Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2022 Feb 16;10(2):456.
doi: 10.3390/biomedicines10020456.

PCOS: A Chronic Disease That Fails to Produce Adequately Specialized Pro-Resolving Lipid Mediators (SPMs)

Pedro-Antonio Regidor  1   2 , Xavier de la Rosa  3 , Anna Müller  1 , Manuela Mayr  1 , Fernando Gonzalez Santos  4 , Rafael Gracia Banzo  5 , Jose Miguel Rizo  2
Affiliations

PCOS: A Chronic Disease That Fails to Produce Adequately Specialized Pro-Resolving Lipid Mediators (SPMs)

Pedro-Antonio Regidor et al. Biomedicines. .

Abstract

Introduction: Polycystic ovary syndrome (PCOS) is an endocrinological disorder that affects 5-15% of women of their reproductive age and is a frequent cause of infertility. Major symptoms include hyperandrogenism, ovulatory dysfunction, and often obesity and/or insulin resistance. PCOS also represents a state of chronic low-grade inflammation that is closely interlinked with the metabolic features. "Classical" pro-inflammatory lipid mediators such as prostaglandins (PG), leukotrienes (LT), or thromboxanes (TX) are derived from arachidonic acid (AA) and are crucial for the initial response. Resolution processes are driven by four families of so-called specialized pro-resolving mediators (SPMs): resolvins, maresins, lipoxins, and protectins. The study aimed to establish lipid mediator profiles of PCOS patients compared to healthy women to identify differences in their resolutive and pro-inflammatory lipid parameters.

Material and methods: Fifteen female patients (18-45 years) were diagnosed with PCOS according to Rotterdam criteria, and five healthy women, as a comparator group, were recruited for the study. The main outcome measures were: pro-inflammatory lipid mediators (PG, LT, TX) and their precursor AA, SPMs (resolvins, maresins, protectins, lipoxins), their precursors EPA, DHA, DPA, and their active biosynthesis pathway intermediates (18-HEPE, 17-HDHA, 14-HDHA).

Results: The level of pro-inflammatory parameters in serum was significantly higher in PCOS-affected women. The ratio (sum of pro-inflammatory molecules)/(sum of SPMs plus hydroxylated intermediates) reflecting the inflammatory state was significantly lower in the group of healthy women.

Conclusion: There is a strong pro-inflammatory state in PCOS patients. Further research will clarify whether supplementation with SPMs or their precursors may improve this state.

Keywords: PCOS; inflammation; obesity; specialized pro-resolving mediators (SPMs).

PubMed Disclaimer

Conflict of interest statement

Pedro-Antonio Regidor is an employee of Exeltis Healthcare. Anna Müller and Manuela Sailer are employees of Exeltis Germany. Fernando Gonzalez Santos and Rafael Gracia Banzo are employees of Solutex Spain. Jose Miguel Rizo is an employee of Chemo OTC Spain. Xavier de la Rosa declares no conflict of interest.

Figures

Figure 1
Figure 1
Results of the ARA-derived pro-inflammatory mediators of the healthy and PCOS patients. * = significant difference (p < 0.05); ** p < 0.005.
Figure 2
Figure 2
Results of the quantified free-fatty-acid precursors of resolving mediators. Ns = not significant.
Figure 3
Figure 3
Results of the ratio pro-inflammatory parameters/SPMs, including the monohydroxylates in the serum compared to the plasma. ns = not significant; ** p < 0.005.
Figure 4
Figure 4
Heat map results in pg/mL of the human plasma analyses of the healthy and PCOs patients.
Figure 5
Figure 5
Heat map results in pg/mL of the human serum analyses of the healthy and PCOs patients.
See this image and copyright information in PMC

References

    1. Ehrmann D.A. Polycystic ovary syndrome. N. Engl. J. Med. 2005;352:1223–1236. doi: 10.1056/NEJMra041536. - DOI - PubMed
    1. Homburg R. Polycystic ovary syndrome—From gynecological curiosity to multisystem endocrinopathy. Hum. Reprod. 1996;11:29–39. doi: 10.1093/oxfordjournals.humrep.a019031. - DOI - PubMed
    1. Diamanti-Kandarakis E., Kandarakis H., Legro R.S. The role of genes and environment in the etiology of PCOS. Endocrine. 2006;30:19–26. doi: 10.1385/ENDO:30:1:19. - DOI - PubMed
    1. Rotterdam ESHRE/ASRM-Sponsored PCOS Consensus Workshop Group Revised 2003 consensus on diagnostic criteria and long-term health risks related to polycystic ovary syndrome (PCOS) Hum. Reprod. 2004;19:41–47. doi: 10.1093/humrep/deh098. - DOI - PubMed
    1. Sam S. Obesity and Polycystic Ovary Syndrome. Obes Manag. 2007;3:69–73. doi: 10.1089/obe.2007.0019. - DOI - PMC - PubMed

Grants and funding