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Streptozotocin Induced Diabetes In Mice Protocol

Black Ginseng Extract Counteracts Streptozotocin-induced Diabetes In Mice

Black Ginseng Extract Counteracts Streptozotocin-induced Diabetes In Mice

Abstract Black ginseng, a new type of processed ginseng that has a unique ginsenoside profile, has been shown to display potent pharmacological activities in in vitro and in vivo models. Although red ginseng is considered beneficial for the prevention of diabetes, the relationship between black ginseng and diabetes is unknown. Therefore, this study was designed to evaluate the anti-diabetic potential of black ginseng extract (BGE) in streptozotocin (STZ)-induced insulin-deficient diabetic mice, in comparison with red ginseng extract (RGE). HPLC analyses showed that BGE has a different ginsenoside composition to RGE; BGE contains Rg5 and compound k as the major ginsenosides. BGE at 200 mg/kg reduced hyperglycemia, increased the insulin/glucose ratio and improved islet architecture and β-cell function in STZ-treated mice. The inhibition of β-cell apoptosis by BGE was associated with suppression of the cytokine—induced nuclear factor–κB—mediated signaling pathway in the pancreas. Moreover, these anti-diabetic effects of BGE were more potent than those of RGE. Collectively, our data indicate that BGE, in part by suppressing cytokine—induced apoptotic signaling, protects β-cells from oxidative injury and counteracts diabetes in mice. Figures Citation: Kim JH, Pan JH, Cho HT, Kim YJ (2016) Black Ginseng Extract Counteracts Streptozotocin-Induced Diabetes in Mice. PLoS ONE 11(1): e0146843. Editor: Nigel Irwin, University of Ulster, UNITED KINGDOM Received: October 31, 2015; Accepted: December 22, 2015; Published: January 11, 2016 Copyright: © 2016 Kim et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original autho Continue reading >>

Streptozotocin - Vckd

Streptozotocin - Vckd

2014 Vanderbilt Center for Kidney Disease To induce type I diabetes, we can use the cell toxin, streptozotocin (STZ). In order to mitigate non-specific cytotoxicity, we will use the AMDCC protocol of multiple low-dose STZ injections, which induces diabetes mellitus by inducing repetitive low-grade -cell damage without significant extrapancreatic toxicity (2). We have found that STZ-induced diabetes in DBA mice leads to progressive diabetic nephropathy.In addition, type I diabetes can be induced in eNOS-/- mice by streptozotocin, which induces an accelerated and more severe diabetic nephropathy (1) Nakagawa T, Sato W, Glushakova O, Heinig M, Clarke T, Campbell-Thompson M, Yuzawa Y, Atkinson MA, Johnson RJ, Croker B. Diabetic endothelial nitric oxide synthase knockout mice develop advanced diabetic nephropathy. J Am Soc Nephrol (2007) 18:539-50 The pathogenesis of diabetic nephropathy remains poorly defined, and animal models that represent the human disease have been lacking. It was demonstrated recently that the severe endothelial dysfunction that accompanies a diabetic state may cause an uncoupling of the vascular endothelial growth factor (VEGF)-endothelial nitric oxide (eNO) axis, resulting in increased levels of VEGF and excessive endothelial cell proliferation. It was hypothesized further that VEGF-NO uncoupling could be a major contributory mechanism that leads to diabetic vasculopathy. For testing of this hypothesis, diabetes was induced in eNO synthase knockout mice (eNOS KO) and C57BL6 controls. Diabetic eNOS KO mice developed hypertension, albuminuria, and renal insufficiency with arteriolar hyalinosis, mesangial matrix expansion, mesangiolysis with microaneurysms, and Kimmelstiel-Wilson nodules. Glomerular and peritubular capillaries were increased with endo Continue reading >>

New Mouse Model To Study Islet Transplantation In Insulin-dependent Diabetes Mellitus

New Mouse Model To Study Islet Transplantation In Insulin-dependent Diabetes Mellitus

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[full Text] Streptozotocin-induced Type 1 Diabetes In Rodents As A Model For Study | Dmso

