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How To Induce Diabetes In Mice

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 >>

Mouse Models Of Diabetic Nephropathy

Mouse Models Of Diabetic Nephropathy

*Vanderbilt University and VA Medical Center, Nashville, Tennessee; Mount Sinai Medical School, New York, New York; University of Michigan, Ann Arbor, Michigan; Duke University and Durham VA Medical Centers, Durham, North Carolina; Departments of Medicine and Cellular & Molecular Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland; and Dorrance Hamilton Research Laboratories, Thomas Jefferson University, Philadelphia, Pennsylvania Dr. Matthew D. Breyer, Division of Nephrology and Departments of Medicine and Molecular Physiology and Biophysics, Vanderbilt University Medical School, S3223 MCN, Division of Nephrology, Nashville, TN 37232. Phone: 615-343-9867; Fax: 615-343-4704; E-mail: matthew.breyer{at}vanderbilt.edu Mice provide an experimental model of unparalleled flexibility for studying mammalian diseases. Inbred strains of mice exhibit substantial differences in their susceptibility to the renal complications of diabetes. Much remains to be established regarding the course of diabetic nephropathy (DN) in mice as well as defining those strains and/or mutants that are most susceptible to renal injury from diabetes. Through the use of the unique genetic reagents available in mice (including knockouts and transgenics), the validation of a mouse model reproducing human DN should significantly facilitate the understanding of the underlying genetic mechanisms that contribute to the development of DN. Establishment of an authentic mouse model of DN will undoubtedly facilitate testing of translational diagnostic and therapeutic interventions in mice before testing in humans. Diabetic nephropathy (DN) is the major single cause of ESRD in the United States ( 1 ), with costs for care of these patients projected to be $12 billion/yr by 2010 ( 1 ). Despite Continue reading >>

Portulaca Oleracea L. Alleviates Liver Injury In Streptozotocin-induced Diabetic Mice

Portulaca Oleracea L. Alleviates Liver Injury In Streptozotocin-induced Diabetic Mice

Editor who approved publication: Dr Tuo Deng Guoyin Zheng,1,* Fengfeng Mo,2,* Chen Ling,3,* Hao Peng,1 Wei Gu,1 Min Li,2 Zhe Chen1 1Department of Traditional Chinese Medicine, Changhai Hospital, 2Department of Military Hygiene, Second Military Medical University, 3Department of Biology, School of LifeScience, Fudan University, Shanghai, Peoples Republic of China *These authors contributed equally tothis work Abstract: Purslane is a widespread succulent herb that exhibits various pharmacological effects. The purpose of this study was to evaluate the protective effect of Portulaca oleracea L. (purslane) on streptozotocin-induced diabetes in mice. Oral glucose-tolerance tests were carried out to assess blood glucose levels and body weight and food intake were recorded. The biochemical parameters anti-aspartate aminotransferase, alanine aminotransferase, insulin, triglycerides, total cholesterol, IL-6, IL-1, and TNF were also measured. The pathological condition of liver tissues were examined by hematoxylineosin staining. Rho, ROCK1, ROCK2, NFBp65, p-NFBp65, IB, and p-IB expression in liver tissue were analyzed by Western blot. Purslane increased body weight and decreased food intake. Purslane also significantly reduced concentrations of glucose, anti-aspartate aminotransferase, alanine aminotransferase, triglycerides, total cholesterol, IL-6, IL-1, and TNF in serum. Serum insulin was elevated with purslane treatment. In addition, pathologic liver changes in diabetic mice were also alleviated by purslane. Obtained data revealed that purslane restored the levels of RhoNFB signaling-related proteins in comparison with those of diabetic mice. Above all, it can be assumed that purslane might play a positive role in regulating streptozotocin-induced liver injury through suppres Continue reading >>

Jci -multiple Low-dose Streptozotocin-induced Diabetes In The Mouse. Evidence For Stimulation Of A Cytotoxic Cellular Immune Response Against An Insulin-producing Beta Cell Line.

