Effect of Seleno-L-methionine on Oxidative Stress in the Pancreatic Islets of a Short-Term Induced Diabetic Mouse Model in Insufficient Selenium Status
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- Ueno Hitoshi
- Faculty of Pharmaceutical Sciences, Setsunan University
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- Shimizu Ryo
- Faculty of Pharmaceutical Sciences, Hiroshima International University
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- Okuno Tomofumi
- Faculty of Pharmaceutical Sciences, Setsunan University
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- Ogino Hirofumi
- Faculty of Pharmaceutical Sciences, Setsunan University
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- Arakawa Tomohiro
- Faculty of Pharmaceutical Sciences, Setsunan University
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- Murano Koichi
- Faculty of Pharmaceutical Sciences, Setsunan University
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- Nakamuro Katsuhiko
- Faculty of Science and Engineering, Setsunan University
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Abstract
<p>The protective effects of seleno-L-methionine (SeMet) on oxidative stress in pancreatic islets were investigated with a short-term nicotinamide (NA) and streptozotocin (STZ)-induced diabetic mouse model. ICR mice were intraperitoneally injected twice with 100 mg/kg STZ and 120 mg/kg NA at a 1-d interval and were then orally administered 158 µg Se/kg SeMet with free access to a selenium-deficient diet for 5 weeks. Administration of SeMet significantly improved the levels of glycated hemoglobin (HbA1c), non-fasting and oral glucose tolerance-tested (OGTT) blood glucose, plasma adiponectin and hepatic glycogen that deteriorated by NA/STZ treatment. However, supplementary SeMet did not restore non-fasting plasma insulin levels in NA/STZ treatment group and significantly suppressed OGTT plasma insulin levels in the control group. Although SeMet significantly suppressed 8-hydroxy-2′-deoxyguanosine density in pancreatic islets, SeMet did not restore insulin density. The hepatic and pancreatic mRNA levels of glutathione peroxidase 1 (GPX1) increased by NA/STZ treatment or SeMet administration. These results suggest that although a physiological level of SeMet improves glucose tolerance by exhibiting insulin-mimetic activity in a short-term induced diabetic mouse model under insufficient Se status, the suppression of pancreatic oxidative stress with the induction GPX1 by SeMet supplementation is unlikely to restore insulin storage and secretion.</p>
Journal
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- Biological and Pharmaceutical Bulletin
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Biological and Pharmaceutical Bulletin 41 (1), 80-85, 2018
The Pharmaceutical Society of Japan
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Details 詳細情報について
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- CRID
- 1390001204634265728
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- NII Article ID
- 130006301211
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- NII Book ID
- AA10885497
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- ISSN
- 13475215
- 09186158
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- NDL BIB ID
- 028739344
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- PubMed
- 29311486
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- Text Lang
- en
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- Data Source
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- JaLC
- NDL
- Crossref
- PubMed
- CiNii Articles
- KAKEN
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- Abstract License Flag
- Disallowed