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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 >>

A Practical Guide For Induction Of Type-2 Diabetes In Rat: Incorporating A High-fat Diet And Streptozotocin - Sciencedirect

A Practical Guide For Induction Of Type-2 Diabetes In Rat: Incorporating A High-fat Diet And Streptozotocin - Sciencedirect

A practical guide for induction of type-2 diabetes in rat: Incorporating a high-fat diet and streptozotocin Author links open overlay panel SevdaGheibiab KhosrowKashfic AsgharGhasemia Feeding a high fat diet (HFD) to rats causes insulin resistance. Administration of low-dose streptozotocin (STZ) causes -cell dysfunction. Combining a HFD with low-dose STZ induces type-2 diabetes (T2D). HFD-STZ-T2D exhibits the metabolic characteristics similar to those seen in human T2D. Prevalence of diabetes, a serious public health problem is rapidly increasing worldwide. Type-2 diabetes is the common form of diabetes characterized by insulin resistance and abnormalities in insulin production. Despite the current development of therapeutic agents, there is no effective treatment without side effects; it is therefore necessary to find new prevention strategies and better treatments. For this purpose animal models of diabetes are appropriate tools, of which rodents due to the short generation time and economic considerations are the first choice. The aim of this review is to present features of a frequently used model of type-2 diabetes in rat, induced by a high fat diet and streptozotocin, taking into account its advantages/disadvantages and presenting a practical guide. Continue reading >>

Hypoglycemic And Hypolipidemic Effects Of Bersama Engleriana Leaves In Nicotinamide/streptozotocin-induced Type 2 Diabetic Rats

Hypoglycemic And Hypolipidemic Effects Of Bersama Engleriana Leaves In Nicotinamide/streptozotocin-induced Type 2 Diabetic Rats

BMC Complementary and Alternative Medicine Watcho et al.; licensee BioMed Central Ltd.2012 The present investigation was aimed at evaluating the hypoglycemic and hypolipidemic properties of the aqueous and methanolic extracts from Bersama engleriana leaves in streptozotocin/nicotinamide (STZ-NA)-induced type 2 diabetic rats. Animals were orally treated for 4 consecutive weeks with Bersama engleriana extracts at doses of 300 or 600 mg/kg. The anti-diabetic effect was examined by measuring blood glucose (BG) at 0, 1, 14 and 28 days after STZ-NA treatment and, total cholesterol (TC), high density lipoprotein cholesterol (HDL-C), low density lipoprotein cholesterol (LDL-C) and triglycerides (TG) levels at sacrifice (day 29). Glibenclamide (0.25 mg/kg) was used for comparison. STZ-NA-induced diabetic rats showed moderate to significant increases in the levels of BG, TG, TC, LDL-C while body weight, HDL-C levels and relative weights of liver and pancreas were decreased compared to controls (non diabetic rats). Administration of the plant extracts to STZ-NA diabetic rats resulted in a significant decrease in BG, TG, TC and LDL-C and the dose 600 mg/kg of the methanolic extract was the most effective; HDL-C level was markedly increased after four weeks compared to untreated diabetic rats. A dose-dependent increase in the relative weights of the diabetogenic organs was observed in the Bersama engleriana groups. It can be also noticed that the methanolic extract, especially the dose 600 mg/kg (p<0.001), produced more effects than glibenclamide and aqueous extract. Rats treated with glibenclamide (0.25 mg/kg) generally gave lower results compared to groups treated with plant extracts. Results of the present study showed that Bersama engleriana extracts and especially its methanol Continue reading >>

High-fat Diet/low-dose Streptozotocin-induced Type 2 Diabetes In Rats Impacts Osteogenesis And Wnt Signaling In Bone Marrow Stromal Cells

High-fat Diet/low-dose Streptozotocin-induced Type 2 Diabetes In Rats Impacts Osteogenesis And Wnt Signaling In Bone Marrow Stromal Cells

