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Evaluation of Hepatic Glucose Production in a Polycystic Ovary Syndrome Mouse Model
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Components of the Complement Cascade Differ in Polycystic Ovary Syndrome
Alexandra E Butler1, Abu Saleh Md Moin1, Thozhukat Sathyapalan2
1Research Department, Royal College of Surgeons in Ireland Bahrain, Adliya 15503, Bahrain.
International Journal of Molecular Sciences
|October 27, 2022
Summary
Polycystic ovary syndrome (PCOS) shows increased complement system proteins, particularly the alternative pathway. These changes are linked to obesity, hyperandrogenemia, and insulin resistance, with both pathway activators and inhibitors upregulated.
Area of Science:
- Immunology
- Endocrinology
- Proteomics
Background:
- Polycystic ovary syndrome (PCOS) is associated with complement pathway dysregulation.
- Obesity and insulin resistance may influence complement protein levels in PCOS.
Purpose of the Study:
- To investigate complement system protein expression in women with PCOS.
- To explore correlations between complement proteins and PCOS phenotypes (obesity, insulin resistance, hyperandrogenemia).
Main Methods:
- SOMALogic proteomic analysis of plasma from 234 women (137 PCOS, 97 controls).
- Assessed 26 complement system proteins, including inhibitory factors.
- Statistical analysis to identify significant differences and correlations.
Main Results:
- Alternative complement pathway predominantly upregulated in PCOS (increased C3, properdin, factor B).
- Complement inhibitors also increased (CFHR5, factor H, factor I).
- Downstream factors (iC3b, C3d, C5a) elevated, correlating with hyperandrogenemia, insulin resistance, and BMI.
Conclusions:
- PCOS exhibits a complex dysregulation of the complement system, with both activation and inhibition pathways upregulated.
- These alterations are partially explained by metabolic and hormonal factors like BMI, hyperandrogenemia, and insulin resistance.
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