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Induction Of Diabetes In Mice

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 >>

Guidelines On Use Of Streptozotocin In Rodents

Guidelines On Use Of Streptozotocin In Rodents

Guidelines on Use of Streptozotocin in Rodents To describe the appropriate use of streptozotocin for induction of diabetes mellitus (DM) in rats and mice and associated husbandry procedures To describe the appropriate post-injection monitoring of rodents Investigators using STZ to induce diabetes in rodents Streptozotocin (STZ): An antitumor/antibiotic compound isolated from Streptomyces achromogenes with potent toxicity to beta islet cells of the pancreas Carcinogen: An agent capable of causing cancer Teratogen: An agent capable of causing developmental abnormalities Cytotoxic: Possessing ability to exert toxic effects on a cell Depending on the dose and dose frequency, STZ can be used to induce insulin-dependent Type 1 DM or non insulin-dependent Type 2 DM. Known to cause hepatic and renal toxicity in mice and rats. Due to toxic effects and disease progression, some animal mortality can occur. However, steps to reduce mortality must be taken. Is a carcinogen, teratogen, and has been shown to affect fertility in animal studies. Effect on different strains is variable. ULAM recommends starting at the lower end of the dose ranges until performance for a given strain can be established. Increased appetite, defecation, thirst, and urination Appropriate availability of water must be ensured (e.g., if water bottles are being supplied, consider providing two bottles). Cage change frequency may need to be increased to account for increased urination . Recommended doses vary considerably due to strain, age, and weight differences in susceptibility to STZ, as well as variation in the bioactivity of the STZ itself. A general range for use is 42-65 mg/kg administered intraperitoneally (IP). The compound may also be administered intravenously (IV) or by other less common routes. A 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 >>

The Use Of Animal Models In The Study Of Diabetes Mellitus

The Use Of Animal Models In The Study Of Diabetes Mellitus

Abstract Animal models have enormously contributed to the study of diabetes mellitus, a metabolic disease with abnormal glucose homeostasis, due to some defect in the secretion or the action of insulin. They give researchers the opportunity to control in vivo the genetic and environmental factors that may influence the development of the disease and establishment of its complications, and thus gain new information about its handling and treatment in humans. Most experiments are carried out on rodents, even though other species with human-like biological characteristics are also used. Animal models develop diabetes either spontaneously or by using chemical, surgical, genetic or other techniques, and depict many clinical features or related phenotypes of the disease. In this review, an overview of the most commonly used animal models of diabetes are provided, highlighting the advantages and limitations of each model, and discussing their usefulness and contribution in the field of diabetes research. Type I Diabetes (T1DM) Models T1DM, a multifactorial autoimmune disease involving genetic and environmental factors, is hallmarked by T-cell and macrophages-mediated destruction of pancreatic β-cells, resulting in irreversible insulin deficiency. Diabetic ketoacidosis, a T1DM immediate consequence, can be fatal without treatment, while the long-term vascular T1DM complications affecting several organs and tissues can significantly affect life expectancy. There is no doubt that T1DM susceptibility is MHC-dependent and MHC genes account for approximately 50% of the total contribution to the disease. However, although to date studies corroborate that both HLA-DR and HLA-DQ genes are important in determining disease risk, the effects of individual alleles may be modified by the h Continue reading >>

Alloxan-induced Diabetes In The Mouse: Time Course Of Pancreatie B-cell Destruction As Reflected In An Increased Islet Vascular Permeability

Alloxan-induced Diabetes In The Mouse: Time Course Of Pancreatie B-cell Destruction As Reflected In An Increased Islet Vascular Permeability

, Volume 410, Issue1 , pp 1721 | Cite as Alloxan-induced diabetes in the mouse: Time course of pancreatie B-cell destruction as reflected in an increased islet vascular permeability The extent to which injections of the pancreatic B-cytotoxin alloxan in C57BL/Ks mice induced an increase in islet vascular permeability, and the time course of this increase, were studied. The vascular permeability was monitored by administration of the dye Monastral blue B, which is entrapped in leaky blood vessels with intact basement membranes. The islets were visualized by a freeze-thawing technique which allows identification of stained islets. Not until four hours after the alloxan injections was there an increase in islet uptake of Monastral blue B when compared with saline-treated control animals. Thereafter the islet staining increased further. The process was accompanied by gradual development of hyperglycaemia and a reduction of number of the islets identified in the pancreatic preparations. It is concluded that alloxan causes an increase in islet vascular permeability, which appears to become manifest at a later stage than the cytotoxic B-cell degeneration. This work was supported by grants from the Swedish Medical Research Council (12x-109; K86-12P-7680-01), the Swedish Diabetes Association, the Swedish Society of Medicine, the Nordic Insulin Fund, the C. Groschinsky Memorial Fund, Syskonen Svenssons Fond and the ke Wiberg Foundation This is a preview of subscription content, log in to check access Unable to display preview. Download preview PDF. Asayama K, English D, Slonim AE, Burr IM (1984) Chemiluminescence as an index of drug-induced free radical production in pancreatic islets. Diabetes 33:160163 Google Scholar Cohen G, Heikkila RE (1974) The generation of hydrogen perox Continue reading >>

