In addition to brain, chitosan also evoked the PPAR activity in the stomach. KEGG pathway analysis further revealed that the half of chitosan-regulated pathways in the stomach was related to glucose or lipid metabolism. It has been shown that chitosan and its derivatives markedly prevent the time course-related rise of serum glucose levels in diabetic mice [38]. Moreover, chitosan is well known for its hypotriglyceridemic and hypocholesterolemic effects [39], and exhibits anti-obesity and anti-diabetic effects [1], [9]–[11]. Previous studies showed that chitosan and its derivatives may bind to bile salt components and free fatty acids, resulting in the disrupted lipid absorption in the gut and the increased faecal fat excretion [40]. Chitosan also downregulates the adipogenic molecules such as fatty acid binding protein and glucose transporter 4 via PPAR and CCAAT/enhancer-binding protein α pathways, resulting in the inhibited adipogenesis and differentiation of 3T3-L1 adipocytes [12], [13]. Additionally, plasma proteome analysis showed that chitosan increases the level of adiponectin and decreases the levels of obesity-related proteins, such as resistin, retinol-binding protein 4, TNF-α and interleukin-6 (IL-6), contributing to the anti-diabetic and
