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Streptozotocin Stz )- Induced Diabetes

Black Ginseng Extract Counteracts Streptozotocin-induced Diabetes In Mice

Black Ginseng Extract Counteracts Streptozotocin-induced Diabetes In Mice

Black Ginseng Extract Counteracts Streptozotocin-Induced Diabetes in Mice Affiliation Department of Food and Biotechnology, Korea University, Sejong, Republic of Korea Affiliation Department of Food and Biotechnology, Korea University, Sejong, Republic of Korea Affiliation Department of Food and Biotechnology, Korea University, Sejong, Republic of Korea Affiliation Department of Food and Biotechnology, Korea University, Sejong, Republic of Korea Black Ginseng Extract Counteracts Streptozotocin-Induced Diabetes in Mice 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 -cell function in STZ-treated mice. The inhibition of -cell apoptosis by BGE was associated with suppression of the cytokineinduced nuclear factorBmediated 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 cytokineinduced apoptotic signaling, protects -cells from oxidative injury and counteracts diabetes in mice. Citation: Kim JH, Pan JH, Cho HT, Kim YJ (2 Continue reading >>

A Review Of The Use Of Streptozotocin (stz) In The Induction Of Diabetes In Rats And Subsequent Ocular Tissue Changes | Sithole | African Vision And Eye Health

A Review Of The Use Of Streptozotocin (stz) In The Induction Of Diabetes In Rats And Subsequent Ocular Tissue Changes | Sithole | African Vision And Eye Health

Home South African Optometrist: Vol 68, No 2 (2009) Sithole A review of the use of Streptozotocin (STZ) in the induction of diabetes in rats and subsequent ocular tissue changes African Vision and Eye Health | South African Optometrist: Vol 68, No 2 | a156 | DOI: | 2009 H. L. Sithole | This work is licensed under CC Attribution 4.0 Submitted: 13 December 2009| Published: 13 December 2009 Streptozotocin is widely used in medical research for treating certain cancers of the Islets of Langerhans and to produce an animal model for type 1 diabetes. A study has revealed that when compared to the control group of rats, those injected with STZ exhibited reduced plasma insulin and elevated blood glucose (p < 0.05 in all cases). The study also found that diabetic rats weighed significantly less than control animals (p < 0.05). In relation to ocular tissues, lacrimal glands from diabetic rats were also found to weigh significantly less (p < 0.05) than those from the control group. However, no significant changes in the weights of lens, cornea, sclera and retina were observed between diabeticand control animals. Several other studies found that STZ-induced diabetes can be treated by plant extracts which control the blood sugar level as well as improving the lipid profile and ocular complications such as retinopathy. Experiments are usuallyperformed on male or female rats of a specific body weight, usually between 250 and 300 g. Diabetes is induced in rats by intraperitonial injections of streptozotocin (60 mg/ kg) in citrate buffer, pH 6.3.Animals that exhibit glucosuria after 24 hours, test- ed by urine test strips are considered diabetic. Plant extracts (6 mg/100g body weight) are orally administered into the stomach of STZ-diabetic rats every third day at a certain consistent t Continue reading >>

Long-term Streptozotocin-induced Diabetes In Rats Leads To Severe Damage Of Brain Blood Vessels And Neurons Via Enhanced Oxidative Stress

Long-term Streptozotocin-induced Diabetes In Rats Leads To Severe Damage Of Brain Blood Vessels And Neurons Via Enhanced Oxidative Stress

