According to the American Society for Reproductive Medicine Criteria, presence of any two of the following refers to PCOS and not just visualization of polycysts on imaging [2].

The currently accepted definition of a polycystic ovary is the presence of ≥12 follicles in each ovary, measuring 2–9 mm in diameter and/or increased ovarian volume (>10 mL) [2]. It is also important that the other etiologies (congenital adrenal hyperplasia, androgen-secreting tumors, or Cushing syndrome), potentially resulting in a hyper-androgenic state are excluded [2].

The pathophysiology is complex, multifactorial and incompletely understood. Chronic elevated levels of luteinizing hormone (LH) and insulin resistance are the hallmarks of PCOS [3, 4]. Insulin resistance with type 2 diabetes mellitus (T2DM) and compensatory hyperinsulinemia have been consistently documented in obese women with PCOS [5]. Insulin resistance is related to the chronic visceral fat inflammation seen in patients with metabolic syndrome [6, 7]. Insulin resistance leads to increased production of insulin levels, hence the hyperinsulinemia [8]. It is also interesting to note that the severity of insulin resistance correlates with the severity of the clinical and metabolic phenotype of PCOS [9].

The reason behind elevated levels of LH is not clear. This could probably be the result of relatively high and unchanging concentrations of estrogens that might alter the control of this hormone by the hypothalamic- pituitary axis [10]. This high LH levels along with hyperinsulinemia work synergistically causing ovarian growth, androgen production and cysts formation in the ovaries. High insulin levels also cause decrease of sex hormone binding globulin (SHBG). SHBG binds to sex steroids, especially androgens which then contribute to hyperandrogenism which further inhibits normal follicular maturation. Also, only 50–65 % of PCOS patients are obese. The non-obese groups of patients with PCOS also have been shown to have insulin resistance but the levels of insulin have been lower compared to their obese counterparts. Still they will have evidence of hyperandrogenism and oligo-ovulation/anovulation similar to their obese counterparts [3]. Only a few patients classically present with the triad of hyperandrogenism, insulin resistance and acanthosis nigiricans [11].

The evaluation in obese patients with PCOS referred for bariatric consultation should include an endocrinologist evaluation to rule out pituitary or thyroid disease as the cause of anovulation and premature ovarian failure which is characterized by high FSH levels.

As mentioned previously the other causes of hyperandrogenic state like androgen producing neoplasms, congenital adrenal hyperplasia (high 17-OH progesterone) and Cushings syndrome should be excluded by appropriate evaluation [2].

Diabetic evaluation is important as it is noted that 35–45 % of patients with PCOS will have impaired glucose tolerance and 7–10 % will actually be diabetic. Hence a complete T2DM profile has to be done which includes GTT, HbA1C and HOMA-IR [12, 13]. It is also noted that patients with PCOS have higher chances of developing cardiovascular events. Hence a cardiac evaluation is also important [14].

Endometrial aspiration can be considered in patients above 35 years to rule out endometrial carcinoma. Imaging in the form of ultrasonogram needs to be done to assess the ovaries for polycysts. But it needs to be understood that many PCOS patients may not have cysts and cysts may also be seen in 25 % of healthy women [15].

Sustained weight loss is the only currently available definitive intervention expected to have a lifelong effect on reducing the long-term complications of PCOS. Eventually, any intervention directed at reducing obesity will not only improve the quality of life, but also correct the hyperinsulinism and improve fertility and the lipid and androgen profiles [16]. It has been shown that a modest 5–10 % weight loss can lead to the resumption of ovulation within weeks and improving many features of PCOS [17].

Bariatric surgery is the most effective approach for sustained weight loss in the morbidly obese with effectiveness confirmed in large prospective trials with substantial weight loss and improvements in metabolic effects [18, 19]. Bariatric surgery resulted in improved fertility especially in patients with PCOS where biochemical studies showed normalization of hormones after surgery [20]. In the study by Jaamal M et al., it was shown that weight loss after roux-en-Y bypass (RYGB) had a dramatic effect on several manifestations of PCOS, with a 100 % successful conception rate, even without hormonal therapy. Regulation of the menstrual cycle and remission of T2DM occurred immediately, and improvement in hirsutism occurred relatively slowly. In fact >40 % improvement in the menstrual cycle and T2DM was noted within the first month with an approximate 25 % excess weight loss [10].

It is quite clear that weight loss by both non-surgical means and bariatric surgery has shown better outcomes for successful artificial reproduction technique in obese patients. This has been by improved pregnancy rates and live birth. It has also been shown that following bariatric surgery there is better regularization of menstrual pattern, a decrease in cancellation rates, increase in the number of embryos available for transfer, reduced numbers of ART cycles and decreased miscarriage rates. There was an increased number of natural conceptions noted [21]. Following RYGB, significant improvements were seen in testosterone, fasting glucose, insulin, cholesterol, and triglyceride at 12 months. The improvements in biomarkers, menstrual cycles and hirsutism did not correlate with degree of weight change [22].

No guidelines or consensus exist with the exact timing of pregnancy after a bariatric procedure. Most surgeons generally prefer a minimum of 12 months before pregnancy, as rapid weight loss (relative starvation phase) may be unhealthy for the mother and a baby [23]. Hence it is advisable to delay pregnancy for 12–18 months following the bariatric procedure to avoid nutritional deficiencies [24].

Obesity increases the risk of both maternal and infant morbidity. Obese women who become pregnant face higher risk of developing gestational diabetes (GDM), pregnancy-induced hypertension, and pre-eclampsia [30]. In obese women complicated by GDM, the pregnancy outcome is definitely compromised regardless of the severity of obesity or the treatment modality [25]. They also have a greater incidence of having preterm labor, higher rates of cesarean sections and perioperative morbidity. Infants born to obese women are also expected to have increased rates of macrosomia and congenital anomalies, as well as life-long complications of obesity associated co-morbidities like T2DM, hypertension etc. [26].