Polycystic ovarian syndrome (PCOS) is the most common endocrine disorder affecting reproductive-age women worldwide. [1]. Clinical features of PCOS namely hirsutism, acne, and alopecia originate from high circulating levels of androgens, menstrual irregularities from anovulatory cycles. [2]. and obesity is thought to originate from both the underlying IR and high androgen levels in these patients.[3]. The alarming tribulations associated with the syndrome are past the reproductive axis and these women are at a greater risk of developing the metabolic syndrome at an early age because of IR and obesity observed in 30-60% of PCOS patients. [4,7]. The adipose tissue not only stores a large quantity of fat as an energy source [8]. but also expresses a variety of genes of secretory proteins. [9,13]. The human apM1 gene has been recently discovered, and it is exclusively expressed in white adipose tissue. [14]. The product of this gene is called adiponectin, a 244-amino acid protein with high structural homology to collagen VIII, X, complement C1q, and TNF. [15,16]. Adiponectin expression is increased by peroxisome proliferator-activated receptor agonists. [17,18]. Although the physiological role of adiponectin still has to be clarified, recent findings have indicated that it may be a kind of matrix protein with potential antiatherogenic and anti-inflammatory effects. [19-22]. Because adiponectin is a fat cell product, secreted into the circulating blood, it might be responsible for the metabolic and neuroendocrine derangements characteristic of obesity and obesity-related disease, such as PCOS. Serum adiponectin levels were found to be altered in women with PCOS due to the increased adiposity commonly observed in them. Accordingly, earlier studies have reported decreased adiponectin levels in PCOS women. Further, the altered adiponectin levels are proposed to contribute to the endocrine and metabolic disturbances observed in PCOS women. In this background, the present study was conducted to measure serum adiponectin levels in women with PCOS and to evaluate its association with the biochemical parameters studied.

The present study included 50 women of reproductive age attending the department of Gynecology, tertiary care institute of India and diagnosed with polycystic ovary syndrome based on Rotterdam criteria.

* indicates statistically significance at p≤0.05

Table 2: Association of adiponectin with the parameters studied in women with PCOS

* indicates statistical significance at p≤0.05

r=correlation coefficient; BMI=body mass index; FBS=fasting blood sugar; TGL=triglycerides; HDL-C=high density lipoprotein cholesterol; HOMA-IR= homeostasis model assessment-estimated insulin resistance. The demographic characteristics and biochemical parameters studied in healthy controls and PCOS women were shown in Table 1. Both the study groups were matched concerning age, however, PCOS women were obese when compared to healthy women (p<0.001).

Serum total cholesterol and triglyceride levels were significantly higher (p≤0.05) and serum adiponectin concentration was significantly lower in PCOS women when compared to controls (p≤0.05). HDL cholesterol, fasting insulin and HOMA-IR were similar between cases and controls. Adiponectin did not show significant association with any of the parameters studied (Table 2).

It has been established that adiponectin is almost exclusively produced in adipose tissue. [23. Adiponectin is probably one of the most important adipocytokines of adipose tissue. [24]. It is highly expressed and actively secreted by adipocytes. [25]. it is abundantly present in human circulation and displays a variety of functions, including antiatherogenic, antiinflammatory, and insulin-sensitizing properties. [26,27].

Polycystic ovary syndrome is commonly associated with metabolic disturbances such as glucose intolerance and dyslipidemia in addition to hormonal changes.

A possible explanation for this finding is that lower adiponectin levels in PCOS women might be a result of increasing IR in these patients as supported by our study. [39]. However, the HDL cholesterol levels were similar in PCOS women and controls (p=0.550) [Table 1]. Earlier studies have reported increased total cholesterol and triglycerides and decreased HDL cholesterol in PCOS women, compared to controls.[40]. Dyslipidemia in the setting of polycystic ovary syndrome is multifactorial in origin. The increased prevalence of obesity, insulin resistance and hyperandrogenemia have all been proposed to be involved in the lipoprotein disturbances observed in PCOS women.[41]. Increased lipogenesis, impaired clearance, decreased oxidation of fatty acids and their increased availability and an increased secretion of very-low-density lipoprotein (VLDL) particles by the hepatocytes contribute to the increased triglyceride levels in the presence of insulin resistance. [40]. Adiponectin is actively involved in energy homeostasis through its role in carbohydrate and lipid metabolism and is involved in causing insulin sensitivity. The present study analyzed the association of adiponectin with the studied parameters. It was observed that adiponectin showed a negative but no significant association with age and BMI [Table 2]. These findings are in accord with those of others. [42,43]. who established adiponectin as the only `adipokine' that is suppressed by increased body fat. The adiponectin levels in PCOS women in the present study showed no significant inverse association with fasting insulin levels and HOMA-IR [Table 2]. Similar findings were reported by Ramanand et al. [44]. Adiponectin thus may serve as a useful marker in detecting cases of PCOS with atypical presentation or in individuals with a family history of PCOS. Longitudinal studies are therefore warranted to understand the initiating point in the development of PCOS in females having a family history of PCOS and IR.

Serum adiponectin levels are significantly lower in women with polycystic ovary syndrome compared to healthy women. The hyperandrogenemia which is one of the characteristic features of PCOS leads to a state of adiposity which can further cause a decrease in adiponectin levels. The low adiponectin levels further contribute to the metabolic complications associated with PCOS including insulin resistance and dyslipidemia.