Long-term streptozotocin-induced diabetes in rats leads to severe damage of brain blood vessels and neurons via enhanced oxidative stress Affiliations: Department of Clinical Laboratory, The Second Affiliated Hospital of Kunming Medical University, Kunming 650101, P.R. China, Department of Diabetes, The First Affiliated Hospital of Kunming Medical University, Kunming 650101, P.R. China, Department of Pathophysiology, Kunming Medical University, Kunming 650031, P.R. China, Department of Clinical Laboratory, The First Affiliated Hospital of Dali Medical College, Dali 671000, P.R. China Published online on: December 10, 2012 Metrics: HTML 0 views | PDF 0 views Cited By (CrossRef): 0 citations The aim of this study was to investigate pathophysiological alterations and oxidative stress in various stages of streptozotocin (STZ)induced diabetes mellitus(DM) in rats. Male Sprague-Dawley rats (120) were randomized into DM and control groups. Body mass, plasma glucose, glycated hemoglobin (HbA1c), superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx) levels, as well as aldose reductase (AR) activities, in brain tissue and serum were determined. Electron microscopy was used to observe neuron and vessel changes in the brain. In STZtreated rats, blood glucose, low density lipoproteins, triglycerides and total cholesterol levels increased 1.433.0fold and high density lipoprotein, HbA1c and insulin sensitivity index increased 1.11.23fold compared with control. At week16 following treatment, DM rat serum H2O2 concentration was increased, indicating oxidative stress and mRNA levels of GPx and SOD were 2fold higher than the control. Protein GPx and SOD levels were reduced(P<0.01). DM rats were identified to exhibit early irregular glomerular capillary basement memb Continue reading >>

Hypoglycemic And Hypolipidemic Potential Of Nigella Sativa L. Seedextract In Streptozotocin (stz)-induced Diabetic Rats

Hypoglycemic And Hypolipidemic Potential Of Nigella Sativa L. Seedextract In Streptozotocin (stz)-induced Diabetic Rats

Department of Biochemistry and Molecular Biology University of Rajshahi, Rajshahi-6205, Bangladesh Received October 20, 2015; Accepted October 16, 2015; Published October 23, 2015 Citation: Asaduzzaman M, Nahar L, Rahman MS, Hasan M, Khatun A, et al. (2015) Hypoglycemic and Hypolipidemic Potential of Nigella sativa L. Seed Extract in Streptozotocin (STZ)-Induced Diabetic Rats. J Plant Biochem Physiol 3:158. doi:10.4172/2329-9029.1000158 Copyright: 2015 Asaduzzaman M, 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 author and source are credited. Nigella sativa; Diabetes; CVD; Lipid profile ; CRP Diabetes mellitus (DM) is the most common metabolic disease worldwide. Therapeutic compounds available to treat DM are either synthetic or formulated forms. Type 2 diabetes had global prevalence estimate of 2.8% in the year 2000 and is projected to be 4.4% in 2030 [ 1 ]. Prevention and control of DM is a major challenge and requires moulding lifestyle towards more physical activity and less calorie intake avoiding sedentary habits. However most people find it difficult to change their lifestyle and look for a less cumbersome alternative. A traditional component of food that can reduce appetite, glucose absorption in intestine, hepatic gluconeogenesis, blood glucose level, body weight, and can stimulate glucose induced secretion of insulin from beta-cells in pancreas, may prove to be useful for prevention and control of diabetes mellitus. Therefore, a variety of plants are used in the management and treatment of DM. Chemical and pharmacological studies on antidiabetic herbal remedies are in progress and might lead to i Continue reading >>

The Protective Effect Of Betulinic Acid (ba) Diabetic Nephropathy On Streptozotocin (stz)-induced Diabetic Rats

The Protective Effect Of Betulinic Acid (ba) Diabetic Nephropathy On Streptozotocin (stz)-induced Diabetic Rats

