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Streptozotocin-diabetic Rats (streptozotocin-diabetic + rat)
Selected AbstractsGREEN TEA EXTRACT IMPEDES DYSLIPIDAEMIA AND DEVELOPMENT OF CARDIAC DYSFUNCTION IN STREPTOZOTOCIN-DIABETIC RATSCLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 12 2006PV Anandh Babu SUMMARY 1The efficacy of green tea extract (GTE) on serum and cardiac lipids was investigated in streptozotocin (STZ)-diabetic rats. 2Diabetes was induced in rats by a single intraperitoneal injection of STZ (60 mg/kg bodyweight). Six weeks after the induction of diabetes, GTE was administered orally for 4 weeks (300 mg/kg bodyweight daily). Bodyweight, heart weight, heart weight : bodyweight ratio, blood glucose, serum and cardiac lipids were determined in experimental rats. 3In diabetic rats, there was a significant decrease in bodyweight with an increase in heart weight : bodyweight ratio and blood glucose. Diabetic rats had significantly increased serum levels of cholesterol, triglycerides, free fatty acids and low-density lipoprotein,cholesterol (LDL-C) and decreased levels of high-density lipoprotein,cholesterol (HDL-C). In the hearts of diabetic rats, there was a significant increase in cholesterol, triglycerides and free fatty acids levels, with an increase in lipoprotein lipase activity. 4The administration of GTE to diabetic rats resulted in significant recovery in bodyweight, heart weight : bodyweight ratio and blood glucose levels. The administration of GTE reduced cholesterol, triglyceride, free fatty acid and LDL-C levels, and increased HDL-C levels, in the serum of diabetic rats. In addition, GTE decreased cholesterol, triglyceride, free fatty acids levels and lipoprotein lipase activity in the myocardium of diabetic rats. These beneficial effects of GTE are ascribed to its antihyperglycaemic and hypolipidaemic activity. In conclusion, green tea can reduce the risk of cardiovascular disease in diabetes with a significant improvement in lipid metabolism. [source] DOSE-DEPENDENT EFFECT OF CAPTOPRIL ON AORTIC REACTIVITY OF STREPTOZOTOCIN-DIABETIC RATSCLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 5-6 2004Tourandokht Baluchnejadmojarad Summary 1.,Diabetes mellitus is a primary risk factor for cardiovascular disorders. Strategies that interrupt the renin,angiotensin system have been known to reduce cardiovascular disease. The present study was performed to investigate the effect of sub-chronic administration of captopril on the aortic reactivity of streptozotocin-diabetic rats. 2.,Streptozotocin-diabetic rats received captopril (30 and 50 mg/kg per day) for 2 months. Contractile responses to phenylephrine (PE) and relaxation responses to acetylcholine (ACh) and isosorbide dinitrate (ISD) were obtained from aortic rings. 3.,Concentration,response curves from captopril-treated diabetic rats to PE were attenuated compared with vehicle (Saline)-treated diabetic rats, especially at a dose of 50 mg/kg captopril. In addition, endothelium-dependent relaxation responses induced by ACh were significantly higher in captopril-treated diabetic rats compared with diabetic rats. The endothelium-independent relaxation responses for ISD were found not to be significantly different among the groups. 4.,Therefore, sub-chronic treatment of diabetic rats with captopril in a dose-dependent manner could prevent the functional changes in vascular reactivity in diabetic rats. [source] Morphometric and Quantitative Evaluation of the NADH-Diaphorase Positive Myenteric Neurons of the Jejunum of Streptozotocin-Diabetic Rats Supplemented with Acetyl-L-CarnitineANATOMIA, HISTOLOGIA, EMBRYOLOGIA, Issue 3 2005M. H. de Miranda Neto Summary In this study we investigated the effect of the acetyl-L-carnitine (ALC) supplementation on the myenteric neurons of the jejunum of rats made diabetic at the age of 105 days by streptozotocin (35 mg/kg body weight). Four groups were used: non-diabetic (C), non-diabetic supplemented with ALC (CC), diabetic (D), diabetic supplemented with ALC (DC). After 15 weeks of diabetes induction the blood was collected by cardiac puncture to evaluate glycaemia and glycated haemoglobin. Next the animals were killed and the jejunum was collected and subjected to whole-mount preparation to evidence the myenteric neurons through the histochemical technique of the NADH-diaphorase. The neuronal counts were made in 80 microscopic fields, in tissue samples of five animals of each group. The profiles of the cell bodies