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-a and interleukin6, contributing to the anti-diabetic and anti-obesity potentials in ob/ob mice. Our data showed that chitosan significantly regulated the IL-6 and TNF-a Gomisin-D signaling pathways in the guts, which were consistent with previous findings. Moreover, we newly identified that chitosan significantly regulated the glucose metabolic pathways, such as glycolysis/gluconeogenesis and insulin signaling pathway, which might contribute to the hypoglycemic effect of chitosan. Microarray data showed that chitosan downregulated the expressions of apoB and ghrelin genes in the stomach. ApoB, a large amphipathic protein, is mainly expressed in the liver and is present on very-low density lipoproteins, intermediate density lipoproteins, and low-density lipoproteins. ApoB is required for the formation of VLDL in the liver. Binding of apoB to the microsomal transport protein results in the incorporation of lipids into the apoB molecule and leads to the formation of VLDL particles. In clinical practice, apoB can be used as a marker to estimate the total number of atherogenic lipoprotein particles. Elevated apoB is a hallmark of several inherited disorders associated with atherosclerosis. However, patients with extremely low levels of apoB seem to be protected against cardiovascular diseases. Because apoB is an essential component of lipoprotein, the down-regulated expression of apoB gene by chitosan might contribute to the hypotriglyceridemic and hypocholesterolemic Glycitin effects of chitosan. Ghrelin is a peptide hormone mainly produced by the stomach. Ghrelin is a potent stimulator of growth hormone secretion. Moreover, it is the only circulatory hormone that potently enhances the feeding and weight gain, increases the gastrointestinal mobility, and regulates the energy homeostasis. Furthermore, ghrelin-based components may have therapeutic effects in treating malnutrition. Because ghrelin has a great impact on the food intake or body weight, the down-regulated expression of ghrelin gene by chitosan might explain why chitosan exhibited the anti-obestic effect. In conclusion, we applied PPAR bioluminescent imagingguided transcriptomic analysis to evaluate the organs that chitosan acted on and to analyze the molecular mechanisms of chitosan in this study. We found that administration of chitosan induced the PPAR-driven bioluminescent signals in brain and stomach. Microarray analysis showed that several pathways associated with lipid and glucose metabolism were regulated by chitosan. Moreover, we newly identified that chitosan may exhibit hypocholestemic and anti-obestic effects via downregulated expression of apoB and ghrelin genes.