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| Content Provider | PubMed Central |
|---|---|
| Author | Shao, Chen Gu, Jianqiu Meng, Xin Zheng, Hongzhi Wang, Difei |
| Copyright Year | 2015 |
| Abstract | Objectives: Glucose fluctuation is suggested to be the leading cause of beta-cell damages. To determine how it induces beta-cell dysfunction, we systematically evaluated the effects of intermittent high glucose (IHG) in INS-1 rat pancreatic beta-cells on their proliferation activity, apoptosis, insulin secretion, reactive oxygen species (ROS), intracellular concentration of Ca2+ ([Ca2+]i), and the PTEN expression as well as AKT phosphorylation. Methods: Prior to the examinations, INS-1 cells were treated with normal glucose (NG, 11.1 mmol/L), sustained high glucose (SHG, 33 mmol/L), IHG (switching per 12 h in 11.1 mmol/l or 33 mmol/L), NG+α-lipoic acid (LA, pretreated with LA 12 h before exposure to NG), SHG+LA (pretreated with LA 12 h before being exposed to 33.3 mmol/L glucose) and IHG+LA (pretreated with LA 12 h before being cultured with IHG). The cells in each group were cultured with indicated concentrations of glucose for 3 days. The evaluations were carried out on the cell viability, apoptosis rate, insulin secretion, [Ca2+]i, ROS and the expressions of PTEN and p-AKT. Results: The current study determined that IHG induces more apoptosis and significant increases of [Ca2+]i and intracellular ROS levels, compared to SHG and NG treatments to INS-1 cells. Moreover, IHG leads to more than 20% decrease on cell viability and over 50% reduction on insulin secretion (from 5.48±0.79 mIU/L to 2.51±0.58 mIU/L). The negative regulation of IHG on insulin signaling in beta-cells is identified via western blot analysis with results of the elevated expression of PTEN and lowered phosphorylation levels of AKT post IHG treatment. While the pretreatment of the antioxidant LA can significantly suppress the above responses induced by high glucose treatment. Conclusions: This study demonstrated that IHG plays a detrimental role in the viability, expansion, and function of beta-cells. IHG could be more harmful to the INS-1 cells than the SHG treatment. The rate increase of apoptosis in beta-cells could be caused by the suppressed insulin signaling, which is resulted from the raised ROS level by abnormal glucose treatments. Undergoing oxidative stress induced by high glucose treatments, including SHG and IHG, might be an important player in mediating the injury process to beta-cells, concluded from the beneficial rescue by the antioxidant LA treatment. |
| Ending Page | 5469 |
| Starting Page | 5462 |
| File Format | |
| ISSN | 19405901 |
| e-ISSN | 19405901 |
| Journal | International Journal of Clinical and Experimental Medicine |
| Issue Number | 4 |
| Volume Number | 8 |
| Language | English |
| Publisher | e-Century Publishing Corporation |
| Publisher Date | 2015-04-15 |
| Access Restriction | Open |
| Rights Holder | e-Century Publishing Corporation |
| Subject Keyword | Research in Higher Education |
| Content Type | Text |
| Resource Type | Article |
| Subject | Biochemistry, Genetics and Molecular Biology |
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