[full Text] Streptozotocin-induced Type 1 Diabetes In Rodents As A Model For Study | Dmso

Editor who approved publication: Professor Ming-Hui Zou 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 cell glucotoxicity in diabetes. As diabetes induced by a single STZ injection is often referred to as type 1 diabetes that is caused by STZs 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 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 cell glucotoxicity. Evidence presented includes: 1) continued 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 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 cell dysfunction are also discussed. Keywords: diabetes, cell, glucotoxicity, mitochondria, redox imbalance, streptozotocin Diabetes mellitus and its complications are chronic glucotoxicity diseases. The concept of cell glucotoxicity (and other cells as well) implicates that persistent excessive glucose can exert adverse or toxic effect on cell function after the Continue reading >>

Death Of Retinal Neurons In Streptozotocin-induced Diabetic Mice | Iovs | Arvo Journals

Death Of Retinal Neurons In Streptozotocin-induced Diabetic Mice | Iovs | Arvo Journals

Death of Retinal Neurons in Streptozotocin-Induced Diabetic Mice From the Departments of Cellular Biology and Anatomy, From the Departments of Cellular Biology and Anatomy, From the Departments of Cellular Biology and Anatomy, From the Departments of Cellular Biology and Anatomy, Ophthalmology, Medical College of Georgia, Augusta, Georgia. Investigative Ophthalmology & Visual Science September 2004, Vol.45, 3330-3336. doi:10.1167/iovs.04-0247 Death of Retinal Neurons in Streptozotocin-Induced Diabetic Mice You will receive an email whenever this article is corrected, updated, or cited in the literature. You can manage this and all other alerts in My Account Pamela M. Martin, Penny Roon, Tracy K. Van Ells, Vadivel Ganapathy, Sylvia B. Smith; Death of Retinal Neurons in Streptozotocin-Induced Diabetic Mice. Invest. Ophthalmol. Vis. Sci. 2004;45(9):3330-3336. doi: 10.1167/iovs.04-0247. ARVO (1962-2015); The Authors (2016-present) purpose. Neuronal cell death has been reported in retinas of humans with diabetic retinopathy and in diabetic rat models. Little is known about neuronal cell death in mouse models of diabetic retinopathy. This study was designed to determine whether neurons are lost in diabetic mouse retinas and whether the loss involves an apoptotic process. methods. Three-week-old C57Bl/6 mice were made diabetic with streptozotocin. They were studied over the course of 14 weeks after onset of diabetes. Eyes were processed for morphometric analysis and detection of apoptotic cells by TUNEL analysis and activated caspase-3 and were subjected to electron microscopy. results. Morphometric analysis of retinal cross sections of mice that had been diabetic 14 weeks showed 20% to 25% fewer cells in the ganglion cell layer compared with age-matched control mice. There w Continue reading >>

A New Method For Targeted And Sustained Induction Of Type 2 Diabetes In Rodents

A New Method For Targeted And Sustained Induction Of Type 2 Diabetes In Rodents

A New Method for Targeted and Sustained Induction of Type 2 Diabetes in Rodents Scientific Reportsvolume7, Articlenumber:14158 (2017) Type 2 diabetes is a chronic metabolic disorder that is becoming a leading cause of morbidity and mortality. The prolonged time-course of human type 2 diabetes makes modelling of the disease difficult and additional animal models and methodologies are needed. The goal of this study was to develop and characterise a new method that allows controlled, targeted and sustained induction of discrete stages of type 2 diabetes in rodents. Using adult, male rats, we employed a three-week high fat-diet regimen and confirmed development of obesity-associated glucose intolerance, a key feature of human type 2 diabetes. Next, we utilised osmotic mini-pumps to infuse streptozotocin (STZ; doses ranging 80200 mg/kg) over the course of 14-days to decrease insulin-producing capacity thus promoting hyperglycemia. Using this new approach, we demonstrate a dose-dependent effect of STZ on circulating glucose and insulin levels as well as glucose tolerance, while retaining a state of obesity. Importantly, we found that insulin secretion in response to a glucose load was present, but reduced in a dose-dependent manner by increasing STZ. In conclusion, we demonstrate a novel method that enables induction of discrete stages of type 2 diabetes in rodents that closely mirrors the different stages of type 2 diabetes in humans. Among the different forms of diabetes, type 2 diabetes accounts for approximately 90% of cases and current estimates indicate that by 2040, approximately 642 million world-wide people will be living with type 2 diabetes 1 , 2 . This is likely to be a conservative estimate given that for every case of diagnosed type 2 diabetes, we know there is Continue reading >>

