Effects of Simvastatin on Glucose Metabolism in Mouse MIN6 Cells

The aim of this study was to investigate the effects of simvastatin on insulin secretion in mouse MIN6 cells and the possible mechanism. MIN6 cells were, respectively, treated with 0 μM, 2 μM, 5 μM, and 10 μM simvastatin for 48 h. Radio immunoassay was performed to measure the effect of simvastatin...

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Main Authors: Jieqiong Zhou, Weihua Li, Qiang Xie, Yuxi Hou, Shaopeng Zhan, Xi Yang, Xiaofeng Xu, Jun Cai, Zhengrong Huang
Format: Article
Language:English
Published: Wiley 2014-01-01
Series:Journal of Diabetes Research
Online Access:http://dx.doi.org/10.1155/2014/376570
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author Jieqiong Zhou
Weihua Li
Qiang Xie
Yuxi Hou
Shaopeng Zhan
Xi Yang
Xiaofeng Xu
Jun Cai
Zhengrong Huang
author_facet Jieqiong Zhou
Weihua Li
Qiang Xie
Yuxi Hou
Shaopeng Zhan
Xi Yang
Xiaofeng Xu
Jun Cai
Zhengrong Huang
author_sort Jieqiong Zhou
collection DOAJ
description The aim of this study was to investigate the effects of simvastatin on insulin secretion in mouse MIN6 cells and the possible mechanism. MIN6 cells were, respectively, treated with 0 μM, 2 μM, 5 μM, and 10 μM simvastatin for 48 h. Radio immunoassay was performed to measure the effect of simvastatin on insulin secretion in MIN6 cells. Luciferase method was used to examine the content of ATP in MIN6 cells. Real-time PCR and western blotting were performed to measure the mRNA and protein levels of inward rectifier potassium channel 6.2 (Kir6.2), voltage-dependent calcium channel 1.2 (Cav1.2), and glucose transporter-2 (GLUT2), respectively. ATP-sensitive potassium current and L-type calcium current were recorded by whole-cell patch-clamp technique. The results showed that high concentrations of simvastatin (5 μM and 10 μM) significantly reduced the synthesis and secretion of insulin compared to control groups in MIN6 cells (P<0.05). ATP content in simvastatin-treated cells was lower than in control cells (P<0.05). Compared with control group, the mRNA and protein expression of Kir6.2 increased with treatment of simvastatin (P<0.05), and mRNA and protein expression of Cav1.2 and GLUT2 decreased in response to simvastatin (P<0.05). Moreover, simvastatin increased the ATP-sensitive potassium current and reduced the L-type calcium current. These results suggest that simvastatin inhibits the synthesis and secretion of insulin through a reduction in saccharometabolism in MIN6 cells.
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language English
publishDate 2014-01-01
publisher Wiley
record_format Article
series Journal of Diabetes Research
spelling doaj-art-645e03cae8204f76bc0a9f589bf9efa12025-02-03T06:07:02ZengWileyJournal of Diabetes Research2314-67452314-67532014-01-01201410.1155/2014/376570376570Effects of Simvastatin on Glucose Metabolism in Mouse MIN6 CellsJieqiong Zhou0Weihua Li1Qiang Xie2Yuxi Hou3Shaopeng Zhan4Xi Yang5Xiaofeng Xu6Jun Cai7Zhengrong Huang8Department of Cardiology, The First Affiliated Hospital of Xiamen University, 55 Zhenhai Road, Xiamen 361003, ChinaDepartment of Cardiology, The First Affiliated Hospital of Xiamen University, 55 Zhenhai Road, Xiamen 361003, ChinaDepartment of Cardiology, The First Affiliated Hospital of Xiamen University, 55 Zhenhai Road, Xiamen 361003, ChinaDepartment of Cardiology, The First Affiliated Hospital of Xiamen University, 55 Zhenhai Road, Xiamen 361003, ChinaDepartment of Cardiology, The First Affiliated Hospital of Xiamen University, 55 Zhenhai Road, Xiamen 361003, ChinaDepartment of Cardiology, The First Affiliated Hospital of Xiamen University, 55 Zhenhai Road, Xiamen 361003, ChinaDepartment of Cardiology, The First Affiliated Hospital of Xiamen University, 55 Zhenhai Road, Xiamen 361003, ChinaDepartment of Cardiology, Chaoyang Hospital, Capital Medical University, 8th Gongtinanlu Road, Chaoyang District, Beijing 100020, ChinaDepartment of Cardiology, The First Affiliated Hospital of Xiamen University, 55 Zhenhai Road, Xiamen 361003, ChinaThe aim of this study was to investigate the effects of simvastatin on insulin secretion in mouse MIN6 cells and the possible mechanism. MIN6 cells were, respectively, treated with 0 μM, 2 μM, 5 μM, and 10 μM simvastatin for 48 h. Radio immunoassay was performed to measure the effect of simvastatin on insulin secretion in MIN6 cells. Luciferase method was used to examine the content of ATP in MIN6 cells. Real-time PCR and western blotting were performed to measure the mRNA and protein levels of inward rectifier potassium channel 6.2 (Kir6.2), voltage-dependent calcium channel 1.2 (Cav1.2), and glucose transporter-2 (GLUT2), respectively. ATP-sensitive potassium current and L-type calcium current were recorded by whole-cell patch-clamp technique. The results showed that high concentrations of simvastatin (5 μM and 10 μM) significantly reduced the synthesis and secretion of insulin compared to control groups in MIN6 cells (P<0.05). ATP content in simvastatin-treated cells was lower than in control cells (P<0.05). Compared with control group, the mRNA and protein expression of Kir6.2 increased with treatment of simvastatin (P<0.05), and mRNA and protein expression of Cav1.2 and GLUT2 decreased in response to simvastatin (P<0.05). Moreover, simvastatin increased the ATP-sensitive potassium current and reduced the L-type calcium current. These results suggest that simvastatin inhibits the synthesis and secretion of insulin through a reduction in saccharometabolism in MIN6 cells.http://dx.doi.org/10.1155/2014/376570
spellingShingle Jieqiong Zhou
Weihua Li
Qiang Xie
Yuxi Hou
Shaopeng Zhan
Xi Yang
Xiaofeng Xu
Jun Cai
Zhengrong Huang
Effects of Simvastatin on Glucose Metabolism in Mouse MIN6 Cells
Journal of Diabetes Research
title Effects of Simvastatin on Glucose Metabolism in Mouse MIN6 Cells
title_full Effects of Simvastatin on Glucose Metabolism in Mouse MIN6 Cells
title_fullStr Effects of Simvastatin on Glucose Metabolism in Mouse MIN6 Cells
title_full_unstemmed Effects of Simvastatin on Glucose Metabolism in Mouse MIN6 Cells
title_short Effects of Simvastatin on Glucose Metabolism in Mouse MIN6 Cells
title_sort effects of simvastatin on glucose metabolism in mouse min6 cells
url http://dx.doi.org/10.1155/2014/376570
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