Source:http://linkedlifedata.com/resource/pubmed/id/12007724
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
1
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pubmed:dateCreated |
2002-5-14
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pubmed:abstractText |
Oxidative stress is induced under diabetic conditions and causes various forms of tissue damage in patients with diabetes. Recently, pancreatic beta-cells have emerged as a putative target of oxidative stress-induced tissue damage and this seems to explain in part the progressive deterioration of beta-cell function in type 2 diabetes. As a step toward clinical trial of antioxidant for type 2 diabetes, we investigated the possible anti-diabetic effects of probucol, an antioxidant widely used as an anti-hyperlipidemic agent, on preservation of beta-cell function in diabetic C57BL/KsJ-db/db mice. Probucol-containing diet was given to mice from 6 to 16 weeks of age. Immunostaining for oxidative stress markers such as 4-hydroxy-2-nonenal (HNE)-modified proteins and heme oxygenase-1 revealed that probucol treatment decreased reactive oxygen species (ROS) in pancreatic islets of diabetic animals. Oxidative stress is known to enhance apoptosis of beta-cells and to suppress insulin biosynthesis, but probucol treatment led to preservation of beta-cell mass and the insulin content. According to intraperitoneal glucose tolerance tests, the probucol treatment preserved glucose-stimulated insulin secretion and improved glucose tolerance at 10 and 16 weeks: insulin, 280+/-82 vs. 914+/-238 pmol/l (120 min, at 16 weeks; P<0.05); glucose, 44.6+/-2.4 vs. 35.2+/-2.6 mmol/l (120 min, at 16 weeks; P<0.05). Thus, our present observations demonstrate the potential usefulness of probucol for treatment of type 2 diabetes.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Jul
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pubmed:issn |
0168-8227
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pubmed:author |
pubmed-author:GorogawaShin ichiS,
pubmed-author:HoriMasatsuguM,
pubmed-author:KajimotoYoshitakaY,
pubmed-author:KanetoHideakiH,
pubmed-author:KawamoriDanD,
pubmed-author:KurodaAkioA,
pubmed-author:MatsuhisaMunehideM,
pubmed-author:UmayaharaYutakaY,
pubmed-author:WatadaHirotakaH,
pubmed-author:YamasakiYoshimitsuY,
pubmed-author:YasudaTetsuyukiT
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pubmed:issnType |
Print
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pubmed:volume |
57
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1-10
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pubmed:dateRevised |
2011-11-17
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pubmed:meshHeading |
pubmed-meshheading:12007724-Animals,
pubmed-meshheading:12007724-Antioxidants,
pubmed-meshheading:12007724-Blood Glucose,
pubmed-meshheading:12007724-Diabetes Mellitus, Type 2,
pubmed-meshheading:12007724-Female,
pubmed-meshheading:12007724-Injections, Intraperitoneal,
pubmed-meshheading:12007724-Insulin,
pubmed-meshheading:12007724-Islets of Langerhans,
pubmed-meshheading:12007724-Mice,
pubmed-meshheading:12007724-Mice, Inbred C57BL,
pubmed-meshheading:12007724-Oxidative Stress,
pubmed-meshheading:12007724-Probucol
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pubmed:year |
2002
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pubmed:articleTitle |
Probucol preserves pancreatic beta-cell function through reduction of oxidative stress in type 2 diabetes.
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pubmed:affiliation |
Department of Internal Medicine and Therapeutics (A8), Osaka University Graduate School of Medicine, 2-2 Yamadaoka, Suita City, Osaka Pref, Japan.
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pubmed:publicationType |
Journal Article
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