Yan Hua, Gao Yan-Qiong, Zhang Ying, Wang Huan, Liu Gui-Sheng, Lei Jian-Yuan
Department of Geratology, Shaanxi Provincial People's Hospital, Third Affiliated Hospital of Xi'an Jiaotong University, Xi'an 710068, China.
J Biosci. 2018 Jun;43(2):287-294.
Non-alcoholic fatty liver disease (NAFLD) is one of the leading causes of chronic liver diseases around the world and commonly associated with insulin resistance and hyperlipidemia. Chlorogenic acid (CG) was reported to have insulinsensitizing activity and exert hypocholesterolemic and hypoglycemic effect. However, the involvement of CG in NAFLD remains far from being addressed. In this study, a high-fat diet-induced NAFLD rat model was used to investigate the biological roles and underlying mechanism of CG in NAFLD. The results showed that high-fat diet-fed rats exhibited an increase in body weight, glucose tolerance, liver injury, insulin resistance, as well as autophagy and C-Jun N-terminal kinase (JNK) pathway. Nevertheless, all these effects were alleviated by CG treatment. Moreover, angiotensin treatment in CG group activated the JNK pathway, and promoted autophagy, insulin resistance, and liver injury. In conclusion, our findings demonstrated that CG ameliorated liver injury and insulin resistance by suppressing autophagy via inactivation of JNK pathway in a rat model of NAFLD. Therefore, CG might be a potential application for the treatment of NAFLD.
非酒精性脂肪性肝病(NAFLD)是全球慢性肝病的主要病因之一,通常与胰岛素抵抗和高脂血症相关。据报道,绿原酸(CG)具有胰岛素增敏活性,并具有降胆固醇和降血糖作用。然而,CG在NAFLD中的作用仍远未得到解决。在本研究中,使用高脂饮食诱导的NAFLD大鼠模型来研究CG在NAFLD中的生物学作用及其潜在机制。结果表明,高脂饮食喂养的大鼠体重增加、葡萄糖耐量降低、肝损伤、胰岛素抵抗以及自噬和c-Jun氨基末端激酶(JNK)通路均增加。然而,CG治疗减轻了所有这些影响。此外,CG组中的血管紧张素治疗激活了JNK通路,并促进了自噬、胰岛素抵抗和肝损伤。总之,我们的研究结果表明,在NAFLD大鼠模型中,CG通过使JNK通路失活来抑制自噬,从而改善肝损伤和胰岛素抵抗。因此,CG可能是治疗NAFLD的一种潜在应用。