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Diabetic Rat Model

Appropriate Insulin Level In Selecting Fortified Diet-fed, Streptozotocin-treated Rat Model Of Type 2 Diabetes For Anti-diabetic Studies

Appropriate Insulin Level In Selecting Fortified Diet-fed, Streptozotocin-treated Rat Model Of Type 2 Diabetes For Anti-diabetic Studies

Abstract Pathophysiological investigation of disease in a suitable animal model is a classical approach towards development of a credible therapeutic strategy. This study examined appropriate insulin level in selecting animal model for type 2 diabetes (T2D) studies. Albino Wistar rats (150-200g) were divided into two groups fed with commercially available normal-diet-feed (NDF) and water or fortified diet feed (FDF) (10g NDF per gram of margarine) with 20% fructose solution as drinking water. After 6 weeks of dietary regimen both groups were divided into 5 sub-groups and injected intraperitoneally with a graded dose of streptozotocin (STZ) (0, 25, 35, 45 & 55mg/kg bw.). Result The result showed that the FDF-fed rats increased significantly in body weight, basal serum insulin, total cholesterol, triglycerides and blood glucose levels as compared to NDF-fed rats. Ten days post STZ induction, the groups treated with STZ (45 & 55 mg/kg) developed frank hyperglycaemia with < 46.8% serum insulin, a severe deficiency typical of diabetes type 1. The NDF25 and NDF35 groups with 75.7% and 64.4% serum insulin respectively presented relative normoglycemia, whereas the FDF35 (85.8% serum insulin) were notably hyperglycaemia (>300 mg/dL) throughout the 6weeks post diabetes confirmation. These FDF35 rats were sensitive to glibenclamide, metformin and pioglitazone in lowering hyperglycaemia, hypertriglyceridemia and hypercholesterolemia The hyperglycaemia stability of the FDF35 rats (85.5% insulin) together with their sensitivity to 3 different hypoglycaemic drugs strongly suggests their suitability as a non-genetic model of T2D. Hence the study shows that circulating serum insulin ≥ 85.8% with overt hyperglycaemia may be utilized as the benchmark in selecting rat models for T2D stud 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 >>

Combination Of High-fat/high-fructose Diet And Low-dose Streptozotocin To Model Long-term Type-2 Diabetes Complications

Combination Of High-fat/high-fructose Diet And Low-dose Streptozotocin To Model Long-term Type-2 Diabetes Complications

Combination of high-fat/high-fructose diet and low-dose streptozotocin to model long-term type-2 diabetes complications Scientific Reportsvolume8, Articlenumber:424 (2018) The epidemic of type 2 diabetes mellitus (T2DM) is fueled by added fructose consumption. Here, we thus combined high-fat/high-fructose diet, with multiple low-dose injections of streptozotocin (HF/HF/Stz) to emulate the long-term complications of T2DM. HF/HF/Stz rats, monitored over 56 weeks, exhibited metabolic dysfunctions associated with the different stages of the T2DM disease progression in humans: an early prediabetic phase characterized by an hyperinsulinemic period with modest dysglycemia, followed by a late stage of T2DM with frank hyperglycemia, normalization of insulinemia, marked dyslipidemia, hepatic fibrosis and pancreatic -cell failure. Histopathological analyses combined to [18F]-FDG PET imaging further demonstrated the presence of several end-organ long-term complications, including reduction in myocardial glucose utilization, renal dysfunction as well as microvascular neuropathy and retinopathy. We also provide for the first time a comprehensive -PET whole brain imaging of the changes in glucose metabolic activity within discrete cerebral regions in HF/HF/Stz diabetic rats. Altogether, we developed and characterized a unique non-genetic preclinical model of T2DM adapted to the current diet and lifestyle that recapitulates the major metabolic features of the disease progression, from insulin resistance to pancreatic -cell dysfunction, and closely mimicking the target-organ damage occurring in type 2 diabetic patients at advanced stages. Type 2 diabetes is a long-term metabolic disorder that represents a global public health challenge, affecting not only industrialized countries, but Continue reading >>