The protective effect of betulinic acid (BA) diabetic nephropathy on streptozotocin (STZ)-induced diabetic rats b Department of Endocrinology, Huai'an First People's Hospital, Nanjing Medical University, Huai'an, P. R. China The present study was designed to investigate the protective effect of betulinic acid (BA) on streptozotocin (STZ)-induced diabetic rats. The rats were intraperitoneally injected with STZ (35 mg kg ). 7 days later, the animals were intragastrically administered with metformin (MET, 150 mg kg ) once daily for consecutive 30 days. The blood glucose, the contents of insulin, interleukin-6 (IL-6), interleukin-1 (IL-1) and tumor necrosis factor- (TNF-) in serum were examined. The levels of IL-6, IL-1, TNF-, superoxide dismutase (SOD), catalase (CAT) and malondialdehyde (MDA) in kidney tissues were measured. Moreover, the histopathological alteration and the protein expressions of the signaling pathway were detected by hematoxylin and eosin (H&E) staining and western blotting, respectively. BA significantly decreased the levels of serum insulin, IL-6, IL-1, TNF- and blood glucose. In addition, BA increased the activities of SOD, CAT and reduced the contents of MDA, IL-6, IL-1, and TNF- in kidney tissues. BA also ameliorated the histopathological condition. Furthermore, BA attenuated the phosphorylations of p-adenosine 5-monophosphate-activated protein kinase (AMPK), nuclear factor kappaB (NF-B), and an inhibitor of NF-B (IB) and the expressions of NF-E2-related factor 2 (Nrf2) and heme oxygenase (HO)-1. These findings demonstrated that BA exhibited a protective effect on diabetic nephropathy in STZ-induced rats possibly through the AMPK/NF-B/Nrf2 pathway. The article was received on 31 Oct 2016, accepted on 30 Nov 2016and first published on 06 Dec 2016 T Continue reading >>

Deterioration Of Bone Quality By Streptozotocin (stz)-induced Type 2 Diabetes Mellitus In Rats

Deterioration Of Bone Quality By Streptozotocin (stz)-induced Type 2 Diabetes Mellitus In Rats

, Volume 140, Issue3 , pp 342353 | Cite as Deterioration of Bone Quality by Streptozotocin (STZ)-Induced Type 2 Diabetes Mellitus in Rats Patients with diabetes mellitus (DM) have various skeletal disorders and bone quality can be impaired in DM leading to fractures. Wistar albino male rats (270300g; n = 16) were assigned randomly to nondiabetic and diabetic rats (single dose intravenous injection of 45mg/kg streptozotocin). All rats in each group were perpetuated for 8weeks, and blood glucose levels as well as body weights were measured once weekly. Biomechanical measurements were performed at the mid-diaphysis of the left femur with tensile test. Extrinsic and intrinsic properties were measured or calculated. Bone mineral density (BMD) was also evaluated and measured by dual-energy X-ray absorptiometry. Cross-sectional area of the femoral shaft was evaluated by computerized tomography. Blood glucose levels in diabetic rats were significantly increased compared to that of the nondiabetic rats, while the body and femur weights were decreased (P < 0.05). In respect to the BMD, cross-sectional area and femur length, there were no statistically significant differences between the nondiabetic and diabetic rats (P > 0.05). The maximum load, ultimate stress, and toughness endpoints in diabetic rats were significantly decreased compared to that of the nondiabetics (P < 0.05). There were no statistically significant differences between the nondiabetic and diabetic rats with regard to the displacement and stiffness (P > 0.05). Femurs of diabetic rats had less absorbed energy than that in nondiabetics (P < 0.05). Ultimate strain was lower in diabetic rats than that in nondiabetics, while the elastic modulus was higher (P > 0.05). The bone quality of rats is decreased by streptoz Continue reading >>

Effects Of Streptozotocin (stz)-induced Diabetes And Insulin Replacement On Ratventral Prostate.

Effects Of Streptozotocin (stz)-induced Diabetes And Insulin Replacement On Ratventral Prostate.