Animal Models In Diabetes And Pregnancy

Animal Models In Diabetes And Pregnancy

Laboratory of Reproduction and Metabolism, Centro de Estudios Farmacologicos y BotanicosConsejo Nacional de Investigaciones Cientificas y Tecnicas, School of Medicine, University of Buenos Aires, 1121ABG Buenos Aires, Argentina Address all correspondence and requests for reprints to: Alicia Jawerbaum, Laboratory of Reproduction and Metabolism, Centro de Estudios Farmacologicos y BotanicosConsejo Nacional de Investigaciones Cientificas y Tecnicas-School of Medicine, University of Buenos Aires. Paraguay 2155, 17th floor (C1121ABG), 1121ABG Buenos Aires, Argentina. Search for other works by this author on: Laboratory of Reproduction and Metabolism, Centro de Estudios Farmacologicos y BotanicosConsejo Nacional de Investigaciones Cientificas y Tecnicas, School of Medicine, University of Buenos Aires, 1121ABG Buenos Aires, Argentina Search for other works by this author on: Endocrine Reviews, Volume 31, Issue 5, 1 October 2010, Pages 680701, Alicia Jawerbaum, Veronica White; Animal Models in Diabetes and Pregnancy, Endocrine Reviews, Volume 31, Issue 5, 1 October 2010, Pages 680701, The worldwide increase in the incidence of diabetes, the increase in type 2 diabetes in women at reproductive ages, and the cross-generation of the intrauterine programming of type 2 diabetes are the bases for the growing interest in the use of experimental diabetic models in order to gain insight into the mechanisms of induction of developmental alterations in maternal diabetes. In this scenario, experimental models that present the most common features of diabetes in pregnancy are highly required. Several important aspects of human diabetic pregnancies such as the increased rates of spontaneous abortions, malformations, fetoplacental impairments, and offspring diseases in later life can be appr 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 >>

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 >>

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 >>

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 >>

Virus-induced Diabetes In Mice - Sciencedirect

Virus-induced Diabetes In Mice - Sciencedirect

Get rights and content As recently reported, a variant of the encephalomyocarditis virus can induce a diabetic syndrome in mice. Forty-six animals were inoculated and followed by urinary glucose every other day. Eighteen of 30 which survived the infection were sacrificed on the 4th, 8th, 12th, and 24th postinfection day. Six of 30 non-infected mice served as controls. The parameters measured were blood glucose, immunoreactive insulin and pancreatic insulin. Four days after inoculation hyperinsulinemia was apparent, without alteration in blood glucose or pancreatic insulin content. Hyperglycemia and glycosuria were present at 8, 12, and 24 days, associated with a reduction of pancreatic insulin. Serum insulin was significantly below control levels only at 12 days following infection. These biochemical findings support the histological evidence that a variant of the encephalomy-ocarditis virus produces pancreatic islet lesions in mice, resulting in a diabetic syndrome. Continue reading >>

Streptozotocin-induced Type 1 Diabetes In Rodents As A Model For Studying Mitochondrial Mechanisms Of Diabetic Cell Glucotoxicity

Streptozotocin-induced Type 1 Diabetes In Rodents As A Model For Studying Mitochondrial Mechanisms Of Diabetic Cell Glucotoxicity

Streptozotocin-induced type 1 diabetes in rodents as a model for studying mitochondrial mechanisms of diabetic cell glucotoxicity Department of Pharmaceutical Sciences, UNT System College of Pharmacy, University of North Texas Health Science Center, Fort Worth, TX, USA Department of Pharmaceutical Sciences, UNT System College of Pharmacy, University of North Texas Health Science Center, Fort Worth, TX, USA Department of Pharmaceutical Sciences, UNT System College of Pharmacy, University of North Texas Health Science Center, Fort Worth, TX, USA Correspondence: Liang-Jun Yan, Department of Pharmaceutical Sciences, UNT System College of Pharmacy, University of North Texas Health Science Center, 3500 Camp Bowie Boulevard, Fort Worth, TX 76107, USA, Tel +1 817 735 2386, Fax +1 817 735 2603, Email [email protected] Author information Copyright and License information Disclaimer Copyright 2015 Wu and Yan. This work is published by Dove Medical Press Limited, and licensed under Creative Commons Attribution Non Commercial (unported, v3.0) License The full terms of the License are available at . Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. This article has been cited by other articles in PMC. 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 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 >>

