**2. Main body**

#### **2.1. Gut-brain axis in controlling eating behavior**

An inability to control eating behavior is the main culprit for eating beyond metabolic needs that result in obesity. Eating behavior is a complex pattern based on communication between specific regulatory and hedonistic centers in hypothalamus and peripheral signals from gastrointestinal tract. The latter system consists of gastric emptying/distention signals and gastrointestinal regulatory (orexigenic and anorexigenic) hormones. In addition, eating behavior is regulated also by cognitive functions and emotional inputs [8, 9].

Orexigenic hormone increases before meal and stimulates hunger and food intake. The most potent known orexigenic hormone ghrelin is released from specific endocrine cells in the stomach and stimulates food intake. On the opposite, hormones, such as cholecystokinin (CCK), peptide tyrosine-tyrosine (PYY) and glucagon-like polipeptide-1 (GLP-1), produce anorexigenic signals and affect peripheral organs and centers in the central nervous system (CNS) in order to stop feeding [8].

Reports about eating behavior in PCOS population are few and the results are not conclusive. It has not been established whether eating behavior is different in obese women with PCOS when compared to weight-matched non-PCOS controls. An increased food intake was reported in animal models and clinical studies with women with PCOS when compared to healthy controls [10–14]. Furthermore, bulimia was associated with an increased frequency of PCOS, suggesting that androgens have appetite-stimulating effects and could impair the impulse control of eating behavior [15]. Disturbed appetite was also associated with altered opioid function demonstrated in PCOS linked to the stimulation of food intake and appetite for high fat/high glucose food through hedonistic centers in hypothalamus [16]. In addition, there are some evidences that disturbed regulation of gastrointestinal signals, in particular incretins, are intrinsic to PCOS [15, 17–21].
