Title:Polycystic Ovary Syndrome as a Proinflammatory State: The Role of Adipokines
VOLUME: 22 ISSUE: 36
Author(s):Georgios K. Dimitriadis, Ioannis Kyrou and Harpal S. Randeva
Affiliation:Division of Translational and Experimental Medicine, Warwick Medical School, University of Warwick, Coventry CV4 7AL, United Kingdom.
Keywords:Polycystic Ovary Syndrome (PCOS), Central Obesity, Hyperandrogenaemia, Insulin Resistance (IR), Adipocyte Hypertrophy
(AH), Adipokines, Inflammation.
Abstract:Background: Polycystic Ovary Syndrome (PCOS) is a complex heterogeneous
disorder and the most common endocrinopathy amongst women of reproductive age. It is
characterized by androgen excess, chronic anovulation and an altered cardiometabolic profile.
PCOS is linked to impaired adipose tissue (AT) physiology and women with this disorder
present with greater risk for insulin resistance (IR), hyperinsulinemia, central adiposity,
nonalcoholic fatty liver disease (NAFLD) and type 2 diabetes mellitus (T2DM) than
matched for age and body mass index (BMI) women without PCOS. Hyperandrogenaemia
appears to be driving adipocyte hypertrophy observed in PCOS under the influence of a
hyperinsulinaemic state. Changes in the function of adipocytes have an impact on the secretion
of adipokines, adipose tissue-derived proinflammatory factors promoting susceptibility
to low grade inflammation.
Methods: In this article, we review the existing knowledge on the interplay between hyperandrogenaemia,
insulin resistance, impaired adipocyte biology, adipokines and chronic low-grade inflammation
in PCOS.
Results: In PCOS, more than one mechanisms have been suggested in the development of a chronic low-grade
inflammation state with the most prevalent being that of a direct effect of the immune system on adipose tissue
functions as previously reported in obese women without PCOS. Despite the lack of conclusive evidence regarding
a direct mechanism linking hyperandrogenaemia to pro-inflammation in PCOS, there have been recent findings
indicating that hyperandrogenaemia might be involved in chronic inflammation by exerting an effect on
adipocytes morphology and attributes.
Conclusion: Increasing evidence suggests that there is an important connection and interaction between proinflammatory
pathways, hyperinsulinemia, androgen excess and adipose tissue hypertrophy and, dysfunction in
PCOS. While lifestyle changes and individualized prescription of insulin-sensitizing drugs are common in managing
PCOS, further studies are warranted to eventually identify an adipokine that could serve as an indirect marker
of adipocyte dysfunction in PCOS, used as a reliable and pathognomic sign of metabolic alteration in this syndrome.