of 1000 neurons per group were analysed. Diabetes induced a significant increase in the area of the cell body and decrease in the number of NADH-diaphorase positive myoenteric neurons. ALC suplementation to the diabetic group promoted smaller hypertrophic effects and less neuronal loss than in the myoenteric neurons of the diabetic rats, and in addition diminished the body weight decrease and reduced the fasting glycaemia. [source] Occurrence of oxidative impairments, response of antioxidant defences and associated biochemical perturbations in male reproductive milieu in the Streptozotocin-diabetic ratINTERNATIONAL JOURNAL OF ANDROLOGY, Issue 6 2007B. Shrilatha Summary Oxidative stress is implicated to play a vital role in the pathogenesis of various diabetic complications. While reproductive dysfunction is a well recognized consequence of diabetes mellitus, the underlying mechanisms are poorly understood. The present study aims to obtain insights into the incidence, extent and progression of oxidative impairments in testis and epididymal sperm (ES) in streptozotocin (STZ)-induced diabetic rat during early and progressive phase. Adult rats (CFT-Wistar strain) rendered diabetic by an acute dose of STZ (60 mg/kg bw, i.p.) were examined for induction of hyperglycaemia at 72 h, followed by the assessment of oxidative impairments in testis and ES over a 6-week period. Oxidative damage was ascertained by measuring the malondialdehyde levels, reactive oxygen species (ROS) generation, alterations in antioxidant defences and extent of protein oxidation. STZ induced a significant (2.5-fold) increase in blood glucose levels. In diabetic rats, both testis and ES showed enhanced status of lipid peroxidation measured as increased TBARS and ROS from week 2 onwards. These impairments in testis were consistent, progressive and accompanied by marked alterations in antioxidant defences and elevated protein carbonyls. Varying degree of reduction in the specific activities of antioxidant enzymes was evident in testis and ES, while the activity of glutathione- S -transferase (GST) was significantly elevated. Reduced glutathione (GSH) and vitamin E levels were consistently reduced in testis. Lipid dysmetabolism measured in terms of increased cholesterol, triglycerides and phospholipids was evident only beyond week 2 in diabetic testis. Taken together, these results indicate that the testis and ES are indeed subjected to significant oxidative stress in the STZ-diabetic rat both during early as well as progressive phase. It is hypothesized that oxidative impairments in testis which develop over time may at least in part contribute towards the development of testicular dysfunction eventually leading to testicular degeneration which culminates in reduced fertility during the progressive phase of STZ-induced diabetes in adult rats. [source] A Sonic Hedgehog (SH) Fusion Protein Corrects Multifocal Defects In Experimental Diabetic NeuropathyJOURNAL OF THE PERIPHERAL NERVOUS SYSTEM, Issue 3 2000Dr Tomlinson Diabetic neuropathy develops from defective interactions between nerve axons and other cells in the endoneurium; such interactions are influenced in development by hedgehog proteins. This study explored the possibility that this might be maintained in the adult and form a basis for therapy in diabetic neuropathies. Streptozotocin-diabetic rats were treated (final 5 weeks of 10 weeks diabetes) with a SH-IgG fusion protein (either 0.3mg/kg or 3.0mg/kg s.c. 3 times per week); control diabetic and non-diabetic rats received vehicle. Conduction velocity (MNCV, SNCV) data and sciatic nerve levels of nerve growth factor (NGF) and neuropeptide Y (NPY) are presented below. Diabetes caused significant (p < 0.05 by ANOVA with SNK tests) reductions in all variables and treatment with SH-IgG either attenuated or prevented (p < 0.05) these reductions. Since it is well-established that the conduction deficits are unrelated to neurotrophic deficits (NGF depletion) and that NPY depletion derives from a neurotrophic defect distinct from NGF, this treatment clearly acts at multiple components of the aetiology of diabetic neuropathy. [source] DOSE-DEPENDENT EFFECT OF CAPTOPRIL ON AORTIC REACTIVITY OF STREPTOZOTOCIN-DIABETIC RATSCLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 5-6 2004Tourandokht Baluchnejadmojarad Summary 1.,Diabetes mellitus is a primary risk factor for cardiovascular disorders. Strategies that interrupt the renin,angiotensin system have been known to reduce cardiovascular disease. The present study was performed to investigate the effect of sub-chronic administration of captopril on the aortic reactivity of streptozotocin-diabetic rats. 2.,Streptozotocin-diabetic rats received captopril (30 and 50 mg/kg per day) for 2 months. Contractile responses to phenylephrine (PE) and relaxation responses to acetylcholine (ACh) and isosorbide dinitrate (ISD) were obtained from aortic rings. 