Fig. 2

Inflammatory consequences and possible markers related to polycystic ovary syndrome (PCOS): Considering the dietary influence, excessive intake of carbohydrates and fats causes obesity and hyperinsulinemia/insulin resistance (IR) in young women. Obesity and IR have a positive influence on the pathogenesis of PCOS. The obesity-induced hypertrophic adipocytes sharply increase the level of adiponectin, leptin, IL-6, and TNF-α which cumulatively contribute to the inflammation of adipose tissue. This hypertrophic adipose tissue resulted in androgen excess which might contribute to IR. The stimulated hepatocytes produce acute phase response protein CRP. The pro-inflammatory cytokines and leptins cause chronic low-grade inflammation via the activation of NF-κB. The excessive production of reactive oxygen species (ROS) and cortisol is responsible for the onset of stress-induced immune alterations as well as attenuated T cell response. Simultaneously, the increased macrophage activation, higher neutrophil-to-lymphocyte ratio (NLR), and mean platelet volume (MPV) are observed as the hallmarks of PCOS