In this study, leptin/BMI ratio in serum and peritoneal fluid and gene expression of leptin and long form leptin receptor (OB-RL) were assessed in eutopic and ectopic endometria of women with endometriosis and controls. Increased serum leptin/BMI ratio was found in endometriosis patients. Leptin and OB-RL gene expression was significantly higher in ectopic versus eutopic endometrium of patients and controls. A positive, significant correlation was observed between leptin and OB-RL transcripts in ectopic endometria and also in eutopic endometria in endometriosis and control groups. A negative and significant correlation was found between OB-RL mRNA expression and peritoneal fluid leptin/BMI ratio only in endometriosis. These data suggest that, through a modulatory interaction with its active receptor, leptin might play a role in the development of endometrial implants. 1. Introduction Endometriosis is defined as the presence of endometrial glands and/or stroma outside the uterus. In women with endometriosis, the eutopic endometrium has specific characteristics that favor tissue survival, adhesion, and growth outside the uterine cavity. Several studies have demonstrated that endometriosis is associated with abnormal peritoneal and endometrial production of proinflammatory cytokines and growth and angiogenic factors [1, 2]. Leptin, a hormone produced mainly by adipocytes, is expressed in endometrium [3] and has been implicated in the regulation of sex hormone production, ovulation, endometrial cell physiology, and early embryo development and implantation [4]. It may also play a role in endometriosis through its inflammatory and angiogenic properties. Nevertheless, studies evaluating serum and peritoneal fluid (PF) levels of leptin in patients with endometriosis report conflicting results: some describe increased levels [2, 5–10], while others report no differences between patients with endometriosis and controls [7, 11–14]. Moreover, the possibility of an association between PF leptin levels and severity of endometriosis is also controversial, with some studies suggesting a negative correlation [2, 6, 8] and others showing a positive correlation with more severe forms of peritoneal endometriosis [5, 7, 13, 15]. Interestingly, only a few studies so far have evaluated leptin receptor gene and/or protein expression in endometrial tissue of women with endometriosis [16–18]. Lima-Couy et al. [16] evaluated the three isoforms of leptin receptor—total (OB-RT), long (OB-RL), and short (HuB219.3)—in the eutopic endometrium of patients with moderate and severe
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