Jci -multiple Low-dose Streptozotocin-induced Diabetes In The Mouse. Evidence For Stimulation Of A Cytotoxic Cellular Immune Response Against An Insulin-producing Beta Cell Line.

Mice were examined for the presence of splenocytes specifically cytotoxic for a rat insulinoma cell line (RIN) during the induction of diabetes by streptozotocin (SZ) in multiple low doses (Multi-Strep). Cytotoxicity was quantitated by the release of 51Cr from damaged cells. A low but statistically significant level of cytolysis (5%) by splenocytes was first detectable on day 8 after the first dose of SZ. The cytotoxicity reached a maximum of approximately 9% on day 10 and slowly decreased thereafter, becoming undetectable 42 d after SZ was first given. The time course of the in vitro cytotoxic response correlated with the degree of insulitis demonstrable in the pancreata of the Multi-Strep mice. The degree of cytotoxicity after Multi-Strep was related to the number of effector splenocytes to which the target RIN cells were exposed and was comparable to that detectable after immunization by intraperitoneal injection of RIN cells in normal mice. The cytotoxicity was specific for insulin-producing cells; syngeneic, allogeneic, and xenogeneic lymphocytes and lymphoblasts, 3T3 cells, and a human keratinocyte cell line were not specifically lysed by the splenocytes of the Multi-Strep mice. This phenomenon was limited to the Multi-Strep mice. Splenocytes from mice made diabetic by a single, high dose of SZ exhibited a very low level of cytotoxicity against the RIN cells. The cytotoxic response was also quantitated in splenocytes from control and Multi-Strep mice (10 d after the first dose of SZ) before and after culture with mitomycin-treated RIN cells in the presence of T cell growth factor (TCGF). The cytotoxicity of the Multi-Strep splenocytes was enhanced more than fivefold after such culture, suggesting the proliferation of an effector cell that could be stimulated and Continue reading >>

The Streptozotocin-induced Diabetic Nude Mouse Model: Differences Between Animals From Different Sources

The Streptozotocin-induced Diabetic Nude Mouse Model: Differences Between Animals From Different Sources

The Streptozotocin-Induced Diabetic Nude Mouse Model: Differences between Animals from Different Sources Schulze Diabetes Institute, Department of Surgery, University of Minnesota, Minneapolis, Minnesota. *Corresponding author. Email: [email protected] Received 2010 Dec 8; Revised 2010 Jan 9; Accepted 2011 Feb 20. Copyright American Association for Laboratory Animal Science This article has been cited by other articles in PMC. Diabetes is induced in mice by using streptozotocin (STZ), a compound that has a preferential toxicity toward pancreatic cells. We evaluated nude male mice from various sources for their sensitivity to a single high dose (160 to 240 mg/kg) of STZ. Diabetes was induced in male mice (age: median, 12 wk; interquartile range, 11 to 14 wk; body weight, about 30 g) from Taconic Farms (TAC), Jackson Laboratories (JAX), and Charles River Laboratories (CRL). Mice were monitored for 30 d for adverse side effects, blood glucose, and insulin requirements. In CRL mice given 240 mg/kg STZ, more than 95% developed diabetes within 4 to 5 d, and loss of body weight was relatively low (mean, 0.4 g). In comparison, both TAC and JAX mice were more sensitive to STZ, as evidenced by faster development of diabetes (even at a lower STZ dose), greater need for insulin after STZ, greater body weight loss (mean: TAC, 3.5 g; JAX, 3.7 g), and greater mortality. We recommend conducting exploratory safety assessments when selecting a nude mouse source, with the aim of limiting morbidity and mortality to less than 10%. Abbreviations: CRL, Charles River Laboratories; JAX, Jackson Laboratories; STZ, streptozotocin; TAC, Taconic Farms. Rodent models commonly are used to study immunologic mechanisms and metabolic function in diabetes. 19 In our institution, the mouse diabetes model 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 >>

