Anti-Obesity Effect and Mechanism of Chitooligosaccharides Were Revealed Based on Lipidomics in Diet-Induced Obese Mice

Chitooligosaccharide (COS) is a natural product from the ocean, and while many studies have reported its important role in metabolic diseases, no study has systematically elaborated the anti-obesity effect and mechanism of COS. Herein, COSM (MW & LE; 3000 Da) was administered to diet-induced obese mice by oral gavage once daily for eight weeks. The results show that COSM administration reduced body weight; slowed weight gain; reduced serum Glu, insulin, NEFA, TC, TG, and LDL-C levels; increased serum HSL and HDL-C levels; improved inflammation; and reduced lipid droplet size in adipose tissue. Further lipidomic analysis of adipose tissue revealed that 31 lipid species are considered to be underlying lipid biomarkers in COS therapy. These lipids are mainly enriched in pathways involving insulin resistance, thermogenesis, cholesterol metabolism, glyceride metabolism and cyclic adenosine monophosphate (cAMP), which sheds light on the weight loss mechanism of COS. The Western blot assay demonstrated that COSM intervention can improve insulin resistance, inhibit de novo synthesis, and promote thermogenesis and & beta;-oxidation in mitochondria by the AMPK pathway, thereby alleviating high-fat diet-induced obesity. In short, our study can provide a more comprehensive direction for the application of COS in obesity based on molecular markers.

Automated summary

This study investigated the anti-obesity effect and mechanism of chitooligosaccharide (COS) in diet-induced obese mice. The results showed that COS administration reduced body weight, improved lipid metabolism, and alleviated inflammation. Lipidomic analysis revealed underlying lipid biomarkers involved in insulin resistance, thermogenesis, cholesterol metabolism, glyceride metabolism, and cyclic adenosine monophosphate (cAMP) pathways. Western blot assay confirmed that COS intervention improved insulin resistance, inhibited de novo synthesis, and promoted thermogenesis and β-oxidation through the AMPK pathway.