Animal Models In Diabetes And Pregnancy

Animal Models In Diabetes And Pregnancy

Laboratory of Reproduction and Metabolism, Centro de Estudios Farmacologicos y BotanicosConsejo Nacional de Investigaciones Cientificas y Tecnicas, School of Medicine, University of Buenos Aires, 1121ABG Buenos Aires, Argentina Address all correspondence and requests for reprints to: Alicia Jawerbaum, Laboratory of Reproduction and Metabolism, Centro de Estudios Farmacologicos y BotanicosConsejo Nacional de Investigaciones Cientificas y Tecnicas-School of Medicine, University of Buenos Aires. Paraguay 2155, 17th floor (C1121ABG), 1121ABG Buenos Aires, Argentina. Search for other works by this author on: Laboratory of Reproduction and Metabolism, Centro de Estudios Farmacologicos y BotanicosConsejo Nacional de Investigaciones Cientificas y Tecnicas, School of Medicine, University of Buenos Aires, 1121ABG Buenos Aires, Argentina Search for other works by this author on: Endocrine Reviews, Volume 31, Issue 5, 1 October 2010, Pages 680701, Alicia Jawerbaum, Veronica White; Animal Models in Diabetes and Pregnancy, Endocrine Reviews, Volume 31, Issue 5, 1 October 2010, Pages 680701, The worldwide increase in the incidence of diabetes, the increase in type 2 diabetes in women at reproductive ages, and the cross-generation of the intrauterine programming of type 2 diabetes are the bases for the growing interest in the use of experimental diabetic models in order to gain insight into the mechanisms of induction of developmental alterations in maternal diabetes. In this scenario, experimental models that present the most common features of diabetes in pregnancy are highly required. Several important aspects of human diabetic pregnancies such as the increased rates of spontaneous abortions, malformations, fetoplacental impairments, and offspring diseases in later life can be appr Continue reading >>

Diabetes-induced Impairment In Visual Function In Mice: Contributions Of P38 Mapk, Rage, Leukocytes, And Aldose Reductase | Iovs | Arvo Journals

Diabetes-induced Impairment In Visual Function In Mice: Contributions Of P38 Mapk, Rage, Leukocytes, And Aldose Reductase | Iovs | Arvo Journals

Visual Psychophysics and Physiological Optics| May 2014 Diabetes-Induced Impairment in Visual Function in Mice: Contributions of p38 MAPK, RAGE, Leukocytes, and Aldose Reductase Case Western Reserve University, Cleveland, Ohio, United States Case Western Reserve University, Cleveland, Ohio, United States The Second Hospital of Jilin University, Changchun, Jilin, China St. Louis School of Medicine, St. Louis, Missouri, United States University of Colorado Denver Health Sciences Center, Aurora, Colorado, United States University Hospitals Eye Institute, Case Western Reserve University, Cleveland, Ohio, United States Case Western Reserve University, Cleveland, Ohio, United States Case Western Reserve University, Cleveland, Ohio, United States Case Western Reserve University, Cleveland, Ohio, United States Case Western Reserve University, Cleveland, Ohio, United States Stokes Veterans Administration Medical Center, Cleveland, Ohio, United States Case Western Reserve University, Cleveland, Ohio, United States University Hospitals Eye Institute, Case Western Reserve University, Cleveland, Ohio, United States Stokes Veterans Administration Medical Center, Cleveland, Ohio, United States Case Western Reserve University, Cleveland, Ohio, United States Stokes Veterans Administration Medical Center, Cleveland, Ohio, United States Correspondence: Timothy S. Kern, Department of Medicine, 441 Wood Building, Case Western Reserve University, 10900 Euclid Avenue, Cleveland, OH 44106; [email protected] . Investigative Ophthalmology & Visual Science May 2014, Vol.55, 2904-2910. doi:10.1167/iovs.13-11659 Diabetes-Induced Impairment in Visual Function in Mice: Contributions of p38 MAPK, RAGE, Leukocytes, and Aldose Reductase You will receive an email whenever this article is corrected, updated, Continue reading >>

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