Springerprotocols: Full Text: Streptozotocin, Type I Diabetes Severity And Bone

Springerprotocols: Full Text: Streptozotocin, Type I Diabetes Severity And Bone

Streptozotocin, Type I Diabetes Severity and Bone As many as 50% of adults with type I (T1) diabetes exhibit bone loss and are at increased risk for fractures. Therapeutic development to prevent bone loss and/or restore lost bone in T1 diabetic patients requires knowledge of the molecular mechanisms accounting for the bone pathology. Because cell culture models alone cannot fully address the systemic/metabolic complexity of T1 diabetes, animal models are critical. A variety of models exist including spontaneous and pharmacologically induced T1 diabetic rodents. In this paper, we discuss the streptozotocin (STZ)-induced T1 diabetic mouse model and examine dose-dependent effects on disease severity and bone. Five daily injections of either 40 or 60mg/kg STZ induce bone pathologies similar to spontaneously diabetic mouse and rat models and to human T1 diabetic bone pathology. Specifically, bone volume, mineral apposition rate, and osteocalcin serum and tibia messenger RNA levels are decreased. In contrast, bone marrow adiposity and aP2 expression are increased with either dose. However, high-dose STZ caused a more rapid elevation of blood glucose levels and a greater magnitude of change in body mass, fat pad mass, and bone gene expression (osteocalcin, aP2). An increase in cathepsin K and in the ratio of RANKL/OPG was noted in high-dose STZ mice, suggesting the possibility that severe diabetes could increase osteoclast activity, something not seen with lower doses. This may contribute to some of the disparity between existing studies regarding the role of osteoclasts in diabetic bone pathology. Examination of kidney and liver toxicity indicate that the high STZ dose causes some liver inflammation. In summary, the multiple low-dose STZ mouse model exhibits a similar bone p Continue reading >>

Modified Dio Protocols Improve Type 2 Diabetes Models

Modified Dio Protocols Improve Type 2 Diabetes Models

Modified DIO Protocols Improve Type 2 Diabete... Modified DIO Protocols Improve Type 2 Diabetes Models Animal models of diet-induced obesity (DIO) are commonly used to model metabolic syndrome, but have some limitations. Can a modified DIO protocol produce better type 2 diabetes models? DIO C57BL/6 mice are obese, glucose intolerant, insulin resistant, and display mild hyperglycemia. To better model Type 2 diabetes, researchers at the University of Colorado and NYU Langone Medical Center recently developed a modified protocol which combines diet induction and streptozotocin treatment in C57BL/6NTac mice . Yu and colleagues obtained DIO B6 mice from Taconic Biosciences and continued feeding the high fat diet D12492 for an additional five weeks. Some mice were then administered low doses of streptozotocin (STZ), a drug which is commonly used to induce Type 1 diabetes by destroying pancreatic beta cells. In this case, the lower STZ dose produced less severe insulin deficiency. The modified protocol of high fat diet + low dose STZ produced mice with higher blood glucose levels and plasma triglycerides compared to Black 6 mice on high fat diet alone. The high fat diet + STZ mice also demonstrated mild body weight loss (~10%). Researchers evaluated the new model by studying its response to canaglifozin, a diabetes treatment which works by inhibiting sodium-glucose transporter 2 ( SGLT2 ). In the clinic, canaglifozin controls hyperglycemia, with some improvement also in lipid profiles. As in humans, treatment of the high fat diet + STZ mice with canaglifozin resulted in lower blood glucose. They also showed lower total plasma cholesterol compared to mice treated with either insulin or a placebo. Although canaglifozin treatment decreased plasma triglycerides in some clinical s Continue reading >>

