Streptozotocin Diabetes
Streptozotocin Diabetes - Related Videos
10:03
A Zebrafish Model of Diabetes Mellitus and Metabolic Memory
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Cited by 69 •
2013
Metabolic memory is the phenomenon by which diabetic complications persist and progress unimpeded even after euglycemia is achieved pharmaceutically. Here we describe a diabetes mellitus zebrafish model which is unique in that it allows for the examination of the mitotically transmissible epigenetic components of metabolic memory in vivo.
10:43
Transplantation of Pancreatic Islets Into the Kidney Capsule of Diabetic Mice
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Cited by 98 •
2007
Our protocol was developed to cleanly and easily deliver islets or cells under the kidney capsule of mice. Cells are concentrated into pellets in the final tubing used for transplanting the cells under the kidney capsule. The ease of this technique reduces stress to the cells and the mouse.
16:59
Neo-Islet Formation in Liver of Diabetic Mice by Helper-dependent Adenoviral Vector-Mediated Gene Transfer
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Cited by 5 •
2012
We describe hepatic neo-islet formation in STZ (streptozotocin)-induced diabetic mice by gene transfer of Neurogenin3 (Ngn3) and Betacellulin (Btc) using helper-dependent adenoviral vector (HDAd) and the reversal of hyperglycemia. Our method takes advantages of helper-dependent adenoviral vectors with their highly efficient in vivo transduction and the long lasting gene expression.
16:26
Regulatory T cells: Therapeutic Potential for Treating Transplant Rejection and Type I Diabetes
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Cited by 2 •
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09:15
Come to the Light Side: In Vivo Monitoring of Pseudomonas aeruginosa Biofilm Infections in Chronic Wounds in a Diabetic Hairless Murine Model
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Cited by 8 •
2017
Here we describe a novel diabetic murine model utilizing hairless mice for real-time, non-invasive, monitoring of biofilm wound infections of bioluminescent Pseudomonas aeruginosa. This method can be adapted to evaluate infection of other bacterial species and genetically modified microorganisms, including multi-species biofilms, and test the efficacy of antibiofilm strategies.
FAQs
Glucose transporter 2 provides the entry route that allows streptozotocin to reach pancreatic beta cells. Once inside, the compound produces DNA damage and cellular stress, disrupting the cells responsible for insulin production. This transporter-linked selectivity helps create an experimental condition centered on beta-cell dysfunction rather than a generalized injury to all cell types.
Sustained hyperglycemia provides the physiological context for examining how diabetes changes host defense. In the Streptozotocin Diabetes model, investigators can assess immune behavior under insulin-deficient conditions and determine how those conditions influence innate and adaptive responses. This makes the model useful for connecting metabolic disturbance with altered susceptibility to infection and impaired tissue repair.
The key sequence includes streptozotocin entry through glucose transporter 2, followed by DNA damage and cellular stress in pancreatic beta cells. These injuries compromise beta-cell function and reduce insulin production, producing the insulin-deficient state required for the model. The sequence is important because it links the initiating chemical exposure to the metabolic and immune consequences studied experimentally.
After the model produces sustained hyperglycemia, researchers examine whether diabetic conditions alter host defense against infection. Studies can focus on both innate and adaptive immune responses, allowing investigators to evaluate how diabetes changes the behavior or effectiveness of these defense systems. The model therefore supports research into why infection-related outcomes may differ under insulin-deficient conditions.
Streptozotocin Diabetes provides a setting for examining tissue repair when insulin deficiency and sustained hyperglycemia are present. Investigators can compare repair-related outcomes with the immune responses observed in the same diabetic context. This is relevant because the model connects metabolic disruption with two interacting research concerns: host defense and the restoration of damaged tissue.
The model can be used to evaluate potential interventions aimed at immune mechanisms or diabetes-associated complications. Investigators apply the experimental condition, examine immune responses, infection susceptibility, or tissue-repair outcomes, and then assess whether an intervention changes those effects. Its value lies in testing candidate approaches under diabetic conditions rather than in a non-diabetic experimental setting.