1. Biomed Pharmacother. 2009 Jan;63(1):43-50. doi: 10.1016/j.biopha.2008.01.002.Epub 2008 Feb 11. Effects of streptozotocin (STZ)-induced diabetes and insulin replacement on ratventral prostate. Suthagar E(1), Soudamani S, Yuvaraj S, Ismail Khan A, Aruldhas MM,Balasubramanian K. (1)Department of Endocrinology, Dr. ALM Post Graduate Institute of Basic Medical Sciences, University of Madras, Taramani, Chennai, India. BACKGROUND: Diabetes mellitus due to insulin deficiency has adverse effect on allorgan systems including reproductive organs. Streptozotocin (STZ)-induceddiabetes in rats provides a relevant model to study reproductive dysfunctionunder diabetic conditions, as they exhibit a number of deficits in reproductivefunction that resemble those seen in humans. The present investigation wasdesigned to delineate the impact of STZ-induced diabetes and insulin replacement on the rat ventral prostate.METHODS: Healthy adult male rats of Wistar strain were divided into three groups:Group I: Control; Group II: STZ-diabetic (rats were treated with a singleintraperitoneal injection of streptozotocin (STZ) at a dose of 65 mg/kg bodyweight); Group III: Insulin replaced (after 3 days of STZ treatment, a group ofadult male diabetic rats was given insulin at a dose of 3U/100g body weight intwo equally divided doses at 08:00 and 18:00 h). All the rats were killed after20 days of treatment and ventral prostate was removed and processed forbiochemical estimations such as glucose oxidation, nuclear and cytosolic androgenand estrogen receptors, fructose, acid and alkaline phosphatases.RESULTS: STZ-diabetes significantly decreased the body weight. Glucose oxidation,androgen and estrogen receptor concentration were also decreased in ventralprostate, but the fructose concentration was incr Continue reading >>

Vascular Dysfunction In Streptozotocin-induced Experimental Diabetes Strictly Depends On Insulin Deficiency

Vascular Dysfunction In Streptozotocin-induced Experimental Diabetes Strictly Depends On Insulin Deficiency

Free access is sponsored by an educational grant of the European Society for Microcirculation Vascular Dysfunction in Streptozotocin-Induced Experimental Diabetes Strictly Depends on Insulin Deficiency Oelze M.a Knorr M.a Schuhmacher S.a Heeren T.a Otto C.a Schulz E.a Reifenberg K.b Wenzel P.a Mnzel T.a Daiber A.a Prof. Dr. Andreas Daiber, II. Medizinische Klinik Labor fr Molekulare Kadiologie Universittsmedizin der Johannes Gutenberg-Universitt Mainz Verfgungsgebude fr Forschung und Entwicklung Raum 00349 Obere Zahlbacher Strasse 63, DE55101 Mainz (Germany) Tel. +49 6131 179 722, Fax +49 6131 179 723, E-Mail [email protected] Objective: In previous studies we and others have shown that streptozotocin (STZ)-induced diabetes in rats is associated with vascular oxidative stress and dysfunction. In the present study, we sought to determine whether vascular dysfunction and oxidative stress strictly depend on insulin deficiency. Methods: The effects of insulin (2.5 U/day s.c., 2 weeks) therapy on vascular disorders in STZ-induced (60 mg/kg i.v., 8 weeks) diabetes mellitus (type I) were studied in Wistar rats. The contribution of NADPH oxidase to overall oxidative stress was investigated by in vivo (30 mg/kg/day s.c., 4 days) and in vitro treatment with apocynin. Results: Insulin therapy completely normalized blood glucose, body weight, vascular dysfunction and oxidative stress as well as increased cardiac reactive oxygen and nitrogen species formation in diabetic rats, although diabetes was already established for 6 weeks before insulin therapy was started for the last 2 weeks of the total treatment interval. Apocynin normalized cardiac NADPH oxidase activity, and L-NAME effects suggest a role for uncoupled endothelial nitric oxide synthase in diabetic vascular co 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 Effect Of Streptozotocin-induced Diabetes On Dopamine2, Serotonin1a And Serotonin2a Receptors In The Rat Brain

The Effect Of Streptozotocin-induced Diabetes On Dopamine2, Serotonin1a And Serotonin2a Receptors In The Rat Brain