Animal Models Of Type 2 Diabetes: The Gk Rat

Animal Models Of Type 2 Diabetes: The Gk Rat

Animal Models of Type 2 Diabetes: The GK Rat Animal Models of Type 2 Diabetes: The GK Rat Studying the long-term complications of diabetic pathology is more relevant than ever, driving increased interest in animal models of type 2 diabetes. According to the World Health Organization (WHO) the number of people with diabetes (includes both type 1 and type 2) has risen from 108 million in 1980 to 422 million in 2014. "[Diabetes] is a major cause of blindness, kidney failure, heart attacks, stroke, and lower limb amputation. Over time, diabetes can damage the heart, blood vessels, eyes, kidneys, and nerves. Adults with diabetes have a 2-3-fold increased risk of heart attacks and strokes. Combined with reduced blood flow, neuropathy in the feet increases the chance of foot ulcers, infection and eventual need for limb amputation. Diabetic retinopathy is an important cause of blindness and occurs as a result of long-term accumulated damage to the small blood vessels in the retina. 2.6% of global blindness can be attributed to diabetes. Diabetes is among the leading causes of kidney failure." (WHO Media Center, 2016). There are a variety of mouse and rat models which can be used to study aspects of type 2 diabetes: Varying aspects and severity of complications + More robust diet induced obesity in C57BL/6NTac (Gareski T, 2009) Studying Long-term Pathology in Animal Models of Type 2 Diabetes The ob/ob and db/db mice, as well as the Zucker Diabetic Fatty rat, are all well-characterized and frequently-used diabetic models which exhibit a mutation in the leptin (ob/ob) or leptin receptor gene (ZDF, db/db). They are useful for studying particular disease characteristics, but do not necessarily represent the human disease state as mutations in these genes are not frequently the caus Continue reading >>

The Streptozotocin-diabetic Rat As A Model Of The Chronic Complications Of Human Diabetes - Sciencedirect

The Streptozotocin-diabetic Rat As A Model Of The Chronic Complications Of Human Diabetes - Sciencedirect

Get rights and content Background: Diabetes in humans induces chronic complications such as cardiovascular damage, cataracts and retinopathy, nephropathy and polyneuropathy. The most common animal model of human diabetes is streptozotocin (STZ)-induced diabetes in the rat. Methods: This project assessed cardiovascular, ocular and neuropathic changes over a period of 24 weeks post STZ administration in rats. Results: STZ-diabetic rats (n = 96) showed stable signs of diabetes (hyperglycaemia, increased water and food intake with no increase in bodyweight): 52% of untreated STZ-diabetic rats (n = 50) survived 24 weeks after STZ administration. STZ-diabetic rats were normotensive with slowly developing systolic and diastolic dysfunction and an increased ventricular stiffness. Ventricular action potential durations were markedly prolonged. STZ-diabetic rats developed stable tactile allodynia. Cataracts developed to presumed blindness at 16 weeks but proliferative retinopathy was not observed even after 24 weeks. Conclusion: The chronic STZ-diabetic rat mimics many but not all of the chronic complications observed in the diabetic human. The chronic STZ-diabetic rat may be a useful model to test therapeutic approaches for amelioration of chronic diabetic complications in humans. Continue reading >>

New Rat Model Of Diabetic Macrovascular Complication | Cardiovascular Research | Oxford Academic

New Rat Model Of Diabetic Macrovascular Complication | Cardiovascular Research | Oxford Academic

Objectives: Age-related medial calcification (elastocalcinosis) of large arteries is accelerated in diabetes and appears mainly in distal arteries. The aim was to devise a rat model of elastocalcinosis in association with diabetes to examine the hypothesis that diabetes accelerates vascular calcification experimentally. Methods: Male Wistar rats received a high fat diet during 2months followed by a low dose of streptozotocin to induce diabetes (D). Elastocalcinosis was facilitated by 3weeks of treatment with warfarin and vitamin K (WVK). We started WVK treatment 1week (D4WVK) and 4weeks (D7WVK) after the injection of streptozotocin and in age-matched healthy rats. Measurements of hemodynamic and metabolic parameters, aortic and femoral calcium content, and immunohistochemistry for alkaline phosphatase, osteopontin, tumor necrosis factor (TNF)-, and transforming growth factor (TGF)-TGF- were performed. Results: Three weeks of WVK treatment alone did not increase the calcium content in the aorta and femoral arteries. However, in the D7WVK group, femoral calcification, but not aortic calcium content, increased significantly as compared to the WVK group. This response was not observed in the D4WVK group. In femoral arteries, strong immunostaining for alkaline phosphatase and osteopontin was observed in the D7WVK group. TNF- and TGF- expressions were mainly localized in the adventitia of arteries from diabetic rats. Conclusion: We have established a model of accelerated elastocalcinosis in diabetes related to its duration and localized in distal arteries. The modification of local protein expression is also in accordance with clinical data, suggesting that this model could be useful to investigate mechanisms related to this important clinical macrovascular complication of d Continue reading >>

