FABP2 and polycystic ovary syndrome: Tremellen et al. proposed the “gut barrier-endotoxemia-inflammation mechanism” hypothesis, which reflects PCOS pathogenesis (Tremellen and Pearce, 2012), where changes in serum markers such as zonulin, intestinal fatty acid-binding protein 2 (FABP2), and bacterial lipopolysaccharide (LPS) are a result of intestinal barrier damage and inflammation (Sturgeon and Fasano, 2016; Stevens et al., 2018).