High-Fat Diet/Low-Dose Streptozotocin-Induced Type 2 Diabetes in Rats Impacts Osteogenesis and Wnt Signaling in Bone Marrow Stromal Cells Contributed equally to this work with: Chao Qian, Chenyuan Zhu Affiliation: Department of Prosthodontics, School of Stomatology, Ninth Peoples Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai Key Laboratory of Stomatology. Shanghai, 200011, Peoples Republic of China Contributed equally to this work with: Chao Qian, Chenyuan Zhu Affiliation: Department of Prosthodontics, School of Stomatology, Ninth Peoples Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai Key Laboratory of Stomatology. Shanghai, 200011, Peoples Republic of China Affiliation: Department of Prosthodontics, School of Stomatology, Ninth Peoples Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai Key Laboratory of Stomatology. Shanghai, 200011, Peoples Republic of China * E-mail: [email protected] (FZ); [email protected] (XJ) Affiliation: Department of Prosthodontics, School of Stomatology, Ninth Peoples Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai Key Laboratory of Stomatology. Shanghai, 200011, Peoples Republic of China These authors also contributed equally to this work. * E-mail: [email protected] (FZ); [email protected] (XJ) Affiliation: Department of Prosthodontics, School of Stomatology, Ninth Peoples Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai Key Laboratory of Stomatology. Shanghai, 200011, Peoples Republic of China These authors also contributed equally to this work. Bone regeneration disorders are a significant problem in patients with type 2 diabetes mellitus. Bone marrow stromal cells (BMSCs) are recognized as ideal seed cells for tissue engineerin 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

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 This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at and incorporate the Creative Commons Attribution - Non Commercial (unported, v3.0) License . By accessing the work you hereby Continue reading >>

Feruloylated Oligosaccharides From Maize Bran Alleviate The Symptoms Of Diabetes In Streptozotocin-induced Type 2 Diabetic Rats

Feruloylated Oligosaccharides From Maize Bran Alleviate The Symptoms Of Diabetes In Streptozotocin-induced Type 2 Diabetic Rats

Feruloylated oligosaccharides from maize bran alleviate the symptoms of diabetes in streptozotocin-induced type 2 diabetic rats a College of Traditional Chinese Medicine, Jinan University, Guangzhou 510632, China b Department of Food Science, Rutgers, The State University of New Jersey, 65 Dudley Road, New Brunswick 08901, USA c Department of Pharmaceutical Sciences, School of Pharmacy, Texas Tech University Health Sciences Center, Amarillo 79106, USA d Out-patient Department of University, The First Affiliated Hospital, Jinan University, Guangzhou 510632, China e Department of Food Science and Engineering, Jinan University, Guangzhou 510632, China This study investigated the therapeutic effect of feruloylated oligosaccharides (FOs) extracted from maize bran on type 2 diabetic rats and its potential mechanism. Streptozotocin (STZ) induced type 2 diabetic male rats were orally administered with different levels of FOs for 8 weeks, and ferulic acid (FA) treatment was conducted as the positive control. Among all the treatments, the oral administration of 600 mg per kg bw per d FOs showed the best therapeutic effects on the diabetic rats by significantly lowering the levels of fasting plasma glucose (FPG), fasting insulin, TG, LDL-c, aspartate transaminase, creatine kinase and lactate dehydrogenase in plasma, while increasing the level of plasma HDL-c. In addition, the intake of FOs at 600 mg per kg bw per d exhibited the best antioxidant effects in the plasma, liver, kidney and heart of the diabetic rats, and the highest inhibitory effects on the formation of AGEs and CML in the organs, which might explain the alleviating effects of FOs on abdominal aorta injury observed in the current study. FOs presented better regulation effects on FPG, plasma lipid and the protection 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 >>

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 >>

Streptozotocin/high Fat Diet-induced Type 2 Diabetes

Streptozotocin/high Fat Diet-induced Type 2 Diabetes

Home Streptozotocin/High Fat Diet-induced Type 2 Diabetes | Bienta Streptozotocin/High Fat Diet-induced Type 2 Diabetes Background: Unlike type 1 diabetes, type 2 diabetes (T2D) is associated with resistance to insulin action. To develop the corresponding animal pathology model, High Fat Diet (HFD) is often used. HFD leads to the development of obesity, metabolic syndrome and decrease in insulin sensitivity in mice, in contrast to low fat diet (LFD). Combination of HFD and single streptozotocin (STZ) injection leads to metabolic changes that are characteristic of Type 2 Diabetes, including peripheral insulin resistance and pancreas -cell impairment. HFD/STZ-induced model of experimental T2D can be used for efficacy testing of anti-diabetic and anti-obesity drugs. The induction of disease can be carried out in rats or mice. This model is suitable not only for the study of the effectiveness of the drugs stimulating the production/release of insulin from beta cells, but also drugs that reduce the production of glucose in the liver, improve the sensitivity of tissues to insulin, regulate the production of incretins, etc. Service details: To induce T2D in C57BL/6 mice, the standard HFD (Research Diets, Inc.) in combination with a single high dose (95 mg/kg) of STZ is used. Development of the diabetic state is monitored by routine tests food and water intake, body weight gain, glucose levels, glycosylated hemoglobin in the blood, GTT and ITT. Various markers of diabetes side effects can be monitored upon request. To develop the HFD/STZ model of Type 2 diabetes for testing a drug candidate, we suggest using 8-10 animals per each planned experimental group, 12 weeks of high fat diet for obesity induction and post-HFD/STZ treatment monitoring to confirm that the mice are diabet Continue reading >>

