Some adults are either obese or overweight. Complications related with obesity are diverse, and some may relate to the degree of insulin resistance. The obesity and insulin resistance might initiate or worsen polycystic ovarian syndrome (PCOS) and negatively impact on fertility and reproductive outcomes.
PCOS is among the most typical endocrine disorders in women of reproductive age. The main features of PCOS include menstrual disorder secondary to anovulation and indications of hyperandrogenism. To be able to diagnose PCOS, patients need to have at least two following signs: oligo- or anovulation, clinical or biochemical indications of hyperandrogenism and sonographic proof of polycystic ovaries.
The obesity also worsens the seriousness of ovulatory and menstrual disorder. However, the reproductive function improves after weight reduction in obese patients. A modest weight reduction of 5% bodyweight continues to be proven to lead in significant enhancements in ovulatory function. Therefore, it is quite important to reduce weight through dieting and exercise as the first-line therapy to obese patients.
There is a growing evidence that the endometrium in PCOS patients is structural and sure contributors to subfertility. A spontaneous abortion rate in women with PCOS is considered to be 20%-40% greater compared to the general. Even if ovulation is restored, those patients still exhibit decreased cumulative pregnancy rates. Despite advances in assisted reproduction technology (ART) in allowing the selection of high-rank embryos, PCOS patients proved to possess considerably lower implantation rates than other infertile patients.
It was discovered that the obese patients have deregulated expression of markers of uterine receptivity. The lower expression of uterine receptivity markers can lead towards the observed negative effects on reproduction seen in women with PCOS. However, besides the hormonal profile in women with PCOS affect endometrial receptivity, the chronic unopposed estrogen exposure that occurs in this disorder leads to an elevated risk of endometrial hyperplasia and endometrial carcinoma. The decrease in ovulatory events in this condition results in deficient progesterone secretion. Consequently, endometrial growth and differentiation in women with PCOS suffer from estrogen, androgens and insulin without progesterone opposition. In the setting of anovulation and insufficient progesterone regulation, those patients have constant mutagenic stimulation of the endometrium by estradiol, without progesterone for endometrial differentiation, resulting in endometrial overgrowth, structural uterine bleeding, hyperplasia and perhaps cancer.
The hormonal changes connected with obesity have a significant effect on endometrial function, embryo implantation and abnormal proliferation resulting in endometrial hyperplasia. It is clear that obesity affects reproductive function at various levels, such as the ovary and the endometrium. However, it is difficult to determine which system is more adversely affected and the mechanism through which this happens. Generally, the subfertility felt by obese women is probably associated with effects on the oocyte, the embryo and the endometrium. Thus, obese women of reproductive age should be counseled that weight reduction can improve reproductive outcomes significantly and may lessen the incidence of unexpected cases.