Polycystic ovary syndrome (PCOS) is a common endocrine metabolic disorder in women of reproductive age, with a prevalence between 8% and 12% in this population. The causes of PCOS are still unclear, and are known to be influenced by both genetic and environmental factors. Hyperandrogenemia and insulin resistance, hyperinsulinemia are important pathophysiological changes of PCOS. Sixty to 80% of patients with PCOS are combined with overweight or obesity, especially the accumulation of abdominal fat, and even patients with normal weight may present with excessive accumulation of fat in the abdomen, upper arms, and waist. Therefore, obesity is considered to be closely related to the development of PCOS. However, it is known that not all obese patients are combined with hyperandrogenemia, and therefore, this feature is not included in the diagnostic criteria and clinical staging of PCOS. So, how do patients with PCOS with or without obesity differ in terms of clinical presentation, fat distribution and function? Do they require different treatment strategies? Differences in clinical features According to the Rotterdam criteria, PCOS can be classified into 4 types: (1) hyperandrogenemia with sporadic ovulation and ultrasound suggestive of polycystic ovaries; (2) hyperandrogenemia with sporadic ovulation but ultrasound suggestive of normal ovaries; (3) hyperandrogenemia with ultrasound suggestive of polycystic ovaries; (4) sporadic ovulation with ultrasound suggestive of polycystic ovaries but no hyperandrogenemia. The National Institutes of Health ( NIH) classifies PCOS as types A and B, while the Androgen Excess Society (AES) classifies PCOS as types A, B and C. Moran et al. divided 172 patients into 3 types according to classical typing, and then divided each type into obese and non-obese groups according to body weight, and found that 48.2% of type A patients were obese and 16.3% were non-obese; 22.7% of type B patients were obese and 9.9% were non-obese. Obese people accounted for 9.9%; obese people accounted for 1.7% and non-obese people accounted for 1.2% in type C. Due to the different diagnostic criteria applied, the conclusions of different studies vary as to whether there are differences in the clinical characteristics of obese and non-obese patients. Most studies concluded that insulin resistance is an independent feature of PCOS, and insulin sensitivity in normal weight PCOS patients can be reduced by 50% compared to matched weight controls, but PCOS patients with obesity have more pronounced insulin resistance and hyperinsulinemia, and their insulin levels at all points in the oral glucose tolerance test are significantly higher than those of non-obese patients, suggesting that obesity can aggravate the degree of insulin resistance in PCOS patients. The degree of insulin resistance in patients with PCOS is suggested to be aggravated by obesity. Overweight and obese PCOS patients have progressively higher androgen levels compared to normal weight individuals. Studies have shown that there is a linear correlation between body mass index (BMI) and free testosterone index (FAI) in obese patients with or without PCOS due to the decrease in sex hormone binding protein, which does not correlate with total testosterone, but in the PCOS population, androstenedione levels increase with increasing BMI in a linear correlation, and the exact mechanism is unclear. and adrenal glands, and one study found that patients with higher androgens from adrenal dehydroepiandrosterone sulfate sources tended to be leaner, younger and more severely hirsute patients. In addition, the amplitude of luteinizing hormone (LH) pulses was significantly higher in non-obese patients with PCOS compared to obese patients, and although the frequency was slightly lower, the total 24h LH concentration was significantly higher than in obese patients. Thus, the LH/folliculopoietin (FSH) ratio was higher in non-obese patients compared to obese patients. Overweight and obese PCOS patients are more likely to have ovarian polycystic changes, less frequent menstruation with ovulation than normal weight patients, and a lower chance of pregnancy, all of which can be improved when the patient loses weight. Approximately 47% of patients with PCOS develop metabolic syndrome. Obese patients have more pronounced dyslipidemia (high free fatty acids, total cholesterol and LDL cholesterol) as well as hypertension and insulin resistance, thickening of the carotid intima-media, and impaired endothelial function, and these changes persist even after correction for weight. However, some researchers have concluded that PCOS does not independently increase the risk of atherosclerotic vasoembolic disease in patients if matched for weight, and that the risk of coronary heart disease in young, obese PCOS patients is either attributable to obesity or is not actually significant at this stage. Differences in fat distribution and function Some scholars have measured the thickness of subcutaneous fat at different sites in patients with PCOS using a lipid meter and found that the fat distribution in patients with PCOS was characterized by a male-type fat distribution, i.e. a thickened fat layer in the trunk and a thinner fat layer in the thighs. Further analysis of the subcutaneous fat thickness from the neck to the calf (subcutaneous fat topography, or SAT-Top) showed that the fat distribution of non-obese PCOS patients continued to be “child-like” (similar to the fat distribution of children aged 7 to 11 years before the emergence of sex characteristics), and did not develop into a normal female-like distribution. In contrast, the fat distribution of obese PCOS patients shows a “diabetic-like” distribution, with the typical upper part of obesity even more pronounced than that of diabetic women, tending to male fat distribution. Adipose tissue can secrete various adipokines, such as leptin, adiponectin, resistin, endolipin, etc. Leptin can act on the corresponding receptors in the hypothalamus through the blood-brain barrier, suppressing appetite, increasing thermogenesis and regulating systemic energy balance, while its receptors can exist in the ovaries, serving as a bridge between nutrition and reproduction. It has been shown that leptin levels in PC0S patients with obesity are ≥ normal women, and the study by Remsberg et al. suggests that leptin reflects total body fat and is