Streptozotocin - Wikipedia

Streptozotocin - Wikipedia

Streptozotocin or streptozocin ( INN , USP ) (STZ) is a naturally occurring alkylating antineoplastic agent that is particularly toxic to the insulin-producing beta cells of the pancreas in mammals. It is used in medicine for treating certain cancers of the islets of Langerhans and used in medical research to produce an animal model for hyperglycemia in a large dose, as well as type 2 diabetes or type 1 diabetes with multiple low doses. Streptozotocin is approved by the U.S. Food and Drug Administration (FDA) for treating metastatic cancer of the pancreatic islet cells . Since it carries a substantial risk of toxicity and rarely cures the cancer, its use is generally limited to patients whose cancer cannot be removed by surgery. In these patients, streptozotocin can reduce the tumor size and reduce symptoms (especially hypoglycemia due to excessive insulin secretion by insulinomas ). [1] A typical dose is 500mg/m2/day by intravenous injection, for 5 days, repeated every 46 weeks. Due to its high toxicity to beta cells, in scientific research, streptozotocin has also been long used for inducing insulitis and diabetes on experimental animals . [2] Streptozotocin is a glucosamine - nitrosourea compound. As with other alkylating agents in the nitrosourea class, it is toxic to cells by causing damage to the DNA , though other mechanisms may also contribute. DNA damage induces activation of poly ADP-ribosylation , which is likely more important for diabetes induction than DNA damage itself. [3] Streptozotocin is similar enough to glucose to be transported into the cell by the glucose transport protein GLUT2 , but is not recognized by the other glucose transporters. This explains its relative toxicity to beta cells, since these cells have relatively high levels of GLUT2. [4] Continue reading >>

The Characterization Of High-fat Diet And Multiple Low-dose Streptozotocin Induced Type 2 Diabetes Rat Model

The Characterization Of High-fat Diet And Multiple Low-dose Streptozotocin Induced Type 2 Diabetes Rat Model

The Characterization of High-Fat Diet and Multiple Low-Dose Streptozotocin Induced Type 2 Diabetes Rat Model Department of Pharmacology, School of Basic Medical Sciences, Jilin University, Changchun, Jilin 130021, China Received 5 June 2008; Revised 14 October 2008; Accepted 19 November 2008 Copyright 2008 Ming Zhang 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. Aim. Based on the previously established method, we developed a better and stable animal model of type 2 diabetes mellitus by high-fat diet combined with multiple low-dose STZ injections. Meanwhile, this new model was used to evaluate the antidiabetic effect of berberine. Method. Wistar male rats fed with regular chow for 4 weeks received vehicle (control groups), rats fed with high-fat diet for 4 weeks received different amounts of STZ once or twice by intraperitoneal injection (diabetic model groups), and diabetic rats were treated with berberine (100 mg/kg, berberine treatment group). Intraperitoneal glucose tolerance test and insulin tolerance test were carried out. Moreover, fasting blood glucose, fasting insulin, total cholesterol, and triglyceride were measured to evaluate the dynamic blood sugar and lipid metabolism. Result. The highest successful rate (100%) was observed in rats treated with a single injection of 45 mg/kg STZ, but the plasma insulin level of this particular group was significantly decreased, and ISI has no difference compared to control group. The successful rate of 30 mg/kg STZ twice injection group was significantly high (85%) and the rats in this group presented a typical characteristic of T2DM as insulin res Continue reading >>

Streptozotocin, Type I Diabetes Severity And Bone.

Streptozotocin, Type I Diabetes Severity And Bone.

1. Biol Proced Online. 2009 Mar 6;11:296-315. doi: 10.1007/s12575-009-9000-5. Streptozotocin, type I diabetes severity and bone. (1)Departments of Physiology and Radiology, Biomedical Imaging Research Center, Michigan State University, 2201 Biomedical Physical Science Bldg., East Lansing, MI 48824 USA. As many as 50% of adults with type I (T1) diabetes exhibit bone loss and are atincreased risk for fractures. Therapeutic development to prevent bone loss and/orrestore lost bone in T1 diabetic patients requires knowledge of the molecularmechanisms accounting for the bone pathology. Because cell culture models alonecannot fully address the systemic/metabolic complexity of T1 diabetes, animalmodels are critical. A variety of models exist including spontaneous andpharmacologically induced T1 diabetic rodents. In this paper, we discuss thestreptozotocin (STZ)-induced T1 diabetic mouse model and examine dose-dependenteffects on disease severity and bone. Five daily injections of either 40 or60mg/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 aredecreased. In contrast, bone marrow adiposity and aP2 expression are increasedwith either dose. However, high-dose STZ caused a more rapid elevation of bloodglucose 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 theratio of RANKL/OPG was noted in high-dose STZ mice, suggesting the possibilitythat severe diabetes could increase osteoclast activity, something not seen with lower doses. This may contribute to some of the disparity between existingstudies rega 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 >>

