The role of adipokines in uterine contractility.

Obesity is currently an important public health issue, registering a rapid increase in recent decades and affecting young people more and more frequently. The result is an increasing number of overweight or obese patients who reach reproductive age and become pregnant. Obesity is considered as an increased volume of adipose tissue which has well-known negative effects on multiple systems, but also on reproductive function. This piece of information led to the search for the existence of a connection between an increased Body Mass Index and the dysfunction of uterine contractility. Most cases of post-term pregnancy which usually require the induction of childbirth are observed in patients with increased Body Mass Index. The most important adipokines are represented by adiponectin, leptin, ghrelin, visfatin and apelin. Leptin has been demonstrated to act at smooth muscle fiber level in the vascular wall where it produces a decrease in calcium release from the sarcoplasmic reticulum, thus reducing the uterine contractile force. Leptin has an inhibitory effect on the frequency and amplitude of uterine contractions. Increased serum levels of leptin in obese women are involved in the inhibition of the apoptotic phenomenon involved in uterine involution. Visfatin exerts a more potent inhibitory effect compared to leptin upon uterine contractions. The inhibitory effect of ghrelin on uterine contractility involves a possible role in the regulation of myometrial activity. Apelin exerts a potent inhibitory effect on myometrial cells, causing a reduction in both the amplitude and the frequency of uterine contractions. Adipose tissue is currently regarded as a real endocrine organ, responsible for the production of bioactive polypeptides, adipocytokins. Adipokines exert modulating effects during pregnancy and there is evidence of their involvement in the pathophysiology of pregnancy-related complications. [ABSTRACT FROM AUTHOR]