الفهرس 
INTRODUCTIONOnly 14 pages are availabe for public view
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Abstract
The mechanism of fetal growth and the factors regulating fetal growth are not certain yet. There are several factors that have been investigated repeatedly with controversial outcomes; leptin is among these factors.
The role of leptin in fetal growth is not clear and has been a subject of debate.
Leptin is a 16-kD protein produced predominantly in white adipose tissue and, to a lesser extent, in the placenta, skeletal muscle, and stomach fundus in rats. Leptin has a myriad of functions in carbohydrate, bone, and reproductive metabolism that are still being unraveled, but its role in body weight regulation is the main reason it came to prominence.(1-3)
The major role of leptin in body-weight regulation is to signal satiety to the hypothalamus and, thus, reduce dietary intake and fat storage while modulating energy expenditure and carbohydrate metabolism to prevent further weight gain.(4-6_ Unlike the Ob/Ob mouse model in which this peptide was first characterized, most humans who are obese are not leptin deficient but rather leptin resistant. Therefore, they have elevated circulating levels of leptin. Elevated circulating leptin in obesity reflects leptin receptor resistance. Leptin receptors, members of the gp130 family of cytokine receptors, are expressed in the hypothalamus.(7-8)
Leptin, the ob gene product, plays an important role in the regulation of body fat mass and weight. In previous studies, it was demonstrated that leptin is detectable in human fetal cord blood as early as at 18 weeks of gestation.(9-14)
Fetal macrosomia has been defined in several ways. The definitions include birth weight greater than 4000 g or greater than 90th percentile for the newborn adjusted for race, sex, and gestational age.(143-144)
Based on these definitions, macrosomia occurs in 1-10% of all deliveries. Macrosomia may place the mother and fetus or neonate at risk for adverse outcomes. Antenatal risk factors reportedly may predict macrosomia at birth. Identification of those at-risk pregnancies may allow intervention to reduce the risk, to provide appropriate counseling, and to implement appropriate plans for monitoring and follow-up care during pregnancy and after delivery.(143-144)
The aim of this work was to see if there is a correlation between the circulating levels of leptin hormone in the maternal and cord serum and the increase of birth weight of the full term newborns, in medically free mothers; with the ultimate goal to know if leptin level is implicated in macrosomia.
This study was conducted on a group of 50 medically free pregnant women attended to the obstetrics unit of the hospital for delivery. All participants were fully counseled about the study and an informed consent was obtained prior to participation in the study.
The selected patients were subdivided randomly in two groups
Group A(control group): 25 cases delivered fullterm normal weight infants.
Group B (study group): 25 cases delivered fullterm macrosomic infants.
Immediately after delivery patients of group A (control group having normal weight infants) and group B (study group having macrosomic infants) were included in our study.
Maternal serum samples and fetal cord samples were withdrawn immediately after birth of the full term infants.
1. Umbilical cord samples of the fetus were withdrawn immediately after birth.
2. Maternal serum samples were withdrawn immediately after birth.
3. Samples were stored at -20 Celsius in the laboratory till analysis.
4. Samples were analyzed by a solid phase ELISA designed to measure human leptin in serum and plasma.it employs the quantitative sandwich enzyme immunoassay principle.
The results of the study were tabulated and statistically analyzed and showed that:
-There is a statistically significant correlation between fetal plasma leptin levels and neonatal birth weight, which suggests that leptin level is related directly to quantity of body fat tissue in fetal macrosomia. so leptin has important clinical implications for predicting fetal macrosmia.
- On the other hand we didn’t find a statistically significant difference between the two groups as regards the relation between maternal leptin level and fetal birth weight.
- Also no correlation was found between maternal and cord leptin concentrations, which is consistent with a non-communicatory two-compartment model of feto-placental leptin regulation.