Effects of Administering Sodium Selenite, Methylseleninic Acid, and Seleno-L-methionine on Glucose Tolerance in a Streptozotocin/Nicotinamide-Induced Diabetic Mouse Model
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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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- Sakazaki Fumitoshi
- Faculty of Pharmacy, Osaka Ohtani University
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- Nakamuro Katsuhiko
- Faculty of Science and Engineering, Setsunan University
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Abstract
The effects of administering the selenocompounds, sodium selenite, methylseleninic acid (MSA), and seleno-L-methionine (SeMet) on glucose tolerance were compared in the nicotinamide (NA) and streptozotocin (STZ)-induced diabetic mouse model. ICR mice were intraperitoneally treated twice with STZ (100 mg/kg) 15 min after an injection of NA (120 mg/kg) at a 1-d interval. Non-fasting blood glucose levels were then monitored weekly while orally administering the selenocompounds at 158 µg Se/kg body weight with free access to a selenium-deficient diet for 5 weeks. The mean body weights of NA/STZ-induced diabetic mice were partly restored by the administration of selenocompounds, while SeMet led to a higher selenium content and glutathione peroxidase 1 activity in the pancreas. Non-fasting and oral glucose tolerance-tested blood glucose levels, which were elevated by NA/STZ, were significantly suppressed by the administration of SeMet. These results suggest that SeMet may improve glucose tolerance in a NA/STZ-induced mild diabetic mouse model by increasing bioavailability in the pancreas.
Journal
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- Biological and Pharmaceutical Bulletin
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Biological and Pharmaceutical Bulletin 37 (9), 1569-1574, 2014
The Pharmaceutical Society of Japan
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Details 詳細情報について
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- CRID
- 1390282679610462720
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- NII Article ID
- 130004684798
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- NII Book ID
- AA10885497
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- COI
- 1:STN:280:DC%2BC2M%2FmvFKgtw%3D%3D
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- ISSN
- 13475215
- 09186158
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- NDL BIB ID
- 025737111
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- PubMed
- 25177039
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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