related to the distribution of body fat, but in PCOS patients, abdominal subcutaneous or white fat can be a good predictor of serum leptin levels. In addition, PCOS patients with lower BMI had lower leptin levels than controls, while overweight and obese patients had progressively higher leptin levels, but their leptin levels appeared to be undersecreted relative to their total body fat and high insulin levels due to the competitive effect of adipocyte insulin resistance and hyperandrogenism on leptin. The results of the measurement of serum lipocalin and resistin in PCOS patients with different body weights found that lipocalin was lower in obese and overweight PCOS patients than in the control population, while resistin did not change significantly in either obese or normal weight PCOS patients, and that lipocalin/resistin was positively correlated with LH and FSH levels and negatively correlated with free testosterone index. Therefore, it is believed that this ratio may play an important role in hormonal disorders. Endolipin is strongly associated with insulin resistance. a study by Kowalska et al. in a PCOS population showed that endolipin levels in non-obese PCOS patients were associated with their insulin resistance and that it was an independent predictor of serum testosterone levels and free testosterone index (FAI), a marker of hyperandrogenemia. Obesity is recognized as a chronic low cascade inflammatory state. This inflammatory state is now also considered to contribute to the pathogenesis of PCOS and may be a novel entry point for the treatment of PCOS in the future. Increased infiltration of mononuclear macrophages occurs in over-accumulated adipose tissue, and these cells can secrete inflammatory factors such as tumor necrosis factor (TNF)-α, which in turn can alter the secretion of adipocytokines via paracrine pathways, while inflammatory factors and adipocytokines presumably may directly stimulate the ovaries to produce more androgens. Recent studies have proposed that in obese PCOS patients, hyperandrogenism instead plays an anti-inflammatory role, and they suggest that circulating androgens are pleiotropic and their direction of action depends on the individual’s weight status. Adipose tissue is not only an organ for energy storage, but also an important site for steroid metabolism. It is known that adipose tissue contains more than a dozen enzymes that catalyze the synthesis and inactivation of steroid hormones. The hormonal regulation that occurs in adipose tissue and involves sex hormone converting enzymes is called “pre-receptor regulation” of hormones, and they believe that abnormalities in this regulation can lead to significant changes in local sex hormone levels and thus play an important role in the development of metabolic diseases. Increased expression of 11β hydroxysteroid dehydrogenase type 1 (11β-HSD1, responsible for catalyzing the conversion of cortisol from inactive to active form) in subcutaneous fat of PCOS patients compared to controls in the following order: lean controls < fat controls < fat PCOS < lean PCOS, an alteration that increases the level of active cortisol in peripheral adipose tissue, the latter being associated with the patient's peripheral insulin resistance and the development of central obesity, and PCOS and obesity are independently associated with the expression of 11βHSD1. Barber et al. showed that increased expression of 17β-HSD5 (responsible for catalyzing the conversion of androstenedione to testosterone) and 5α-reductase (responsible for catalyzing the conversion of testosterone to dihydrotestosterone) in adipose tissue was associated with weight gain and hyperandrogenemia in patients with PCOS. The local pattern of sex hormone metabolism in adiposity may also play an important role in determining the distribution of "male" (central) or "female" (peripheral) adiposity, as inactivation of progesterone (which has an anti-glucocorticoid effect) in adiposity and It has been shown that the inactivation of progesterone (which has an anti-glucocorticoid effect) and the simultaneous increase in androgen synthesis in fat are positively associated with obesity in women. Treatment options for PCOS include lifestyle interventions, reduction of androgen and LH levels, regulation of menstruation, improvement of insulin resistance, and promotion of ovulation. Whether or not obesity is combined has an important reference value for the development of treatment plans for patients. Trolle et al. found that metformin was effective only in obese patients, reducing body weight to improve insulin sensitivity and thus lowering testosterone levels, but normal weight patients did not benefit. Metformin 1500 mg/d for 3 months significantly improved LH, testosterone and insulin resistance related indicators, and there was no difference in the resumption of menstruation between the two groups. Metformin also reduced the magnitude of LH secretion pulse in non-obese PCOS patients and improved high LH/FSH to achieve therapeutic effect. It has also been suggested that metformin is more effective in normal weight PCOS patients than in obese patients, promoting more ovulation (88% vs. 29%) and pregnancy (65% vs. 18%). In obese PCOS patients, lifestyle changes are particularly important. Reducing body weight through food restriction, dietary structure interventions, and physical activity can significantly improve hyperinsulinism and hyperandrogenemia, improve menstruation, and promote the return of ovulation in patients. Metformin does not have much advantage over low-carbohydrate diets in reducing central obesity and chronic inflammation, and even, dietary treatment has a better effect on improving insulin sensitivity than metformin. Therefore, in 2010, the Androgen Excess-PCOS Society (AE-PCOS society) published a consensus in the New England Journal of Medicine: Metformin is recommended only for abnormal glucose tolerance (IGT) states that do not improve with lifestyle interventions and for normal weight patients with IGT but who are not candidates for weight loss treatment. Contraceptives are an important treatment for PCOS patients to regulate menstruation and improve Kaohsiung, but they also have the effect of increasing the risk of developing diabetes, especially in obese PCOS patients. Therefore, the application of such drugs requires an assessment of the potential risks that may exist.