diabetestalk.net

Streptozotocin Induced Diabetes In Mice Protocol

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 >>

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

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

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

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

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

Editor who approved publication: Professor Ming-Hui Zou Department of Pharmaceutical Sciences, UNT System College of Pharmacy, University of North Texas Health Science Center, Fort Worth, TX, USA Abstract: Chronic hyperglycemia and the corresponding glucotoxicity are the main pathogenic mechanisms of diabetes and its complications. Streptozotocin (STZ)-induced diabetic animal models are useful platforms for the understanding of cell glucotoxicity in diabetes. As diabetes induced by a single STZ injection is often referred to as type 1 diabetes that is caused by STZs partial destruction of pancreas, one question often being asked is whether the STZ type 1 diabetes animal model is a good model for studying the mitochondrial mechanisms of cell glucotoxicity. In this mini review, we provide evidence garnered from the literature that the STZ type 1 diabetes is indeed a suitable model for studying mitochondrial mechanisms of diabetic cell glucotoxicity. Evidence presented includes: 1) continued cell derangement is due to chronic hyperglycemia after STZ is completely eliminated out of the body; 2) STZ diabetes can be reversed by insulin treatment, which indicates that cell responds to treatment and shows ability to regenerate; and 3) STZ diabetes can be ameliorated or alleviated by administration of phytochemicals. In addition, mechanisms of STZ action and fundamental gaps in understanding mitochondrial mechanisms of cell dysfunction are also discussed. Keywords: diabetes, cell, glucotoxicity, mitochondria, redox imbalance, streptozotocin Diabetes mellitus and its complications are chronic glucotoxicity diseases. The concept of cell glucotoxicity (and other cells as well) implicates that persistent excessive glucose can exert adverse or toxic effect on cell function after the Continue reading >>

Streptozotocin, Type I Diabetes Severity And Bone

Streptozotocin, Type I Diabetes Severity And Bone

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

Stz Frequently Asked Questions

Stz Frequently Asked Questions

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

Stz Induced Diabetes I Rats

Stz Induced Diabetes I Rats

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

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 >>

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 >>

Streptozotocininduced Diabetic Models In Mice And Rats

Streptozotocininduced Diabetic Models In Mice And Rats

Please review our Terms and Conditions of Use and check box below to share full-text version of article. I have read and accept the Wiley Online Library Terms and Conditions of Use. Use the link below to share a full-text version of this article with your friends and colleagues. Learn more. Streptozotocin (STZ) is an antibiotic that produces pancreatic islet cell destruction and is widely used experimentally to produce a model of type 1 diabetes mellitus (T1DM). Detailed in this unit are protocols for producing STZinduced insulin deficiency and hyperglycemia in mice and rats. Also described are protocols for creating animal models for type 2 diabetes using STZ. These animals are employed for assessing the pathological consequences of diabetes and for screening potential therapies for the treatment of this condition. 2015 by John Wiley & Sons, Inc. Yu-Ting Tseng, Wan-Hsuan Chang, Chih-Cheng Lin, Fang-Rong Chang, Pao-Chu Wu and Yi-Ching Lo, Protective effects of Liuwei dihuang water extracts on diabetic muscle atrophy, Phytomedicine, 10.1016/j.phymed.2018.09.032, 53, (96-106), (2019). Liming Yu, Zhi Li, Xue Dong, Xiaodong Xue, Yu Liu, Shu Xu, Jian Zhang, Jinsong Han, Yang Yang and Huishan Wang, Polydatin Protects Diabetic Heart against Ischemia-Reperfusion Injury via Notch1/Hes1-Mediated Activation of Pten/Akt Signaling, Oxidative Medicine and Cellular Longevity, 2018, (1), (2018). Haiyan Wei, Qiaoyun Hu, Junxia Wu, Chenjuan Yao, Lingfei Xu, Fengjun Xing, Xinyuan Zhao, Shali Yu, Xiaoke Wang and Gang Chen, Molecular mechanism of the increased tissue uptake of trivalent inorganic arsenic in mice with type 1 diabetes mellitus, Biochemical and Biophysical Research Communications, 10.1016/j.bbrc.2018.06.029, 504, 2, (393-399), (2018). Jay Parikh, Alice Zemljic-Harpf, Johnny F 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 >>

Black Ginseng Extract Counteracts Streptozotocin-induced Diabetes In Mice

Black Ginseng Extract Counteracts Streptozotocin-induced Diabetes In Mice

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

Streptozotocin-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 >>

Modified Dio Protocols Improve Type 2 Diabetes Models

Modified Dio Protocols Improve Type 2 Diabetes Models

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

Hypoglycemic Potential Of Alcoholic Root Extract Of Cassia Occidentalis Linn. In Streptozotocin Induced Diabetes In Albino Mice - Sciencedirect

Hypoglycemic Potential Of Alcoholic Root Extract Of Cassia Occidentalis Linn. In Streptozotocin Induced Diabetes In Albino Mice - Sciencedirect

Volume 52, Issue 2 , December 2014, Pages 211-217 Hypoglycemic potential of alcoholic root extract of Cassia occidentalis Linn. in streptozotocin induced diabetes in albino mice Author links open overlay panel SurbhiSharmaa ManjushaChoudharya Open Access funded by Faculty of Pharmacy, Cairo University Cassia occidentalis (CO) (family: Caesalpiniaceae) is a common weed which is widely used to treat inflammation, hepatotoxicity, antimalarial activities, sore eyes, hematuria, rheumatism, typhoid, asthma, leprosy and diabetes in folklore medicine in India. The present study was carried out to investigate the antidiabetic activity of ethanolic extract of C. occidentalis roots. Root extract of C. occidentalis (RCO) was administered orally at two doses (250 and 500mg/kg) to normal and streptozotocin (STZ) induced NIDDM. Fasting blood glucose (FBG) level, biochemical parameters like blood glucose, serum cholesterol, high density lipoprotein (HDL) cholesterol, triglycerides (TG), total protein, urea, creatinine, serum glutamate oxaloacetate transaminase (SGOT), serum glutamate pyruvate transaminase (SGPT) levels and physical parameters like change in body weight, food intake, water intake and levels in liver were performed for the evaluation of hypoglycemic effects. Both the doses of RCO caused a marked decrease in FBG levels in STZ induced type 2 diabetic mice. RCO decreased the blood glucose, food intake, water intake, organ weight, serum cholesterol, TG, creatinine, SGOT and SGPT levels with significant value and increased the levels of HDL cholesterol and total protein with a significant value (P<0.050.01). The decrease in body weight induced by STZ was restored with a significant value (P<0.01) at both doses. The results suggest that ethanolic roots extract of C. occidenta 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 [] Continue reading >>

More in diabetes