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Abstract Title:

Oleanolic acid attenuates PCBs-induced adiposity and insulin resistance via HNF1b-mediated regulation of redox and PPARγ signaling.

Abstract Source:

Free Radic Biol Med. 2018 Jun 4. Epub 2018 Jun 4. PMID: 29879443

Abstract Author(s):

Shuhao Su, Guangyuan Wu, Xiaodong Cheng, Junshu Fan, Jie Peng, Hongfei Su, Zhongrui Xu, Meng Cao, Zi Long, Yiming Hao, Ge Li, Shuang Li, Chunxu Hai, Xin Wang

Article Affiliation:

Shuhao Su

Abstract:

Polychlorinated biphenyls (PCBs) exposure is closely associated with obesity and diabetes. However, the mechanism of PCBs-induced adiposity and insulin resistance is not clear and the intervention is limited. We have found that oleanolic acid (OA) is a natural triterpenoid, possessing antioxidant and anti-diabetic activity, and hepatocyte nuclear factor 1b (HNF1b) is an important regulator of glucose and lipid metabolism. The present study aimed to investigate the effect of OA on Aroclor 1254-induced adiposity and insulin resistance and explore the possible involvement of HNF1b. We showed that OA significantly attenuated Aroclor 1254-induced insulin resistance and abnormal changes of glucose and lipid parameters. OA inhibited the increase of adipose weight and adipocyte size in Aroclor 1254-treated mice and repressed adipocyte differentiation in vitro. In addition, OA markedly inhibited Aroclor 1254-induced increase of ROS, oxidant products, NOX4 expression, decrease of SOD1, SOD2, GCLC, GCLM and Gpx1 expression, and increase of PPARγ signaling. Aroclor 1254 resulted in a decrease of HNF1b expression in adipose of mice and adipocytes, which was inhibited by OA. Upregulation of HNF1b blocked Aroclor 1254-induced oxidative stress, adipocyte differentiation and insulin resistance. Downregulation of HNF1b inhibited OA-induced protective effects against Aroclor 1254-associated oxidative stress, adipocyte differentiation and insulin resistance. The antioxidant Vitamin C reduced Aroclor 1254-induced ROS generation in vitro, but had no significant effect on HNF1b expression, oxidative stress and metabolic dysfunction in vivo. OAcould inhibit PCBs mixture-induced oxidative injury and glucose/lipid metabolic dysfunction via HNF1b-mediated regulation of redox homeostasis. Our data suggest that HNF1b is a new on/off switch of redox homeostasis and OA-stimulated HNF1b-endogenous antioxidant activity is a potential option for the intervention of PCBs exposure-related adiposity and insulin resistance.

Study Type : Animal Study, In Vitro Study

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