The Effect of Streptozotocin-Induced Diabetes on Dopamine2, Serotonin1A and Serotonin2A Receptors in the Rat Brain Neuropsychopharmacology volume 16, pages 183190 (1997) | Download Citation The effect of streptozotocin (STZ)-induced diabetes and a combination of chronic treatment with haloperidol (HPD) on dopamine (DA)D2, serotonin (5-HT) 5-HT1A and 5-HT2A receptors was investigated in rat brain. Rats were randomly assigned to one of four groups: vehicle-vehicle, STZ-vehicle, vehicle-HPD, and STZ-HPD groups. Four weeks after single administration of STZ (65 mg/kg IV) or vehicle (citrate buffer), rats received depot HPD (4 mg/kg IM) or vehicle (sesame oil) once a week for 4 weeks. Sixteen days after the last injection of HPD or vehicle, rats were sacrificed, and the density of binding sites was determined using [3H]spiperone as ligand in the striatum (D2), [3H]8-hydroxy-2-(di-n-propyl)-aminotetraline in the hippocampus (5-HT1A), and [3H]ketanserin in the frontal cortex (5-HT2A). The density of D2 receptors was significantly increased in the vehicle-HPD compared to vehicle-vehicle controls. However, striatal D2 receptor density of the STZ-HPD and the STZ-vehicle were not significantly different from the vehicle-vehicle group. A significant increase in cortical 5- HT2A receptor density was observed only in the group of STZ-vehicle. Treatment with STZ, HPD, or the combination thereof, did not affect the density of 5-HT1A receptors. The affinity constants for D2, 5-HT1A, and 5-HT2A receptors were not affected by any treatment. These results suggest that diabetic state may affect brain serotonergic activity via an increase in the density of 5-HT2A receptors. This may indicate an increased vulnerability to major depression in patients with diabetes. The lack of an effect of t Continue reading >>

Metabolic Disorders And Adipose Tissue Insulin Responsiveness In Neonatally Stz-induced Diabetic Rats Are Improved By Long-term Melatonin Treatment

Metabolic Disorders And Adipose Tissue Insulin Responsiveness In Neonatally Stz-induced Diabetic Rats Are Improved By Long-term Melatonin Treatment

Metabolic Disorders and Adipose Tissue Insulin Responsiveness in Neonatally STZ-Induced Diabetic Rats Are Improved by Long-Term Melatonin Treatment Superior Institute of Biomedical Sciences (A.C.d.O.), State University of Cear, Fortaleza, Cear 60135-420, Brazil Department of Physiology and Biophysics (A.C.d.O., S.A., T.d.S.M.F., F.L.T.-L., A.R.G.d.P., A.B.C., A.H.d.S., R.A.L.S., A.R.C., J.C.-N., F.B.L.), Institute of Biomedical Sciences, University of So Paulo, So Paulo 05508-900, Brazil Search for other works by this author on: Department of Physiology and Biophysics (A.C.d.O., S.A., T.d.S.M.F., F.L.T.-L., A.R.G.d.P., A.B.C., A.H.d.S., R.A.L.S., A.R.C., J.C.-N., F.B.L.), Institute of Biomedical Sciences, University of So Paulo, So Paulo 05508-900, Brazil Search for other works by this author on: Department of Physiology and Biophysics (A.C.d.O., S.A., T.d.S.M.F., F.L.T.-L., A.R.G.d.P., A.B.C., A.H.d.S., R.A.L.S., A.R.C., J.C.-N., F.B.L.), Institute of Biomedical Sciences, University of So Paulo, So Paulo 05508-900, Brazil Search for other works by this author on: Department of Physiology and Biophysics (A.C.d.O., S.A., T.d.S.M.F., F.L.T.-L., A.R.G.d.P., A.B.C., A.H.d.S., R.A.L.S., A.R.C., J.C.-N., F.B.L.), Institute of Biomedical Sciences, University of So Paulo, So Paulo 05508-900, Brazil Search for other works by this author on: Department of Physiology and Biophysics (A.C.d.O., S.A., T.d.S.M.F., F.L.T.-L., A.R.G.d.P., A.B.C., A.H.d.S., R.A.L.S., A.R.C., J.C.-N., F.B.L.), Institute of Biomedical Sciences, University of So Paulo, So Paulo 05508-900, Brazil Search for other works by this author on: Department of Physiology and Biophysics (A.C.d.O., S.A., T.d.S.M.F., F.L.T.-L., A.R.G.d.P., A.B.C., A.H.d.S., R.A.L.S., A.R.C., J.C.-N., F.B.L.), Institute of Biomedical Sc 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 >>

