CHENG LI1,2, JI-YI XIA3, QIN WAN1
1Department of Endocrinology, The Affiliated Hospital of Southwest Medical University, Sichuan Province, Luzhou - 2Department of Endocrinology, The Rongchang District People’s Hospital, Chongqing Province, Rongchang - 3Research Center for Drug and Functional Food of Southwest Medical University, Sichuan Province, Luzhou, P.R.China
Introduction: In pancreatic B cells, the insulin-signaling IRS-PI3K/AKT pathway and the anti-oxidative stress PI3K/AKT- Nrf2/ARE are cross-linked by a PI3K/AKT pathway. This study aims to observe the presence of the IRS-PI3K/AKT-Nrf2/ARE complex pathway in pancreatic B cells.
Materials and methods: A rat model of type 2 diabetes was developed, and the rats were fed a high-sugar, high-fat diet supple- mented with 1% tBHQ, an activator of the Nrf2/ARE pathway, for 8 weeks. Then, various indicators of oxidative stress and inflam- matory response were measured in the serum and pancreatic tissues, and the fluorescence and protein expressions of Nrf2, IRS-2, p- IRS-2, AKTand p-AKT in the islet cells were determined.
Results: Oxidative stress and inflammation of the pancreatic B cells decreased the protein expressions of Nrf2, IRS-2, p-IRS-2, AKT, and p-AKT, and interfered with signal transduction in the IRS-PI3K/AKT-Nrf2/ARE pathway. Activation of the Nrf2/ARE path- way increased the expressions of the above proteins by increasing anti-oxidative stress and anti-inflammatory responses and promot- ing signal transduction in the IRS-PI3K/AKT pathway.
Conclusions: There may exist a complex IRS-PI3K/AKT-Nrf2/ARE pathway for signal transduction in pancreatic B cells. This pathway is likely to play an important role in maintaining a relatively stable environment in the pancreatic B cells.
Nrf2/ARE pathway, IRS-PI3K/AKT pathway, IRS-PI3K/AKT-Nrf2/ARE complex pathway, pancreatic B cell, oxidative stress, chronic inflammation