Metformin Ameliorates Insulitis In Stz-induced Diabetic Mice

Metformin Ameliorates Insulitis In Stz-induced Diabetic Mice

This is an open access article distributed under the terms of the Creative Commons Attribution License , which permits unrestricted use, distribution, reproduction and adaptation in any medium and for any purpose provided that it is properly attributed. For attribution, the original author(s), title, publication source (PeerJ) and either DOI or URL of the article must be cited. Han X, Tao Y, Deng Y, Yu J, Cai J, Ren G, Sun Y, Jiang G. (2017) Metformin ameliorates insulitis in STZ-induced diabetic mice. PeerJ 5:e3155 Metformin is currently the most widely used first-line hypoglycemic agent for diabetes mellitus. Besides glucose-lowering action, there is increasingly interest in the potential anti-inflammatory action of this drug. In the present study, we investigated the actions of metformin on experimental insulitis using STZ-induced diabetic mice. Mice with acute diabetes induced by STZ were administered metformin by gavage. Changes of blood glucose and body weight, and the daily amount of food and water intake were measured. Pancreatic tissues were collected for histologic analyses. Pathological assessment and immunohistochemistry analysis were used to determine the effect of metformin on insulitis. Inflammatory cytokines in the pancreas and insulin levels were measured through ELISA analysis. Metformin significantly reduced blood glucose levels and improved aberrant water intake behavior in experimental diabetic mice. No significant differences were observed in terms of body weight and food intake behavior in metformin-treated animals. In the STZ-induced model of diabetes, we found the appearance of pronounced insulitis. However, metformin administration reduced the severity of insulitis assessed by blind pathological scoring. In addition, metformin treatment improv 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 >>

The Use Of Animal Models In Diabetes Research

The Use Of Animal Models In Diabetes Research

The use of animal models in diabetes research Diabetes Research Group, King's College London, London, UK Aileen King, Diabetes Research Group, Guy's Campus, King's College London, London SE1 1UL, UK. E-mail: [email protected] Received 2011 Aug 19; Revised 2012 Feb 10; Accepted 2012 Feb 13. Copyright 2012 The Author. British Journal of Pharmacology 2012 The British Pharmacological Society This article has been cited by other articles in PMC. Diabetes is a disease characterized by a relative or absolute lack of insulin, leading to hyperglycaemia. There are two main types of diabetes: type 1 diabetes and type 2 diabetes. Type 1 diabetes is due to an autoimmune destruction of the insulin-producing pancreatic beta cells, and type 2 diabetes is caused by insulin resistance coupled by a failure of the beta cell to compensate. Animal models for type 1 diabetes range from animals with spontaneously developing autoimmune diabetes to chemical ablation of the pancreatic beta cells. Type 2 diabetes is modelled in both obese and non-obese animal models with varying degrees of insulin resistance and beta cell failure. This review outlines some of the models currently used in diabetes research. In addition, the use of transgenic and knock-out mouse models is discussed. Ideally, more than one animal model should be used to represent the diversity seen in human diabetic patients. This paper is the latest in a series of publications on the use of animal models in pharmacology research. Readers might be interested in the previous papers. Robinson V (2009). Less is more: reducing the reliance on animal models for nausea and vomiting research. Holmes AM, Rudd JA, Tattersall FD, Aziz Q, Andrews PLR (2009). Opportunities for the replacement of animals in the study of nausea and vomiting. Continue reading >>

Hypoglycemic Effect Of Catalpol On High-fat Diet/streptozotocin-induced Diabetic Mice By Increasing Skeletal Muscle Mitochondrial Biogenesis

Hypoglycemic Effect Of Catalpol On High-fat Diet/streptozotocin-induced Diabetic Mice By Increasing Skeletal Muscle Mitochondrial Biogenesis

