Alterations of polyunsaturated fatty acid metabolism in ovarian tissues of polycystic ovary syndrome rats

Huiyong Yin,Xinli Xue,Wei Liu,Shengxian Li,Rong Huang,Yun Sun,Yuying Wang,Tao Tao

doi:10.1111/jcmm.13614

Abstract

The metabolism of polyunsaturated fatty acids (PUFAs) remains poorly characterized in ovarian tissues of patients with polycystic ovary syndrome (PCOS). This study aimed to explore alterations in the levels of PUFAs and their metabolites in serum and ovarian tissues in a PCOS rat model treated with a high‐fat diet and andronate. Levels of PUFAs and their metabolites were measured using gas/liquid chromatography‐mass spectrometry after the establishment of a PCOS rat model. Only 3 kinds of PUFAs [linoleic acid, arachidonic acid (AA) and docosahexaenoic acid] were detected in both the circulation and ovarian tissues of the rats, and their concentrations were lower in ovarian tissues than in serum. Moreover, significant differences in the ovarian levels of AA were observed between control, high‐fat diet‐fed and PCOS rats. The levels of prostaglandins, AA metabolites via the cyclooxygenase (COX) pathway, in ovarian tissues of the PCOS group were significantly increased compared to those in the controls. Further studies on the mechanism underlying this phenomenon showed a correlation between decreased expression of phosphorylated cytosolic phospholipase A2 (p‐cPLA2) and increased mRNA and protein expression of COX2, potentially leading to a deeper understanding of altered AA and prostaglandin levels in ovarian tissues of PCOS rats.

Highlights

Polycystic ovary syndrome (PCOS) is a common ovulatory disorder among women of childbearing age, with 50% of PCOS patients being accompanied by infertility.[1]
We found higher serum arachidonic acid (AA) levels but lower ovarian tissue AA levels in PCOS rats compared with those of CON and HF rats
In addition to 15-deoxyD12,14-PGJ2, levels of AA metabolites via the COX pathway were increased in PCOS rats

Summary

| INTRODUCTION

Polycystic ovary syndrome (PCOS) is a common ovulatory disorder among women of childbearing age, with 50% of PCOS patients being accompanied by infertility.[1]. Eicosanoids, including prostaglandins (PGs) and leukotrienes, which are cyclooxygenase (COX)-generated metabolites of arachidonic acid (AA),[10] are known to modulate different ovarian functions and luteolysis.[11,12] PGs are biologically active lipid mediators involved in chronic inflammation and regulation of many reproductive events, such as ovulation, corpus luteum regression, implantation and pregnancy establishment.[13] Alterations in dietary PUFAs can change PUFA contents in the cell membrane and PG synthesis, affecting fertility.[14] n-3 PUFAs may be effective in improving hyperandrogenism and insulin resistance in patients with PCOS.[15] Elevated concentrations of AA and linoleic acid (LA) in follicular fluid at the time of oocyte retrieval significantly decrease the ability of oocytes to form pronuclei after intracytoplasmic sperm injection, but levels of AA and LA are not associated with subsequent embryo quality or pregnancy rate.[16]. Lipidomics, a branch of metabolomics, can systematically investigate a broad range of lipids in one biological system, and research on ovarian PUFAs and their derivates in a PCOS rat model by lipidomics might contribute to a deeper understanding of hormonal and metabolic disorders and their mechanisms

| MATERIALS AND METHODS

| Statistical methods

| RESULTS

| DISCUSSION

Findings

CONFLICT OF INTEREST STATEMENT