Streptozotocin-induced Diabetes In Human Apolipoprotein B Transgenic Mice: Effects On Lipoproteins And Atherosclerosis

Streptozotocin-induced Diabetes In Human Apolipoprotein B Transgenic Mice: Effects On Lipoproteins And Atherosclerosis

Streptozotocin-induced diabetes in human apolipoprotein B transgenic mice: effects on lipoproteins and atherosclerosis Department of Medicine, Division of Nutrition and Preventive Medicine, Columbia University College of Physicians and Surgeons, 630 West 168th Street, New York, NY 10032 1 To whom correspondence should be addressed. The effects of diabetes and lipoprotein lipase (LpL) on plasma lipids were studied in mice expressing human apolipoprotein B (HuBTg). Our overall objective was to produce a diabetic mouse model in which the sole effects of blood glucose elevation on atherosclerosis could be assessed. Mice were made diabetic by intraperitoneal injection of streptozotocin, which led to a 2- to 2.5-fold increase in plasma glucose. Lipids were assessed in mice on chow and on an atherogenic Western type diet (WTD), consisting of 21% (wt/wt) fat and 0.15% (wt/wt) cholesterol. Plasma triglyceride and cholesterol were the same in diabetic and non-diabetic mice on the chow diet. On the WTD, male diabetic HuBTg mice had a >50% increase in plasma cholesterol and more very low density lipoprotein (VLDL) cholesterol and triglyceride as assessed by FPLC analysis. A Triton study showed no increase in triglyceride or apolipoprotein B production, suggesting that the accumulation of VLDL was due to a decrease in lipoprotein clearance. Surprisingly, the VLDL increase in these mice was not due to a decrease in LpL activity in postheparin plasma. To test whether LpL overexpression would alter these diabetes-induced lipoprotein changes, HuBTg mice were crossed with mice expressing human LpL in muscle. LpL overexpression reduced plasma triglyceride, but not cholesterol, in male mice on WTD. Aortic root atherosclerosis assessed in 32-week-old mice on the WTD was not greater in diab Continue reading >>

Single Dose Streptozotocin Induced Diabetes: Considerations For Study Design In Islet Transplantation Models

Single Dose Streptozotocin Induced Diabetes: Considerations For Study Design In Islet Transplantation Models

Single Dose Streptozotocin Induced Diabetes: Considerations for Study Design in Islet Transplantation Models We are experimenting with display styles that make it easier to read articles in PMC. The ePub format uses eBook readers, which have several "ease of reading" features already built in. The ePub format is best viewed in the iBooks reader. You may notice problems with the display of certain parts of an article in other eReaders. Generating an ePub file may take a long time, please be patient. Single Dose Streptozotocin Induced Diabetes: Considerations for Study Design in Islet Transplantation Models MC Deeds, JM Anderson, [...], and YC Kudva Streptozotocin (STZ)-induced diabetes mellitus (DM) offers a very cost effective and expeditious technique that can be used in most strains of rodents, opening the field of DM research to an array of genotypic and phenotypic options that would otherwise be inaccessible. Despite widespread use of STZ in small animal models, the data available concerning drug preparation, dosing and administration, time to onset and severity of DM, and any resulting moribundity and mortality are often limited and inconsistent. Because of this, investigators inexperienced with STZ-induced diabetes may find it difficult to precisely design new studies with this potentially toxic chemical and account for the severity of DM it is capable of inducing. Until a better option becomes available, attempts need to be made to address shortcomings with current STZ-induced DM models. In this paper we review the literature and provide data from our pancreatic islet transplantation experiments using single high dose STZ-induced DM in NCr Athymic Nude mice with hopes of providing clarification for study design, suggesting refinements to the process, and develop Continue reading >>

