Chicoric acid prevents obesity by attenuating hepatic steatosis, inflammation and oxidative stress in high-fat diet-fed mice

- Chicoric acid exhibited significant antiobesity activities in vivo.
- Chicoric acid attenuated insulin resistance, liver injury and inflammation in mice.
- Chicoric acid enhanced antioxidant defense system in high-fat diet-fed mice.
- Chicoric acid regulated adipocytokines and adipogenesis-associated proteins levels.

Chicoric acid, a natural phenolic acid, has been found to possess multiple biological properties. However, the antiobesity activity of chicoric acid remains unclear. In the present study, high-fat diet-induced obese C57BL/6J mice were used to investigate the antiobesity effect of chicoric acid in vivo. The results showed that chicoric acid significantly reduced body weight and lowered serum lipid parameters as well as homeostasis model assessment of insulin resistance (HOMA-IR) in HFD-fed mice. Meanwhile, chicoric acid appeared to attenuate high-fat diet-induced liver injury through decreasing hepatic steatosis and fatty acid synthase (FAS) levels, serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels and the Bax/Bcl-2 ratio in liver. Chicoric acid had a positive effect on obesity-associated hepatic inflammation via reducing TNF-α and IL-6 levels as well as protein expressions of COX-2 and p-JNK. High-fat diet mice treated with chicoric acid exhibited enhanced antioxidant defense system and reduced liver lipid peroxidation through increasing the activity of antioxidant enzymes and total antioxidant capacity (TAC) in liver. Furthermore, chicoric acid also regulated the levels of leptin and adiponectin as well as inhibited the protein expressions of peroxisome proliferator-activated receptor γ (PPARγ) and CCAAT/enhancer-binding protein α (C/EBPα). Therefore, chicoric acid efficiently inhibited obesity in high-fat diet-fed mice through attenuating insulin resistance, liver injury and inflammation, enhancing antioxidant defense system, and regulating the secretions of adipocytokines and adipogenesis-associated proteins.