Polycystic Ovary Syndrome as a Proinflammatory State: The Role of Adipokines

被引:26
作者
Dimitriadis, Georgios K. [1 ,2 ,3 ]
Kyrou, Ioannis [1 ,2 ,4 ]
Randeva, Harpal S. [1 ,2 ,4 ]
机构
[1] Univ Warwick, Warwick Med Sch, Div Translat & Expt Med, Coventry CV4 7AL, W Midlands, England
[2] Univ Hosp Coventry & Warwickshire NHS Trust, Warwickshire Inst Study Diabet Endocrinol & Metab, Coventry CV2 2DX, W Midlands, England
[3] Imperial Coll London, Div Endocrinol & Invest Med, Hammersmith Campus, London W12 ONN, England
[4] Aston Univ, Aston Med Sch, Aston Med Res Inst, Birmingham B4 7ET, W Midlands, England
关键词
Polycystic Ovary Syndrome (PCOS); Central Obesity; Hyperandrogenaemia; Insulin Resistance (IR); Adipocyte Hypertrophy (AH); Adipokines; Inflammation; GELATINASE-ASSOCIATED LIPOCALIN; SUBCUTANEOUS ADIPOSE-TISSUE; TUMOR-NECROSIS-FACTOR; C-REACTIVE PROTEIN; INSULIN-RESISTANCE; METABOLIC SYNDROME; WEIGHT-LOSS; ADIPONECTIN LEVELS; OBESE WOMEN; GENE POLYMORPHISM;
D O I
10.2174/1381612822666160726103133
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
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.
引用
收藏
页码:5535 / 5546
页数:12
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