Stz Induced Diabetes I Rats

Stz Induced Diabetes I Rats

I have been working on STZ induced diabetes type I model in rats. I have used 60mg/Kg and 55mg/Kg dose of STZ. induction was good. Can anybody tell me a drug/compound to be used as method control. Ihave used tolbutamide, based on several papers, but it didnt even work slightly. Also I have used Glibenclamide, didnt work. One more thing the blood glucose level rise in my animals was always more than 500mg/dL upto 800mg/dL but most of the papers say 250-350mg/dL. So im confused. Another thing if I reduce the STZ dose will the hyperglycemia level reduce? I fear about the induction percentage.. If you are inducing diabetes type I to make a rat model for the 'first' time you need to standardize your protocol. Have you gone through any research article where STZhas been used to induce this effect? If yes try to follow their protocol and if you are doing it on your own then you need to firt standardize the minimum dosage that precipitates the effects. First check these things then only you should proceed further. As I mentioned earlier too, I have gone through a lot of literature. By the way I have followed a standard protocol after going thru current protocols as well. only thing is I wana know if anybody has any experience with using any standard drug. I have used STZ extensively for the last 3 years. Im a little confused as to what type of control drug you are looking for? As far as the glucose levels in your rats go, if they are hitting 800 mg/dl then you are treating them with too much STZ. Im sure each batch of STZ is different in potency and must be tested for onset of diabetes. In my hands 50mg/kg brought on diabetes 250 mg/dl in 4 weeks after injection. After a few weeks, they animals either went on to full blown diabetes (blood glucose >500 mg/dl) or sometimes recov Continue reading >>

Stz Frequently Asked Questions

Stz Frequently Asked Questions

Streptozotocin (STZ) is an alkylating agent that affects pancreatic islets, inducing diabetes in mice. The males of various strains are differentially susceptible to developing diabetes: FVB/NJ (001800), BALB/cJ (000651), and A/J (000646) males are resistant; C57BL/6J (000664) males are moderately susceptible; and NOD/ShiLtJ (001976) and CBA/J (000656) males are highly susceptible. NOD-congenic strains like NOD.Cg-Prkdcscid Il2rgtm1Wjl/SzJ (NSG; 005557) and NOD.CB17-Prkdcsci/J (NOD scid; 001303) are also highly susceptible. We have developed a multiple low dose STZ protocol that induces diabetes in C57BL/6J, NSG and NOD scid males. What is the JAX protocol for STZ-induced diabetes? Six- to eight-week old C57BL/6J (000664, B6) or NOD.Cg-Prkdcscid Il2rgtm1Wjl/SzJ (005557,NSG) or NOD.CB17-Prkdcscid/JNOD scid ( 001303, NOD scid) males are individually marked, weighed, and their baseline blood glucose levels determined ((OneTouch Ultra monitor) Mice receive daily IP injections of 50 mg STZ/kg body weight (the most effective dose for B6 males) or 40 mg STZ/kg body weight (for NSG males) for five consecutive days; age-matched controls receive bufferonly injections Because mice metabolize STZ for at least 24 hours post-injection, they are housed in disposable cages with appropriate absorbent bedding and food and water ad libitum At least 24-hours after the final injection, all mice are moved to clean cages, weighed, and their blood glucose levels determined The mice are observed daily until 14-16 days post injection, when they are weighed and their blood glucose levels determined (at this time, pancreatic beta-islet cells are totally absent or severely depleted) Blood glucose level and body weight data for individual mice are shipped with the mice How soon and late after being Continue reading >>

Early Myocardial Dysfunction In Streptozotocin-induced Diabetic Mice: A Study Using In Vivo Magnetic Resonance Imaging (mri)

Early Myocardial Dysfunction In Streptozotocin-induced Diabetic Mice: A Study Using In Vivo Magnetic Resonance Imaging (mri)