Hypoglycemic effect of catalpol on high-fat diet/streptozotocin-induced diabetic mice by increasing skeletal muscle mitochondrial biogenesis Key Laboratory of Drug Quality Control and Pharmacovigilance, Ministry of Education Jiangsu Center for Pharmacodynamics Research and Evaluation Jiangsu Center for Pharmacodynamics Research and Evaluation Correspondence address. Tel: +86-25-83271043; Fax: + ; E-mail: [email protected] (T.W.)/ [email protected] (L.Z.) Search for other works by this author on: State Key Laboratory of Natural Medicines Correspondence address. Tel: +86-25-83271043; Fax: + ; E-mail: [email protected] (T.W.)/ [email protected] (L.Z.) Search for other works by this author on: Acta Biochimica et Biophysica Sinica, Volume 46, Issue 9, 1 September 2014, Pages 738748, Xia Li, Zhimeng Xu, Zhenzhou Jiang, Lixin Sun, Jinzi Ji, Jingshan Miao, Xueji Zhang, Xiaojie Li, Shan Huang, Tao Wang, Luyong Zhang; Hypoglycemic effect of catalpol on high-fat diet/streptozotocin-induced diabetic mice by increasing skeletal muscle mitochondrial biogenesis, Acta Biochimica et Biophysica Sinica, Volume 46, Issue 9, 1 September 2014, Pages 738748, Catalpol, an iridoid glycoside, exists in the root of Radix Rehmanniae. Some studies have shown that catalpol has a remarkable hypoglycemic effect in the streptozotocin-induced diabetic model, but the underlying mechanism for this effect has not been fully elucidated. Because mitochondrial dysfunction plays a vital role in the pathology of diabetes and because improving mitochondrial function may offer a new approach for the treatment of diabetes, this study was designed. Catalpol was orally administered together with metformin to high-fat diet/streptozotocin (HFD/STZ)-induced diabetic mice daily for 4 weeks. Body weight (BW), fast Continue reading >>

Insulin Hypersensitivity And Resistance To Streptozotocin-induced Diabetes In Mice Lacking Pten In Adipose Tissue

Insulin Hypersensitivity And Resistance To Streptozotocin-induced Diabetes In Mice Lacking Pten In Adipose Tissue

ABSTRACT In adipose tissue, insulin controls glucose and lipid metabolism through the intracellular mediators phosphatidylinositol 3-kinase and serine-threonine kinase AKT. Phosphatase and a tensin homolog deleted from chromosome 10 (PTEN), a negative regulator of the phosphatidylinositol 3-kinase/AKT pathway, is hypothesized to inhibit the metabolic effects of insulin. Here we report the generation of mice lacking PTEN in adipose tissue. Loss of Pten results in improved systemic glucose tolerance and insulin sensitivity, associated with decreased fasting insulin levels, increased recruitment of the glucose transporter isoform 4 to the cell surface in adipose tissue, and decreased serum resistin levels. Mutant animals also exhibit increased insulin signaling and AMP kinase activity in the liver. Pten mutant mice are resistant to developing streptozotocin-induced diabetes. Adipose-specific Pten deletion, however, does not alter adiposity or plasma fatty acids. Our results demonstrate that in vivo PTEN is a potent negative regulator of insulin signaling and insulin sensitivity in adipose tissue. Furthermore, PTEN may be a promising target for nutritional and/or pharmacological interventions aimed at reversing insulin resistance. Insulin controls metabolism by modulating the uptake and utilization of glucose and lipids in target organs, such as adipose tissue, skeletal muscle, and liver. Glucose homeostasis is, in part, regulated by the insulin-stimulated uptake of glucose in adipose tissue (1, 30, 41, 56). Aberrant glucose uptake due to insulin resistance is a key pathogenic feature of type 2 diabetes mellitus (T2DM). In order to understand glycemic control and the molecular mechanisms responsible for T2DM, significant focus has been placed on the study of insulin signali Continue reading >>

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 >>

Comparison Of Streptozotocin And Alloxan-induced Diabetes In The Rat, Including Volumetric Quantitation Of The Pancreatic Islets