Effects Of Streptozotocin-induced Diabetes On The Pharmacology Of Rat Conduit And Resistance Intrapulmonary Arteries

Effects Of Streptozotocin-induced Diabetes On The Pharmacology Of Rat Conduit And Resistance Intrapulmonary Arteries

Effects of streptozotocin-induced diabetes on the pharmacology of rat conduit and resistance intrapulmonary arteries Gurney and Howarth; licensee BioMed Central Ltd.2009 Poor control of blood glucose in diabetes is known to promote vascular dysfunction and hypertension. Diabetes was recently shown to be linked to an increased prevalence of pulmonary hypertension. The aim of this study was to determine how the pharmacological reactivity of intrapulmonary arteries is altered in a rat model of diabetes. Diabetes was induced in rats by the -cell toxin, streptozotocin (STZ, 60 mg/kg), and isolated conduit and resistance intrapulmonary arteries studied 34 months later. Isometric tension responses to the vasoconstrictors phenylephrine, serotonin and PGF2, and the vasodilators carbachol and glyceryl trinitrate, were compared in STZ-treated rats and age-matched controls. STZ-induced diabetes significantly blunted the maximum response of conduit, but not resistance pulmonary arteries to phenylephrine and serotonin, without a change in pEC50. Agonist responses were differentially reduced, with serotonin (46% smaller) affected more than phenylephrine (32% smaller) and responses to PGF2 unaltered. Vasoconstriction caused by K+-induced depolarisation remained normal in diabetic rats. Endothelium-dependent dilation to carbachol and endothelium-independent dilation to glyceryl trinitrate were also unaffected. The small resistance pulmonary arteries are relatively resistant to STZ-induced diabetes. The impaired constrictor responsiveness of conduit vessels was agonist dependent, suggesting possible loss of receptor expression or function. The observed effects cannot account for pulmonary hypertension in diabetes, rather the impaired reactivity to vasoconstrictors would counteract the d Continue reading >>

Effects Of Streptozotocin (stz)-induced Diabetes And Insulin Replacement On Rat Ventral Prostate.

Effects Of Streptozotocin (stz)-induced Diabetes And Insulin Replacement On Rat Ventral Prostate.

Effects of streptozotocin (STZ)-induced diabetes and insulin replacement on rat ventral prostate. @article{Suthagar2009EffectsOS, title={Effects of streptozotocin (STZ)-induced diabetes and insulin replacement on rat ventral prostate.}, author={Esakky Suthagar and Singh Soudamani and Sambandan Yuvaraj and A Ismail Khan and Michael Mariajoseph Aruldhas and Karundevi Balasubramanian}, journal={Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie}, year={2009}, volume={63 1}, pages={43-50}} BACKGROUNDDiabetes mellitus due to insulin deficiency has adverse effect on all organ systems including reproductive organs. Streptozotocin (STZ)-induced diabetes in rats provides a relevant model to study reproductive dysfunction under diabetic conditions, as they exhibit a number of deficits in reproductive function that resemble those seen in humans. The present investigation was designed to delineate the impact of STZ-induced diabetes and insulin replacement on the rat ventral prostateCONTINUE READING Continue reading >>

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

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

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

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