Journal
DIABETES METABOLIC SYNDROME AND OBESITY-TARGETS AND THERAPY
Volume 8, Issue -, Pages 181-188Publisher
DOVE MEDICAL PRESS LTD
DOI: 10.2147/DMSO.S82272
Keywords
diabetes; beta cell; glucotoxicity; mitochondria; redox imbalance; streptozotocin
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Funding
- National Institute of Neurological Disorders and Stroke [R01NS079792]
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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 beta 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 beta 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 beta cell glucotoxicity. Evidence presented includes: 1) continued beta 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 beta 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 beta cell dysfunction are also discussed.
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