Streptozotocin-induced type 1 diabetes in rodents as a model for studying mitochondrial mechanisms of diabetic β cell glucotoxicity
Jinzi Wu, Liang-Jun Yan Department of Pharmaceutical Sciences, UNT System College of Pharmacy, University of North Texas Health Science Center, Fort Worth, TX, USA Abstract: Chronic hyperglycemia and the corresponding glucotoxicity are the main pathogenic mechanisms of diabetes and its complicatio...
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Dove Medical Press
2015
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oai:doaj.org-article:9626a1c6aeac45c382bfe45a02a281c32021-12-02T02:40:23ZStreptozotocin-induced type 1 diabetes in rodents as a model for studying mitochondrial mechanisms of diabetic β cell glucotoxicity1178-7007https://doaj.org/article/9626a1c6aeac45c382bfe45a02a281c32015-04-01T00:00:00Zhttp://www.dovepress.com/streptozotocin-induced-type-1-diabetes-in-rodents-as-a-model-for-study-peer-reviewed-article-DMSOhttps://doaj.org/toc/1178-7007 Jinzi Wu, Liang-Jun Yan Department of Pharmaceutical Sciences, UNT System College of Pharmacy, University of North Texas Health Science Center, Fort Worth, TX, USA Abstract: Chronic hyperglycemia and the corresponding glucotoxicity are the main pathogenic mechanisms of diabetes and its complications. Streptozotocin (STZ)-induced diabetic animal models are useful platforms for the understanding of β cell glucotoxicity in diabetes. As diabetes induced by a single STZ injection is often referred to as type 1 diabetes that is caused by STZ’s partial destruction of pancreas, one question often being asked is whether the STZ type 1 diabetes animal model is a good model for studying the mitochondrial mechanisms of β cell glucotoxicity. In this mini review, we provide evidence garnered from the literature that the STZ type 1 diabetes is indeed a suitable model for studying mitochondrial mechanisms of diabetic β cell glucotoxicity. Evidence presented includes: 1) continued β cell derangement is due to chronic hyperglycemia after STZ is completely eliminated out of the body; 2) STZ diabetes can be reversed by insulin treatment, which indicates that β cell responds to treatment and shows ability to regenerate; and 3) STZ diabetes can be ameliorated or alleviated by administration of phytochemicals. In addition, mechanisms of STZ action and fundamental gaps in understanding mitochondrial mechanisms of β cell dysfunction are also discussed. Keywords: diabetes, β cell, glucotoxicity, mitochondria, redox imbalance, streptozotocinWu JYan LJDove Medical PressarticleSpecialties of internal medicineRC581-951ENDiabetes, Metabolic Syndrome and Obesity: Targets and Therapy, Vol 2015, Iss default, Pp 181-188 (2015) |
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Specialties of internal medicine RC581-951 Wu J Yan LJ Streptozotocin-induced type 1 diabetes in rodents as a model for studying mitochondrial mechanisms of diabetic β cell glucotoxicity |
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Jinzi Wu, Liang-Jun Yan Department of Pharmaceutical Sciences, UNT System College of Pharmacy, University of North Texas Health Science Center, Fort Worth, TX, USA Abstract: Chronic hyperglycemia and the corresponding glucotoxicity are the main pathogenic mechanisms of diabetes and its complications. Streptozotocin (STZ)-induced diabetic animal models are useful platforms for the understanding of β cell glucotoxicity in diabetes. As diabetes induced by a single STZ injection is often referred to as type 1 diabetes that is caused by STZ’s partial destruction of pancreas, one question often being asked is whether the STZ type 1 diabetes animal model is a good model for studying the mitochondrial mechanisms of β cell glucotoxicity. In this mini review, we provide evidence garnered from the literature that the STZ type 1 diabetes is indeed a suitable model for studying mitochondrial mechanisms of diabetic β cell glucotoxicity. Evidence presented includes: 1) continued β cell derangement is due to chronic hyperglycemia after STZ is completely eliminated out of the body; 2) STZ diabetes can be reversed by insulin treatment, which indicates that β cell responds to treatment and shows ability to regenerate; and 3) STZ diabetes can be ameliorated or alleviated by administration of phytochemicals. In addition, mechanisms of STZ action and fundamental gaps in understanding mitochondrial mechanisms of β cell dysfunction are also discussed. Keywords: diabetes, β cell, glucotoxicity, mitochondria, redox imbalance, streptozotocin |
format |
article |
author |
Wu J Yan LJ |
author_facet |
Wu J Yan LJ |
author_sort |
Wu J |
title |
Streptozotocin-induced type 1 diabetes in rodents as a model for studying mitochondrial mechanisms of diabetic β cell glucotoxicity |
title_short |
Streptozotocin-induced type 1 diabetes in rodents as a model for studying mitochondrial mechanisms of diabetic β cell glucotoxicity |
title_full |
Streptozotocin-induced type 1 diabetes in rodents as a model for studying mitochondrial mechanisms of diabetic β cell glucotoxicity |
title_fullStr |
Streptozotocin-induced type 1 diabetes in rodents as a model for studying mitochondrial mechanisms of diabetic β cell glucotoxicity |
title_full_unstemmed |
Streptozotocin-induced type 1 diabetes in rodents as a model for studying mitochondrial mechanisms of diabetic β cell glucotoxicity |
title_sort |
streptozotocin-induced type 1 diabetes in rodents as a model for studying mitochondrial mechanisms of diabetic β cell glucotoxicity |
publisher |
Dove Medical Press |
publishDate |
2015 |
url |
https://doaj.org/article/9626a1c6aeac45c382bfe45a02a281c3 |
work_keys_str_mv |
AT wuj streptozotocininducedtype1diabetesinrodentsasamodelforstudyingmitochondrialmechanismsofdiabeticbetacellglucotoxicity AT yanlj streptozotocininducedtype1diabetesinrodentsasamodelforstudyingmitochondrialmechanismsofdiabeticbetacellglucotoxicity |
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