Study Suggests Leptin May Promote the Development of Endometrial Implants
This article reports that leptin may play a role in the development of endometrial implants. It explains that endometriosis is defined by the presence of endometrial glands or stroma outside the uterus. Women with endometriosis may have characteristics in the eutopic endometrium that support tissue survival, adhesion, and growth outside the uterine cavity.
The authors report that several studies have linked endometriosis with abnormal peritoneal and endometrial production of pro-inflammatory cytokines, growth factors, and angiogenic factors. They identify leptin, a hormone mainly produced by adipocytes, as one factor of interest because it is expressed in the endometrium and is involved in reproductive processes such as sex hormone regulation, ovulation, endometrial cell physiology, early embryo development, and implantation.
The article notes that only a limited number of studies had examined leptin receptor gene or protein expression in endometrial tissue from women with endometriosis. It refers to previous research that evaluated different isoforms of the leptin receptor in the eutopic endometrium of patients with moderate and severe endometriosis. Those studies reported increased receptor expression during the embryo implantation period, but no clear difference between patients and controls. Other authors also reported leptin receptor expression in both eutopic and ectopic endometrial tissues.
The authors state that the study aimed to assess leptin and long-form leptin receptor gene expression in ectopic and eutopic endometrial tissues from women with endometriosis, as well as in eutopic endometrium from controls without endometriosis. The study also aimed to determine the leptin-to-BMI ratio in serum and peritoneal fluid, evaluate the immunoreactive presence of the long-form leptin receptor in endometrial tissue and endometriotic implants, and investigate relationships among these variables.
The study found that the serum leptin-to-BMI ratio was higher in patients with endometriosis. It also reported that leptin and long-form leptin receptor gene expression were significantly higher in ectopic endometrial tissue than in eutopic endometrial tissue from patients and controls. In addition, the authors observed a positive and significant correlation between leptin and receptor transcripts in ectopic endometria, as well as in eutopic endometria from both endometriosis and control groups.
The authors further report a negative and significant correlation between long-form leptin receptor mRNA expression and the peritoneal-fluid leptin-to-BMI ratio, but only in the endometriosis group. They interpret these findings as evidence that leptin and its active receptor may have a modulatory interaction in ectopic endometrial tissue.
Overall, the article concludes that the serum leptin-to-BMI ratio may be associated with the presence of endometriosis, although its clinical usefulness for predicting the condition still requires confirmation. The increased expression of leptin and its long-form receptor in ectopic endometrium suggests that leptin, as an inflammatory and angiogenic cytokine, may contribute to the initiation or development of endometrial implants.
Source: Hindawi Publishing Corporation, Obstetrics and Gynecology International, Volume 2013, Article ID 879618, 9 pages.
