الفهرس 
InfertilityOnly 14 pages are availabe for public view
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Abstract
Infertility is a condition affecting more than 5 million couples annually with important medical, economic, and psychological implications. The care of the infertile couple must be based on an accurate assessment of factors affecting the fertility of both partners. The postponement of marriage and delay of pregnancy in marriage in the post-World War II generation are largely responsible for the increase in consultations for the evaluation of infertility. With the increased availability of services and improved diagnostic and therapeutic management, more couples are now able to access infertility services.
A couple is said to be infertile if they have been trying to achieve a pregnancy for more than 1 year without success. This definition is arbitrary, and many couples achieve pregnancy after 12 months with no abnormalities and no outside intervention. In English demographic language, the term infecundity refers to the inability to conceive after several years of exposure to the risk of pregnancy. The inability to conceive within two years of exposure to the risk of pregnancy is the epidemiological definition recommended by the world health organization.
Infertility is classified by the woman’s history. Primary infertility implies no antecedent pregnancy, and secondary infertility is defined by a history of any pregnancy, including abortions and ectopic pregnancies.
The general causes of infertility are classified into female infertility, male infertility and unexplained infertility.
While female infertility is divided to tuboperitoneal factor, ovulatory factor, endometriosis, cervical and uterine disorders.
Leptin, the hormone encoded by the obesity (ob) gene, is a 146 aa protein with a tertiary structure similar to that of cytokines. Although leptin was originally thought to be exclusively expressed in white adipose tissue, subsequent reports showed that leptin is expressed in several other areas, such as the hypothalamus, pituitary gland, fundic gastric epithelium, skeletal muscle, syncytiotrophoblast, and mammary epithelium.
Leptin receptors (Ob-Rs) have been identified in the hypothalamus, gonadotrope cells of the anterior pituitary, granulosa, theca, and interstitial cells of the ovary, endometrium and Leydig cells. This multifocal expression of leptin, as well as the dense presence of Ob-Rs at all levels of the hypothalamus-pituitary-gonadal (HPG) axis, implies that the nutritional/leptin regulation of reproduction involves a complex network of interactions at multiple levels to regulate the HPG axis in a paracrine and/or endocrine fashion.
Leptin gene expression is regulated by a variety of hormones, growth factors, and cytokines. Estrogens induce whereas androgens suppress leptin production, providing an explanation for the sexual dimorphism in serum leptin levels. Insulin increases leptin production, and this may contribute to the decrease of plasma leptin levels that occurs during fasting and the hyperleptinemia that accompanies insulin resistance states. Proinflammatory cytokines, such as tumor necrosis factor (TNF) and interleukin 1 (IL-1) may also directly induce leptin gene expression. Leptin regulates food intake and energy expenditure and participates in angiogenesis. In addition, it has been shown to exert direct effects on hypothalamic-pituitary gonadotropin release and follicle stimulating hormone (FSH) and 17- estradiol ovarian synthesis dependant in female rats. This effect was associated with the increased luteinizing hormone (LH) concentrations. Leptin was also found to prevent the ovulation delay induced by Plasma leptin levels directly correlate with body fat mass. (Leptin concentrations in serum increase gradually during the early follicular phase and reach plateau at the time of midcycle gondatropin surge and lower to the baseline during luteal phase in both spontaneous and gonadotropin induced cycles.
As leptin exerts significant effects on female reproductive system, it might be related to infertility, which affects approximately 10% of people at reproductive age and 15% of couples). Although the role of leptin in the pathogenesis of PCOS and endometriosis were investigated in a number of studies, there is still ambiguity and lack of evidence. The present study approved that women with PCOS had significantly lower peritoneal fluid levels of leptin. However, it is difficult to clarify whether reduced follicular development decreases leptin levels in peritoneal environments of PCOS subjects or a “primary” leptin defficiency in peritoneal environment alters ovarian functions in PCOS.
Leptin is exclusively produced by adipose tissue so plasma leptin levels directly correlate with BMI. As PCOS tends to cause weight gain or obesity, it might be related to elevated concentrations of leptin in plasma, leptin concentrations in peritoneal fluid were significantly elevated in women with endometriosis, and directly correlated with the stage of endometriosise and its severity.