Adipose tissue dysfunction, adipokines, and low-grade chronic inflammation in polycystic ovary syndrome

Abstract

Polycystic ovary syndrome (PCOS), a complex condition that affects women of reproductive age, is characterized by ovulatory dysfunction and androgen excess. Women with PCOS present higher prevalence of obesity, central adiposity, and dyslipidemia, and face increased risk of type 2 diabetes. PCOS is closely linked to functional derangements in adipose tissue. Adipocytes seem to be prone to hypertrophy when exposed to androgen excess, as experienced by women with PCOS, and both adipose tissue hypertrophy and hyperandrogenism are related to insulin resistance. Hypertrophic adipocytes are more susceptible to inflammation, apoptosis, fibrosis, and release of free fatty acids. Disturbed secretion of adipokines may also impact the pathophysiology of PCOS through their influence on metabolism and on sex steroid secretion. Chronic low-grade inflammation in PCOS is also related to hyperandrogenism and to the hypertrophy of adipocytes, causing compression phenomena in the stromal vessels, leading to adipose tissue hypoperfusion and altered secretion of cytokines. Lifestyle changes are the first-line intervention for reducing metabolic risks in PCOS and the addition of an insulin-sensitizing drug might be required. Nevertheless, there is not sufficient evidence in favor of any specific pharmacologic therapies to directly oppose inflammation. Further studies are warranted to identify an adipokine that could serve as an indirect marker of adipocyte production in PCOS, representing a reliable sign of metabolic alteration in this syndrome.

Polycystic ovary syndrome is associated with increased osteopontin levels

“…Increased expression of OPN has been reported in obese mice and obese humans (14,15). Adipose tissue dysfunction may also impact the pathophysiology of PCOS through its influence on metabolism and reproductive systems (6). In the present study, circulating OPN levels were significantly elevated in women with PCOS, and also overweight/obese women had significantly higher circulating OPN levels than lean (22) recently reported that OPN might be involved in the regulation of follicular growth and ovulation.…”

“…Although the underlying pathophysiologic mechanisms have not yet been determined clearly, adipose tissue dysfunction exists in PCOS (5,6). Pro-inflammatory immune cell accumulation in adipose tissue is associated with the development of insulin resistance.…”

“…Adipose tissue dysfunction exists in PCOS; this situation causes alteration of secreted adipokines and inflammatory mediators. In addition, disturbed secretion of adipokines contributes to the development of PCOS and also to metabolic abnormalities in the disease (5,6).…”

Adiponectin and resistin: potential metabolic signals affecting hypothalamo-pituitary gonadal axis in females and males of different species

“…Adipokines such as adiponectin and resistin could act as a link between obesity and PCOS (Spritzer et al 2015). Many studies have investigated the concentration of adiponectin and resistin in both plasma and follicular fluid in patients with PCOS and control groups.…”

“…Many studies have investigated the concentration of adiponectin and resistin in both plasma and follicular fluid in patients with PCOS and control groups. However, data are still controversial (Spritzer et al 2015). Several studies have documented a lack of any difference in resistin concentration in serum or follicular fluid of patients with PCOS when compared to the control groups, even though serum adiponectin was significantly lower in obese than that in normalweight women.…”