Spontaneous Type 2 Diabetic Rodent Models

Spontaneous Type 2 Diabetic Rodent Models

Spontaneous Type 2 Diabetic Rodent Models Department of Nephrology, Second Hospital of Jilin University, Changchun 130041, China Received 22 November 2012; Revised 8 January 2013; Accepted 22 January 2013 Copyright 2013 Yang-wei Wang 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. Diabetes mellitus, especially type 2 diabetes (T2DM), is one of the most common chronic diseases and continues to increase in numbers with large proportion of health care budget being used. Many animal models have been established in order to investigate the mechanisms and pathophysiologic progress of T2DM and find effective treatments for its complications. On the basis of their strains, features, advantages, and disadvantages, various types of animal models of T2DM can be divided into spontaneously diabetic models, artificially induced diabetic models, and transgenic/knockout diabetic models. Among these models, the spontaneous rodent models are used more frequently because many of them can closely describe the characteristic features of T2DM, especially obesity and insulin resistance. In this paper, we aim to investigate the current available spontaneous rodent models for T2DM with regard to their characteristic features, advantages, and disadvantages, and especially to describe appropriate selection and usefulness of different spontaneous rodent models in testing of various new antidiabetic drugs for the treatment of type 2 diabetes. In nearly all countries of the world, diabetes mellitus is one of the most common chronic diseases and continues to increase in numbers and significance, because of the reduced physical Continue reading >>

Alterations Of Colonic Contractility In Long-term Diabetic Rat Model

Alterations Of Colonic Contractility In Long-term Diabetic Rat Model

J Neurogastroenterol Motil 2011; 17(4): 372-380 Alterations of Colonic Contractility in Long-term Diabetic Rat Model Sun Joo Kim1, Jae Hyung Park1, Dae Kyu Song1, Kyung Sik Park2*, Jeong Eun Lee2, Eun Soo Kim2, Kwang Bum Cho2, Byoung Kuk Jang2, Woo Jin Chung2, Jae Seok Hwang2, Joong Goo Kwon3 and Tae Wan Kim4 1Department of Physiology, Keimyung University School of Medicine, Daegu, Korea. 2Department of Internal Medicine, Keimyung University School of Medicine, Daegu, Korea. 3Department of Internal Medicine, Catholic University of Daegu School of Medicine, Daegu, Korea. 4Department of Veterinary Physiology, College of Veterinary Medicine, Kyungpook National University, Daegu, Korea. Correspondence to: Correspondence: Kyung Sik Park, MD. Department of Gastroenterology, Dongsan Medical Center, 194 Dongsan-dong, Jung-gu, Daegu 700-712, Korea. Tel: +82-53-250-7088, Fax: +82-53-250-7088, [email protected] Received: June 4, 2011; Revised: July 28, 2011; Accepted: August 6, 2011; Published online: October 31, 2011. The Korean Society of Neurogastroenterology and Motility. All rights reserved. This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License ( ) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited. Dysfunction of the gastrointestinal tract occurs in about 76% of patients who are diabetic for more than 10 years. Although diabetes-related dysfunctions of the stomach such as gastroparesis have been extensively studied over the recent years, studies about the mechanism underlying colonic symptoms in long-term diabetes models are rare. Therefore, the goal of our study was to clarify the nature of colonic dysfunction in a long-te Continue reading >>