Early myocardial dysfunction in streptozotocin-induced diabetic mice: a study using in vivo magnetic resonance imaging (MRI) Yu et al; licensee BioMed Central Ltd.2007 Diabetes is associated with a cardiomyopathy that is independent of coronary artery disease or hypertension. In the present study we used in vivo magnetic resonance imaging (MRI) and echocardiographic techniques to examine and characterize early changes in myocardial function in a mouse model of type 1 diabetes. Diabetes was induced in 8-week old C57BL/6 mice with two intraperitoneal injections of streptozotocin. The blood glucose levels were maintained at 1925 mmol/l using intermittent low dosages of long acting insulin glargine. MRI and echocardiography were performed at 4 weeks of diabetes (age of 12 weeks) in diabetic mice and age-matched controls. After 4 weeks of hyperglycemia one marker of mitochondrial function, NADH oxidase activity, was decreased to 50% of control animals. MRI studies of diabetic mice at 4 weeks demonstrated significant deficits in myocardial morphology and functionality including: a decreased left ventricular (LV) wall thickness, an increased LV end-systolic diameter and volume, a diminished LV ejection fraction and cardiac output, a decreased LV circumferential shortening, and decreased LV peak ejection and filling rates. M-mode echocardiographic and Doppler flow studies of diabetic mice at 4 weeks showed a decreased wall thickening and increased E/A ratio, supporting both systolic and diastolic dysfunction. Our study demonstrates that MRI interrogation can identify the onset of diabetic cardiomyopathy in mice with its impaired functional capacity and altered morphology. The MRI technique will lend itself to repetitive study of early changes in cardiac function in small anima Continue reading >>

Streptozotocin, Type I Diabetes Severity And Bone

Streptozotocin, Type I Diabetes Severity And Bone

Streptozotocin, Type I Diabetes Severity and Bone As many as 50% of adults with type I (T1) diabetes exhibit bone loss and are at increased risk for fractures. Therapeutic development to prevent bone loss and/or restore lost bone in T1 diabetic patients requires knowledge of the molecular mechanisms accounting for the bone pathology. Because cell culture models alone cannot fully address the systemic/metabolic complexity of T1 diabetes, animal models are critical. A variety of models exist including spontaneous and pharmacologically induced T1 diabetic rodents. In this paper, we discuss the streptozotocin (STZ)-induced T1 diabetic mouse model and examine dose-dependent effects on disease severity and bone. Five daily injections of either 40 or 60 mg/kg STZ induce bone pathologies similar to spontaneously diabetic mouse and rat models and to human T1 diabetic bone pathology. Specifically, bone volume, mineral apposition rate, and osteocalcin serum and tibia messenger RNA levels are decreased. In contrast, bone marrow adiposity and aP2 expression are increased with either dose. However, high-dose STZ caused a more rapid elevation of blood glucose levels and a greater magnitude of change in body mass, fat pad mass, and bone gene expression (osteocalcin, aP2). An increase in cathepsin K and in the ratio of RANKL/OPG was noted in high-dose STZ mice, suggesting the possibility that severe diabetes could increase osteoclast activity, something not seen with lower doses. This may contribute to some of the disparity between existing studies regarding the role of osteoclasts in diabetic bone pathology. Examination of kidney and liver toxicity indicate that the high STZ dose causes some liver inflammation. In summary, the multiple low-dose STZ mouse model exhibits a similar bone Continue reading >>

Stz-induced Diabetes

Stz-induced Diabetes

Streptozotocin (STZ) is a chemical used for the destruction of insulin-producing cells and for the generation of Type 1 Diabetes phenotypes in mice. The Jackson Laboratory has extensive experience creating a variety of STZ-induced Diabetes models to facilitate your metabolic research. Protocols designed and tested by JAX scientists STZ-treated immunodeficient mice are ideal preclinical models for testing human cellular therapies for diabetes Alternative diabetes models using NSG , C57BL/6J , and NOD scid strains JAX experts handle and properly dispose of harmful streptozotocin, including byproducts found in mouse excretions Diabetes modeling can be integrated with Efficacy TestingServices and histology services, as needed Standard protocols of streptozotocin (STZ) injections are used to induce diabetes in NSG , C57BL/6J , or NOD scid males Customizable diabetes models using other JAX strains, different STZ doses, and more options, after our feasibility assessment Each injected mouse is periodically weighed, glucose levels measured, recorded, and shipped with your research cohorts Only diabetic mice with non-fasted blood glucose levels of at least 250 mg/dl are shipped We can also inject neonatal C57BL/6J pups for non-alcoholic steatohepatitis (NASH) research and other projects Get started with our STZ-induced Diabetes quote form. Continue reading >>

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