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Inhibition of Calcium Influx Reduces Dysfunction and Apoptosis in Lipotoxic Pancreatic β-Cells via Regulation of Endoplasmic Reticulum Stress.

Lipotoxicity plays an important role in pancreatic [beta]-cell failure during the development of type 2 diabetes. Prolonged exposure of [beta]-cells to elevated free fatty acids level could cause deterioration of [beta]-cell function and induce cell apoptosis. Therefore, inhibition of fatty acids-in... Full description

Journal Title: PloS one 2015, Vol.10(7), p.e0132411
Main Author: Zhou, Yuren
Other Authors: Sun, Peng , Wang, Ting , Chen, Kaixian , Zhu, Weiliang , Wang, Heyao
Format: Electronic Article Electronic Article
Language: English
Subjects:
ID: E-ISSN: 1932-6203 ; DOI: 10.1371/journal.pone.0132411
Link: http://search.proquest.com/docview/1694962920/?pq-origsite=primo
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title: Inhibition of Calcium Influx Reduces Dysfunction and Apoptosis in Lipotoxic Pancreatic β-Cells via Regulation of Endoplasmic Reticulum Stress.
format: Article
creator:
  • Zhou, Yuren
  • Sun, Peng
  • Wang, Ting
  • Chen, Kaixian
  • Zhu, Weiliang
  • Wang, Heyao
subjects:
  • Animals–Drug Effects
  • Apoptosis–Drug Effects
  • Calcium Signaling–Metabolism
  • Cell Line, Tumor–Pathology
  • Diabetes Mellitus, Type 2–Pharmacology
  • Diazoxide–Drug Effects
  • Endoplasmic Reticulum Stress–Metabolism
  • Insulin-Secreting Cells–Pathology
  • Mice–Pharmacology
  • Nifedipine–Toxicity
  • Palmitic Acid–Toxicity
  • Palmitic Acid
  • Nifedipine
  • Diazoxide
ispartof: PloS one, 2015, Vol.10(7), p.e0132411
description: Lipotoxicity plays an important role in pancreatic [beta]-cell failure during the development of type 2 diabetes. Prolonged exposure of [beta]-cells to elevated free fatty acids level could cause deterioration of [beta]-cell function and induce cell apoptosis. Therefore, inhibition of fatty acids-induced [beta]-cell dysfunction and apoptosis might provide benefit for the therapy of type 2 diabetes. The present study examined whether regulation of fatty acids-triggered calcium influx could protect pancreatic [beta]-cells from lipotoxicity. Two small molecule compounds, L-type calcium channel blocker nifedipine and potassium channel activator diazoxide were used to inhibit palmitic acid-induced calcium influx. And whether the compounds could reduce palmitic acid-induced [beta]-cell failure and the underlying mechanism were also investigated. It was found that both nifedipine and diazoxide protected MIN6 pancreatic [beta]-cells and primary cultured murine islets from palmitic acid-induced apoptosis. Meanwhile, the impaired insulin secretion was also recovered to varying degrees by these two compounds. Our results verified that nifedipine and diazoxide could reduce palmitic acid-induced endoplasmic reticulum stress to generate protective effects on pancreatic [beta]-cells. More importantly, it suggested that regulation of calcium influx by small molecule compounds might provide benefits for the prevention and therapy of type 2 diabetes.
language: eng
source:
identifier: E-ISSN: 1932-6203 ; DOI: 10.1371/journal.pone.0132411
fulltext: fulltext
issn:
  • 19326203
  • 1932-6203
url: Link


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titleInhibition of Calcium Influx Reduces Dysfunction and Apoptosis in Lipotoxic Pancreatic β-Cells via Regulation of Endoplasmic Reticulum Stress.
creatorZhou, Yuren ; Sun, Peng ; Wang, Ting ; Chen, Kaixian ; Zhu, Weiliang ; Wang, Heyao
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identifierE-ISSN: 1932-6203 ; DOI: 10.1371/journal.pone.0132411
subjectAnimals–Drug Effects ; Apoptosis–Drug Effects ; Calcium Signaling–Metabolism ; Cell Line, Tumor–Pathology ; Diabetes Mellitus, Type 2–Pharmacology ; Diazoxide–Drug Effects ; Endoplasmic Reticulum Stress–Metabolism ; Insulin-Secreting Cells–Pathology ; Mice–Pharmacology ; Nifedipine–Toxicity ; Palmitic Acid–Toxicity ; Palmitic Acid ; Nifedipine ; Diazoxide
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descriptionLipotoxicity plays an important role in pancreatic [beta]-cell failure during the development of type 2 diabetes. Prolonged exposure of [beta]-cells to elevated free fatty acids level could cause deterioration of [beta]-cell function and induce cell apoptosis. Therefore, inhibition of fatty acids-induced [beta]-cell dysfunction and apoptosis might provide benefit for the therapy of type 2 diabetes. The present study examined whether regulation of fatty acids-triggered calcium influx could protect pancreatic [beta]-cells from lipotoxicity. Two small molecule compounds, L-type calcium channel blocker nifedipine and potassium channel activator diazoxide were used to inhibit palmitic acid-induced calcium influx. And whether the compounds could reduce palmitic acid-induced [beta]-cell failure and the underlying mechanism were also investigated. It was found that both nifedipine and diazoxide protected MIN6 pancreatic [beta]-cells and primary cultured murine islets from palmitic acid-induced apoptosis. Meanwhile, the impaired insulin secretion was also recovered to varying degrees by these two compounds. Our results verified that nifedipine and diazoxide could reduce palmitic acid-induced endoplasmic reticulum stress to generate protective effects on pancreatic [beta]-cells. More importantly, it suggested that regulation of calcium influx by small molecule compounds might provide benefits for the prevention and therapy of type 2 diabetes.
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