Diabetic Rat Model | Springerlink

Diabetic Rat Model | Springerlink

In following chapter we present the basic information about the use of diabetic rats in experimental models. Historic attempts of diabetic model development are discussed. Various breeds of diabetic rats are presented and characterized. Finally we outline organ-specific complications observed in diabetic rats and present our experience in nerve regeneration in Zucker Diabetic Fatty (ZDF) rat model. Diabetes MellitusDiabetic Rat ModelGlycaemia In RatsComplications of DiabetesNerve Regeneration In DiabetesDiabetic Neuropathy Model This is a preview of subscription content, log in to check access. Bliss M. The discovery of insulin. Chicago: University of Chicago Press; 2007. Google Scholar Coleman DL. A historical perspective on leptin. Nat Med. 2010;16(10):10979. doi: 10.1038/nm1010-1097 . PubMed CrossRef Google Scholar Russfield AB. Experimental endocrinopathies. Methods Achiev Exp Pathol. 1975;7:13248. PubMed Google Scholar Fischer LJ, Rickert DE. Pancreatic islet-cell toxicity. CRC Crit Rev Toxicol. 1975;3(2):23163. PubMed CrossRef Google Scholar Rees DA, Alcolado JC. Animal models of diabetes mellitus. Diabet Med. 2005;22(4):35970. PubMed CrossRef Google Scholar King AJ. The use of animal models in diabetes research. Br J Pharmacol. 2012;166(3):87794. doi: 10.1111/j.1476-5381.2012.01911.x . PubMedCentral PubMed CrossRef Google Scholar Mordes JP, Bortell R, Blankenhorn EP, Rossini AA, Greiner DL. Rat models of type 1 diabetes: genetics, environment, and autoimmunity. ILAR J. 2004;45(3):27891. PubMed CrossRef Google Scholar Szkudelski T. The mechanism of alloxan and streptozotocin action in B cells of the rat pancreas. Physiol Res. 2001;50(6):53746. PubMed Google Scholar Cefalu WT. Animal models of type 2 diabetes: clinical presentation and pathophysiological relevance Continue reading >>

A New Rat Model Of Type 2 Diabetes: The Fat-fed, Streptozotocin-treated Rat

A New Rat Model Of Type 2 Diabetes: The Fat-fed, Streptozotocin-treated Rat

Volume 49, Issue 11 , November 2000, Pages 1390-1394 A new rat model of type 2 diabetes: The fat-fed, streptozotocin-treated rat Get rights and content This study was initiated to develop an animal model of type 2 diabetes in a non-obese, outbred rat strain that replicates the natural history and metabolic characteristics of the human syndrome and is suitable for pharmaceutical research. Male Sprague-Dawley rats (n = 31), 7 weeks old, were fed normal chow (12% of calories as fat), or high-fat diet (40% of calories as fat) for 2 weeks and then injected with streptozotocin (STZ, 50 mg/kg intravenously). Before STZ injection, fat-fed rats had similar glucose concentrations to chow-fed rats, but significantly higher insulin, free fatty acid (FFA), and triglyceride (TG) concentrations (P < .01 to .0001). Plasma insulin concentrations in response to oral glucose (2 g/kg) were increased 2-fold by fat feeding (P < .01), and adipocyte glucose clearance under maximal insulin stimulation was significantly reduced (P < .001), suggesting that fat feeding induced insulin resistance. STZ injection increased glucose (P < .05), insulin (P < .05), FFA (P < .05), and TG (P < .0001) concentrations in fat-fed rats (Fat-fed/STZ rats) compared with chow-fed, STZ-injected rats (Chow-fed/STZ rats). Fat-fed/STZ rats were not insulin deficient compared with normal chow-fed rats, but had hyperglycemia and a somewhat higher insulin response to an oral glucose challenge (both P < .05). In addition, insulin-stimulated adipocyte glucose clearance was reduced in Fat-fed/STZ rats compared with both chow-fed and Chow-fed/STZ rats (P < .001). Finally, Fat-fed/STZ rats were sensitive to the glucose lowering effects of metformin and troglitazone. In conclusion, Fat-fed/STZ rats provide a novel animal model 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 >>

How Can I Make A Diabetic Rat Model Using Streptozotocin?

How Can I Make A Diabetic Rat Model Using Streptozotocin?

