PCOS

Introduction

Polycystic ovary syndrome (PCOS) is a prevalent endocrine disorder affecting women of reproductive age. It is characterized by a range of symptoms including menstrual irregularities, hyperandrogenism, and polycystic ovaries. The etiology of PCOS is multifactorial, involving genetic, hormonal, metabolic, and environmental factors. This synthesis aims to consolidate key insights from recent research on PCOS.

Key Insights

Genetic and Hormonal Factors:
- PCOS is influenced by genetic variability, particularly in genes related to antioxidative and inflammatory pathways, which affect the risk and metabolic profile of the syndrome .
- Functional ovarian hyperandrogenism (FOH) is a significant contributor to PCOS, with dysregulation in androgen secretion being a common feature .
- Genome-wide association studies (GWAS) have identified several candidate loci (e.g., FSHR, LHCGR, DENND1A) that are associated with PCOS, suggesting a strong genetic component.
Metabolic and Cardiovascular Risks:
- Women with PCOS have a higher prevalence of insulin resistance, which is independent of but exacerbated by obesity and central adiposity .
- PCOS is associated with an increased risk of type 2 diabetes and cardiovascular diseases, necessitating targeted prevention and management strategies .
Microbiome and Inflammation:
- Alterations in the gut microbiome are linked to PCOS, with evidence suggesting that these changes contribute to insulin resistance and hyperandrogenism through chronic low-grade inflammation.
- The role of the NLRP3 inflammasome and other inflammatory pathways in PCOS pathogenesis highlights the importance of inflammation in the syndrome.
Mitochondrial Dysfunction:
- Mitochondrial dysfunction, including mutations in mitochondrial DNA, may play a role in the pathogenesis and progression of PCOS, contributing to insulin resistance and oxidative stress.
Phenotypic Variability:
- The clinical manifestations of PCOS, such as menstrual irregularities and signs of androgen excess, vary widely among individuals, influenced by both genetic and environmental factors .
- Obesity and central adiposity are more prevalent in severe phenotypes of PCOS, potentially exacerbating reproductive and metabolic features.

Conclusion

PCOS is a complex and multifactorial disorder with significant genetic, hormonal, metabolic, and environmental components. Key insights from recent research highlight the roles of genetic variability, hormonal dysregulation, metabolic and cardiovascular risks, microbiome alterations, inflammation, and mitochondrial dysfunction in the pathogenesis and progression of PCOS. Understanding these diverse factors is crucial for developing targeted diagnostic and therapeutic strategies to manage this heterogeneous condition effectively.

Summary

Introduction

Key Insights

Conclusion

Sources and full results

Genetic, hormonal and metabolic aspects of PCOS: an update

PCOS is a complex endocrine disorder with a multifactorial cause and higher risk of metabolic and cardiovascular diseases.

Microbiome and PCOS: State-of-Art and Future Aspects

The gut microbiome plays a significant role in PCOS, with potential therapeutic approaches including IL-22 and bile acid glycodeoxycholic acid.

Revised 2003 consensus on diagnostic criteria and long-term health risks related to polycystic ovary syndrome (PCOS).

PCOS is a syndrome of ovarian dysfunction with a broader spectrum of symptoms, and is associated with an increased risk of type 2 diabetes and cardiovascular events.

Genetic Variability in Antioxidative and Inflammatory Pathways Modifies the Risk for PCOS and Influences Metabolic Profile of the Syndrome

Genetic variability in antioxidative and inflammatory pathways influences the risk for PCOS and glucose homeostasis in PCOS patients.

The Pathogenesis of Polycystic Ovary Syndrome (PCOS): The Hypothesis of PCOS as Functional Ovarian Hyperandrogenism Revisited.

Polycystic ovary syndrome (PCOS) is a complex condition resulting from the interaction of diverse genetic and environmental factors.

Functional genomics of PCOS: from GWAS to molecular mechanisms

PCOS candidate loci FSHR, LHCGR, INSR, and DENND1A form a hierarchical signaling network that regulates ovarian androgen biosynthesis, offering potential new diagnostic and therapeutic approaches for women with the condition.

Steroidogenic regulatory factor FOS is underexpressed in polycystic ovary syndrome (PCOS) adipose tissue and genetically associated with PCOS susceptibility.

Underexpression of the FOS gene in adipose tissue and genetic association with PCOS suggest a role for this transcription factor in the disorder, potentially linking hyperandrogenism and insulin resistance.

Metabolic risk in PCOS: phenotype and adiposity impact

Women with PCOS have an increased risk of insulin resistance and cardiometabolic features, which are worsened by adiposity, regardless of reproductive phenotype.

Consensus on women's health aspects of polycystic ovary syndrome (PCOS): the Amsterdam ESHRE/ASRM-Sponsored 3rd PCOS Consensus Workshop Group.

Advances in PCOS Pathogenesis and Progression-Mitochondrial Mutations and Dysfunction.

Mitochondrial dysfunction may contribute to the initiation and progression of PCOS complications, such as cardiovascular disease, diabetes mellitus, and cancers.

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