Comparison Of Streptozotocin And Alloxan-induced Diabetes In The Rat, Including Volumetric Quantitation Of The Pancreatic Islets

, Volume 9, Issue3 , pp 178184 | Cite as Comparison of streptozotocin and alloxan-induced diabetes in the rat, including volumetric quantitation of the pancreatic islets Diabetes was induced in rats with equal molar dosages of either streptozotocin or alloxan. The clinical course of the diabetes (mortality, hyperglycemia, weight loss, polydipsia, hyperphagia, polyuria, glycosuria and diabetic indices) was recorded for six weeks before the animals were sacrificed for volumetric quantitation of the pancreatic islets. No significant differences in the pancreas (islet volumes of pancreas; beta, alpha and non-granular cell volumes and vessel volumes of both islet and total pancreas) were seen between the two groups, although differences in the clinical parameters were observed. The diabetic index at three and four weeks post injection was the clinical parameter which best reflected the terminal pancreatic beta cell volume. Analysis of the scanning data adds further empirical support for the accuracy of the linear scan method of quantitation. Streptozotocinalloxandiabetesquantitationislet volumebeta cell volumealpha cell volumevessel volume Supported by USPHS Training Grant No. GM 114. Alrison, R.N., Ciaccio, E.I., Glitzer, M.S., Cassaro, J.A., Pruss, M.P.: Light and electron microscopy of lesions in rats rendered diabetic with streptozotocin. Diabetes16, 5156 (1967). PubMed Google Scholar Brosky, G., Logothetopoulos, J.: Streptozotocin diabetes in the mouse and guinea pig. Diabetes18, 606611 (1969). PubMed Google Scholar Chang, A.Y., Schneider, D.I.: Hepatic enzyme activities in streptozotocin-diabetic rats before and after insulin treatment. Diabetes20, 7177 (1971). PubMed Google Scholar Dulin, W.E., Lund, G.H., Gerritsen, G.C.: Streptozotocin-induced diabetes in the rat. Continue reading >>

Streptozotocin-induced Diabetes Models: Pathophysiological Mechanisms And Fetal Outcomes

Streptozotocin-induced Diabetes Models: Pathophysiological Mechanisms And Fetal Outcomes

Streptozotocin-Induced Diabetes Models: Pathophysiological Mechanisms and Fetal Outcomes D. C. Damasceno ,1,2 A. O. Netto ,1 I. L. Iessi ,1 F. Q. Gallego ,1 S. B. Corvino ,1 B. Dallaqua ,1 Y. K. Sinzato ,1 A. Bueno ,1 I. M. P. Calderon ,1and M. V. C. Rudge 1 1Laboratory of Experimental Research on Gynecology and Obstetrics, Graduate Program in Gynecology, Obstetrics and Mastology, Botucatu Medical School, UNESP-Universidade Estadual Paulista, Distrito de Rubio Jnior S/N, 18618-970 Botucatu, SP, Brazil 2Department of Gynecology and Obstetrics, Botucatu Medical School, UNESP-Univsidade Estadual Paulista, Distrito de Rubio Jnior S/N, 18618-970 Botucatu, SP, Brazil Received 14 March 2014; Revised 30 April 2014; Accepted 14 May 2014; Published 27 May 2014 Copyright 2014 D. C. Damasceno et al. This is an open access article distributed under the Creative Commons Attribution License , which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Glucose homeostasis is controlled by endocrine pancreatic cells, and any pancreatic disturbance can result in diabetes. Because 8% to 12% of diabetic pregnant women present with malformed fetuses, there is great interest in understanding the etiology, pathophysiological mechanisms, and treatment of gestational diabetes. Hyperglycemia enhances the production of reactive oxygen species, leading to oxidative stress, which is involved in diabetic teratogenesis. It has also been suggested that maternal diabetes alters embryonic gene expression, which might cause malformations. Due to ethical issues involving human studies that sometimes have invasive aspects and the multiplicity of uncontrolled variables that can alter the uterine environment during clinical studies, it is neces Continue reading >>

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