Content validity of the PedsQL 3.2 Diabetes Module in newly diagnosed patients with Type 1 diabetes mellitus ages 845 [Show abstract] [Hide abstract] ABSTRACT: Objectives: The content validity of the 28-item PedsQL 3.0 Diabetes Module has not been established in research on pediatric and adult patients with newly diagnosed Type 1 diabetes across a broad age range. This study aimed to document the content validity of three age-specific versions (8-12 years, 13-18 years, and 18-45 years) of the PedsQL Diabetes Module in a population of newly diagnosed patients with Type 1 diabetes.Methods: The study included in-depth interviews with 31 newly diagnosed patients with Type 1 diabetes between the ages of 8 and 45 years, as well as 14 parents and/or caregivers of child and teenage patients between the ages of 8 and 18 years of age; grounded theory data collection and analysis methods; and review by clinical and measurement experts.Results: Following the initial round of interviews, revisions reflecting patient feedback were made to the Child and Teen versions of the Diabetes Module, and an Adult version of the Diabetes Module was drafted. Cognitive interviews of the modified versions of the Diabetes Module were conducted with an additional sample of 11 patients. The results of these interviews support the content validity of the modified 33-item PedsQL 3.2 Diabetes Module for pediatric and adult patients, including interpretability, comprehensiveness, and relevance suitable for all patients with Type 1 Diabetes.Conclusions: Qualitative methods support the content validity of the modified PedsQL 3.2 Diabetes Module in pediatric and adult patients. It is recommended that the PedsQL 3.2 Diabetes Module replaces version 3.0 and is suitable for measuring patient-reported outcomes Continue reading >>

The Streptozotocin-diabetic Rat As A Model Of The Chronic Complications Of Human Diabetes.

The Streptozotocin-diabetic Rat As A Model Of The Chronic Complications Of Human Diabetes.

The streptozotocin-diabetic rat as a model of the chronic complications of human diabetes. Department of Physiology and Pharmacology, School of Biomedical Sciences, University of Queensland, Brisbane, Australia. BACKGROUND: Diabetes in humans induces chronic complications such as cardiovascular damage, cataracts and retinopathy, nephropathy and polyneuropathy. The most common animal model of human diabetes is streptozotocin (STZ)-induced diabetes in the rat. METHODS: This project assessed cardiovascular, ocular and neuropathic changes over a period of 24 weeks post STZ administration in rats. RESULTS: STZ-diabetic rats (n = 96) showed stable signs of diabetes (hyperglycaemia, increased water and food intake with no increase in bodyweight): 52% of untreated STZ-diabetic rats (n = 50) survived 24 weeks after STZ administration. STZ-diabetic rats were normotensive with slowly developing systolic and diastolic dysfunction and an increased ventricular stiffness. Ventricular action potential durations were markedly prolonged. STZ-diabetic rats developed stable tactile allodynia. Cataracts developed to presumed blindness at 16 weeks but proliferative retinopathy was not observed even after 24 weeks. CONCLUSION: The chronic STZ-diabetic rat mimics many but not all of the chronic complications observed in the diabetic human. The chronic STZ-diabetic rat may be a useful model to test therapeutic approaches for amelioration of chronic diabetic complications in humans. Continue reading >>

Modeling Type 2 Diabetes In Rats Using High Fat Diet And Streptozotocin

Modeling Type 2 Diabetes In Rats Using High Fat Diet And Streptozotocin

Modeling type 2 diabetes in rats using high fat diet and streptozotocin 1In vivo Pharmacology Graduate Program, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark Author information Article notes Copyright and License information Disclaimer Received 2014 Feb 14; Revised 2014 Mar 7; Accepted 2014 Mar 14. Copyright 2014 The Author. Journal of Diabetes Investigation published by Asian Association of the Study of Diabetes (AASD) and Wiley Publishing Asia Pty Ltd This is an open access article under the terms of the Creative Commons AttributionNonCommercialNoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is noncommercial and no modifications or adaptations are made. This article has been cited by other articles in PMC. The pathology of type 2 diabetes is complex, with multiple stages culminating in a functional cell mass that is insufficient to meet the body's needs. Although the broad outlines of the disease etiology are known, many critical questions remain to be answered before nextgeneration therapeutics can be developed. In order to further elucidate the pathobiology of this disease, animal models mimicking the pathology of human type 2 diabetes are of great value. One example of a type 2 diabetes animal model is the highfat dietfed, streptozotocin (HFD/STZ)treated rat model. The present review first summarizes the current understanding of the metabolic profile and pathology involved in the different stages of the type 2 diabetes disease progression in humans. Second, the known characteristics of the HFD/STZ rat model are reviewed and compared with the pathophysiology of human type 2 diabetes. Next, the suitability of the HFD/STZ model as a model of type 2 diabet Continue reading >>

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