age or body mass index (BMI). There was no significant difference in the levels of Insulin and glucose between AGA and SGA groups. Resistin level of blood cord in AGA group was 613.76±180.10 (range: 132.6-983.80 ng/ml) and in SGA group it was 1303.47±537.07 (range: 800.9-3001 ng/ml) (P<0.001). Neonates’ weight in AGA group was 3162.82±407.92 g and in SGA group it was 2425.85±32.84 g (P<0.001).

          Conclusion

          In this study resistin level had reverse correlation with fetal weight in term neonates. The SGA neonates with growth insufficiency have higher resistin levels in their cord blood than AGA neonates with same gestational age. It is recommended to conduct more studies in future with larger population of patients to clarify the resistin role in neonatal birth weight.

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          Most cited references18

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          Inverse relationship between plasma adiponectin and leptin concentrations in normal-weight and obese women.

          Adiponectin, a novel adipocyte-derived collagen-like protein, is the gene product of the adipose most-abundant gene transcript 1 (apM1), which has been considered to have anti-inflammatory and anti-atherogenic effects. To characterize the relationship between adiponectin and leptin, the ob gene product, in normal-weight and obese women. In this cross-sectional study, we measured fasting plasma adiponectin by ELISA, leptin concentrations by RIA, and related parameters such as blood pressure, body mass index (BMI), body fat mass, lipids, fasting blood glucose and insulin in 353 non-diabetic adult women with a wide range of BMI values. Plasma adiponectin concentrations in women with the highest tertile of BMI (at least 25.0 kg/m(2)) were decreased compared with those in the middle (22.0-25.0 kg/m(2)) or lowest (
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            Maternal and foetal resistin and adiponectin concentrations in normal and complicated pregnancies.

            The aim of this study was to evaluate how resistin and adiponectin (ApN) are involved in maternal energy metabolism and foetal growth. A cross-sectional study. Resistin and ApN were measured in 30 healthy nonpregnant women, 73 pregnant women [10-41 weeks of gestation; 18 with gestational diabetes mellitus (GDM), five with pregnancy-induce hypertension (PIH), nine with pre-eclampsia (PE), eight with chronic hypertension (CH) and 33 normal] and 40 foetal samples (20-41 weeks of gestation; 18 from GDM mothers and 22 from normal mothers). Resistin levels were significantly higher in normal pregnant women than in nonpregnant controls (13.7 +/- 2.1 vs. 6.3 +/- 1.6 ng/ml; P < 0.005) and showed a negative correlation with gestational age (P < 0.0001, r = -0.7). Only women with PE presented resistin levels significantly lower than normotensive women of the same gestational age (8.2 +/- 1.2 vs. 17.9 +/- 4.3 ng/ml; P < 0.005). ApN levels, although similar in normal pregnant women to those in nonpregnant controls, were significantly lower in women with GDM (37-41 weeks; 5.2 +/- 0.5 vs. 8.2 +/- 0.8 mg/l; P < 0.0001) and PE (20-37 weeks; 5.0 +/- 0.7 vs. 9.5 +/- 0.7 mg/l; P = 0.008) than those found in normal women matched for gestational age. Resistin was detected in the umbilical venous blood in foetuses from 20 to 41 weeks of gestation. In all newborns, both resistin and ApN levels were significantly higher than those recorded in adult life and did not correlate with maternal levels (P = ns, r = 0.03 for resistin and P = ns, r = -0.3 for ApN). Foetuses from diabetic mothers had ApN significantly lower than normal foetuses (26.8 +/- 2.6 vs. 37.5 +/- 3.5 mg/l; P = 0.02), while resistin levels were similar (17.3 +/- 3.7 vs. 18.2 +/- 1.5 ng/ml; P = ns). The secretion pattern of ApN in normal and complicated pregnancies strongly suggests an involvement of ApN in insulin resistance during gestation, while resistin seems to have a minor role. Moreover, the detection of high levels of resistin and ApN in cord blood during gestation is consistent with a regulatory action of these adipokines on tissue differentiation and foetal growth.
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              Hormonal Regulation of Fetal Growth

              Fetal growth is a complex process depending on the genetics of the fetus, the availability of nutrients and oxygen to the fetus, maternal nutrition and various growth factors and hormones of maternal, fetal and placental origin. Hormones play a central role in regulating fetal growth and development. They act as maturational and nutritional signals in utero and control tissue development and differentiation according to the prevailing environmental conditions in the fetus. The insulin-like growth factor (IGF) system, and IGF-I and IGF-II in particular, plays a critical role in fetal and placental growth throughout gestation. Disruption of the IGF1 , IGF2 or IGF1R gene retards fetal growth, whereas disruption of IGF2R or overexpression of IGF2 enhances fetal growth. IGF-I stimulates fetal growth when nutrients are available, thereby ensuring that fetal growth is appropriate for the nutrient supply. The production of IGF-I is particularly sensitive to undernutrition. IGF-II plays a key role in placental growth and nutrient transfer. Several key hormone genes involved in embryonic and fetal growth are imprinted. Disruption of this imprinting causes disorders involving growth defects, such as Beckwith-Wiedemann syndrome, which is associated with fetal overgrowth, or Silver-Russell syndrome, which is associated with intrauterine growth retardation. Optimal fetal growth is essential for perinatal survival and has long-term consequences extending into adulthood. Given the high incidence of intrauterine growth retardation and the high risk of metabolic and cardiovascular complications in later life, further clinical and basic research is needed to develop accurate early diagnosis of aberrant fetal growth and novel therapeutic strategies.
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                Author and article information

                Journal
                Iran J Pediatr
                Iran J Pediatr
                IJPD
                Iranian Journal of Pediatrics
                Tehran University of Medical Sciences
                2008-2142
                2008-2150
                December 2013
                : 23
                : 6
                : 659-663
                Affiliations
                [1 ]University at Buffalo, Buffalo, USA
                [2 ]Pediatric Health Research Center, Tabriz University of Medical Sciences. Department of Pediatrics and Neonatology, Tabriz, Iran
                [3 ]Department of chemistry, Faculty of medicine, Tabriz University of Medical Sciences, Tabriz, Iran
                [4 ]Department of physiology, Faculty of medicine, Tabriz University of medical sciences, Tabriz, Iran
                Author notes
                [* ] Corresponding Author: Address: Pediatric Health Research Center, Tabriz University of Medical Sciences. Department of Pediatrics and Neonatology, Tabriz, Iran. E-mail: gharehbaghimm@ 123456yahoo.com
                Article
                IJPD-23-659
                4025123
                f576632c-1e5e-40a1-bd33-85e712613a17
                © 2013 Iranian Journal of Pediatrics & Tehran University of Medical Sciences

                This is an open-access article distributed under the terms of the Creative Commons Attribution NonCommercial 3.0 License (CC BY-NC 3.0), which allows users to read, copy, distribute and make derivative works for non-commercial purposes from the material, as long as the author of the original work is cited properly.

                History
                : 27 November 2012
                : 11 September 2013
                Categories
                Original Article

                Pediatrics
                small for gestational age,appropriate for gestational age,resistin,insulin,glucose
                Pediatrics
                small for gestational age, appropriate for gestational age, resistin, insulin, glucose

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