Does Stz Make Mice Type 1 Or Type 2?

Does Stz Make Mice Type 1 Or Type 2?

Home > Column > Does STZ make mice Type 1 or Type 2? Since streptozotocin (an N-acetyl--D-glucosaminidase inhibitor; STZ) is cytotoxic to pancreatic beta cells, STZ-induced diabetes models are often considered as a model for Type 1 diabetes mellitus (T1D) which is in definition caused by autoimmune destruction of islet beta cells and characterized by the complete lack of insulin. Indeed, classical STZ models aim to mimic the system of T1D, where insulin is totally deficient and complicated with ketosis. In such models, STZ is typically injected to adult rats or mice at a relatively high dose (160170 mg/kg) to damage the beta cells and induce hyperglycemia due to the lack of insulin function [1]. There is another, later reported STZ model, with the toxin given to neonatal animals (at a dose of 80-100 mg/kg), and thus is called nSTZ [2]. The nSTZ model is distinguished from the adult models in that insulin secretion is low but still remains, and that the impairment is reversible - the features more alike Type 2 diabetes mellitus (T2D). There is evidence supporting the T2D-like characteristics of nSTZ model, including the presence of insulin resistance (IR), impaired glucose tolerance, diabetic complications such as cataract [3], and response to anti-diabetic agents [4]. Interestingly, it is known that susceptibility of beta cells to STZ varies with species, strains, ages or genders [5]. Consequently, by selecting an appropriate combination of animal and dosing regimen of STZ, one can induce multiple diabetic conditions: ranging from the complete abolishment of insulin section like in T1D, to a partial impairment of insulin function seen in early to late T2D. SMC's STAM model (a NASH-HCC model) is produced by a combination of STZ injection and high-fat diet feeding. STZ i Continue reading >>

Rrml - Wistar Rats With Long-term Streptozotocin-induced Type 1 Diabetes Mellitus Replicate The Most Relevant Clinical, Biochemical, And Hematologic Features Of Human Diabetes

Rrml - Wistar Rats With Long-term Streptozotocin-induced Type 1 Diabetes Mellitus Replicate The Most Relevant Clinical, Biochemical, And Hematologic Features Of Human Diabetes

Nr. 23(3)/2015 DOI:10.1515/rrlm-2015-0028 Wistar rats with long-term streptozotocin-induced type 1 diabetes mellitus replicate the most relevant clinical, biochemical, and hematologic features of human diabetes Sobolanii Wistar cu diabet zaharat tip 1 indus cu streptozotocina reproduc cele mai relevante caracteristici clinice, biochimice si hematologice ale diabetului uman Alina Scridon , Marcel Perian , Alina Marginean , Ciprian Fisca , Adriana Vantu , Doina Ghertescu , Philippe Chevalier , Razvan Constantin Serban Background: Experimental models are essential for clarifying the pathogenesis of diabetes mellitus (DM). We aimed to provide an exhaustive description of clinical, biochemical, and hematologic features of rats with streptozotocin (STZ)-induced DM. Methods: Wistar rats were assigned to control (n=14) or DM (n=17) groups. DM was induced using STZ (60 mg/kg, i.p.). If STZ failed to induce DM, rats were reinjected with a similar STZ dose. Bodyweight, 24-h food and water intake were measured weekly during 28 weeks. At the end of the study lipid profile, kidney function, and complete blood count were assessed. Results: STZ induced DM in 58.82% of rats. The second STZ administration induced DM in 71.43% of the remaining rats. Diabetics presented progressive, but less significant bodyweight increase than controls, and higher food and water consumption. At the end of the study, diabetics presented higher white blood cells count, glucose, triglycerides, total and low-density lipoprotein cholesterol, and lower creatinine clearance than controls (all p0.02). No significant difference was observed between diabetics injected once and those that were reinjected, in any of the studied parameters. Conclusions: This study provides one of the longest follow-ups of rats with S Continue reading >>

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