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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
1
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pubmed:dateCreated |
2010-9-6
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pubmed:abstractText |
Angiotensin II receptor blockers (ARBs) have been shown to decrease insulin resistance in obese diabetic animal models and reduce the risk of new-onset diabetes in hypertensive patients. In the present study, we studied whether candesartan, an ARB, can exert a direct effect against fatty acid-induced oxidative stress in pancreatic beta-cells. The effect of candesartan on lipotoxicity was evaluated using mouse insulin-secreting clonal cell, MIN6 and isolated mouse pancreatic islets. Intracellular insulin and triglyceride content, uncoupling protein-2 (UCP-2) mRNA expression, reactive oxygen species, protein kinase C (PKC) and NAD(P)H oxidase activity were examined. Candesartan recovered decreased insulin content in MIN6 exposed to 25mM glucose with 0.5mM palmitate (P<0.01). Candesartan tended to decrease intracellular triglyceride accumulation in cells exposed to 25mM glucose with 0.5mM palmitate. Palmitate-induced up-regulation of UCP-2 mRNA levels was suppressed by candesartan in a dose-dependent manner. Candesartan decreased palmitate-induced reactive oxygen species accumulation in MIN6 cells by 23% and in mouse islets by 59%. Candesartan also decreased palmitate-induced PKC activity by 21% and NAD(P)H oxidase activity by 37% in MIN6 cells. These findings indicated that candesartan attenuated fatty acid-induced oxidative stress and NAD(P)H oxidase activity in pancreatic beta-cells.
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Angiotensin II Type 1 Receptor...,
http://linkedlifedata.com/resource/pubmed/chemical/Antioxidants,
http://linkedlifedata.com/resource/pubmed/chemical/Benzimidazoles,
http://linkedlifedata.com/resource/pubmed/chemical/Insulin,
http://linkedlifedata.com/resource/pubmed/chemical/Ion Channels,
http://linkedlifedata.com/resource/pubmed/chemical/Mitochondrial Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/NADPH Oxidase,
http://linkedlifedata.com/resource/pubmed/chemical/Palmitic Acid,
http://linkedlifedata.com/resource/pubmed/chemical/Protein Kinase C,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger,
http://linkedlifedata.com/resource/pubmed/chemical/Reactive Oxygen Species,
http://linkedlifedata.com/resource/pubmed/chemical/Tetrazoles,
http://linkedlifedata.com/resource/pubmed/chemical/Triglycerides,
http://linkedlifedata.com/resource/pubmed/chemical/candesartan,
http://linkedlifedata.com/resource/pubmed/chemical/mitochondrial uncoupling protein 2
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pubmed:status |
MEDLINE
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pubmed:month |
Oct
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pubmed:issn |
1872-8227
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pubmed:author |
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pubmed:issnType |
Electronic
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pubmed:volume |
90
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
54-9
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pubmed:dateRevised |
2011-11-17
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pubmed:meshHeading |
pubmed-meshheading:20667613-Angiotensin II Type 1 Receptor Blockers,
pubmed-meshheading:20667613-Animals,
pubmed-meshheading:20667613-Antioxidants,
pubmed-meshheading:20667613-Benzimidazoles,
pubmed-meshheading:20667613-Cell Line,
pubmed-meshheading:20667613-Female,
pubmed-meshheading:20667613-Gene Expression Regulation,
pubmed-meshheading:20667613-Hyperglycemia,
pubmed-meshheading:20667613-Insulin,
pubmed-meshheading:20667613-Insulin-Secreting Cells,
pubmed-meshheading:20667613-Ion Channels,
pubmed-meshheading:20667613-Islets of Langerhans,
pubmed-meshheading:20667613-Mice,
pubmed-meshheading:20667613-Mice, Inbred C57BL,
pubmed-meshheading:20667613-Mitochondrial Proteins,
pubmed-meshheading:20667613-NADPH Oxidase,
pubmed-meshheading:20667613-Osmolar Concentration,
pubmed-meshheading:20667613-Oxidative Stress,
pubmed-meshheading:20667613-Palmitic Acid,
pubmed-meshheading:20667613-Protein Kinase C,
pubmed-meshheading:20667613-RNA, Messenger,
pubmed-meshheading:20667613-Reactive Oxygen Species,
pubmed-meshheading:20667613-Tetrazoles,
pubmed-meshheading:20667613-Triglycerides
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pubmed:year |
2010
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pubmed:articleTitle |
Candesartan attenuates fatty acid-induced oxidative stress and NAD(P)H oxidase activity in pancreatic beta-cells.
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pubmed:affiliation |
Division of Endocrinology and Metabolism, Department of Internal Medicine, University of Miyazaki, Faculty of Medicine, Kiyotake, Miyazaki, Japan.
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pubmed:publicationType |
Journal Article
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