3.,Concentration,response curves from captopril-treated diabetic rats to PE were attenuated compared with vehicle (Saline)-treated diabetic rats, especially at a dose of 50 mg/kg captopril. In addition, endothelium-dependent relaxation responses induced by ACh were significantly higher in captopril-treated diabetic rats compared with diabetic rats. The endothelium-independent relaxation responses for ISD were found not to be significantly different among the groups. 4.,Therefore, sub-chronic treatment of diabetic rats with captopril in a dose-dependent manner could prevent the functional changes in vascular reactivity in diabetic rats. [source] Leptin and endothelin-1 mediated increased extracellular matrix protein production and cardiomyocyte hypertrophy in diabetic heart diseaseDIABETES/METABOLISM: RESEARCH AND REVIEWS, Issue 5 2009Pijush Majumdar Abstract Background We investigated the role of leptin and its interaction with endothelin 1 (ET-1) in fibronectin (FN) synthesis and cardiomyocyte hypertrophy, two characteristic features of diabetic cardiomyopathy. Methods Endothelial cells [human umbilical vein endothelial cells (HUVECs)] were examined for FN production and neonatal rat cardiomyocytes for hypertrophy, following incubation with glucose, ET-1, leptin and specific blockers. FN, ET-1, leptin and leptin receptors mRNA expression and FN protein were measured. Myocytes were also morphometrically examined. Furthermore, hearts from streptozotocin-diabetic rats were analysed. Results Glucose caused increased FN mRNA and protein expression in HUVECs and cardiomyocytes hypertrophy along with upregulation of ET-1 mRNA, leptin mRNA and protein. Glucosemimetic effects were seen with leptin and ET-1. Leptin receptor antagonist (leptin quadruple mutant) and dual endothelin A endothelin B (ETA/ETB) receptor blocker bosentan normalized such abnormalities. Hearts from the diabetic animals showed hypertrophy and similar mRNA changes. Conclusion These data indicate that in diabetes increased FN production and cardiomyocyte hypertrophy may be mediated through leptin with its interaction with ET-1. Copyright © 2009 John Wiley & Sons, Ltd. [source] Antihyperlipidemic activity of 3-hydroxymethyl xylitol, a novel antidiabetic compound isolated from Casearia esculenta (Roxb.) root, in streptozotocin-diabetic ratsJOURNAL OF BIOCHEMICAL AND MOLECULAR TOXICOLOGY, Issue 2 2010Govindasamy Chandramohan Abstract Casearia esculenta root (Roxb.) is widely used in traditional system of medicine to treat diabetes in India. An active compound, 3-hydroxymethyl xylitol (3-HMX), has been isolated, and its optimum dose has been determined in a short duration study and patented. In addition, the long-term effect of 3-HMX in type 2 diabetic rats on carbohydrate metabolism was investigated, and its antihyperglycemic effect was shown previously (Chandramohan et al., Eur J Pharmacol 2008;590:437,443). In this study we investigated the effect of 3-HMX on plasma and tissue lipid profiles in streptozotocin-induced diabetic rats. Diabetes was induced in adult male albino rats of the Wistar strain, weighing 180,200 g, by administration of streptozotocin (40 mg/kg of body weight) intraperitoneally. The normal and diabetic rats were treated with 3-HMX (40 mg/kg BW/day) for 45 days. The levels of total cholesterol, triglycerides, free fatty acids, and phospholipids were assayed in the plasma besides lipoprotein-cholesterol (high-density lipoprotein-cholesterol (HDL-C), low-density lipoprotein-cholesterol (LDL-C), and very low density lipoprotein-cholesterol (VLDL-C)) and tissues (liver, kidney, heart, and brain). Total cholesterol, triglyceride, free fatty acid, and phospholipid (LDL-C and VLDL-C in plasma only) levels increased in plasma and tissues significantly, whereas plasma HDL-C significantly decreased in diabetic rats. Treatment with 3-HMX or glibenclamide reversed the above-mentioned changes and improved toward normalcy. Histological study of liver also confirmed the biochemical findings. Thus administration of 3-HMX is able to reduce hyperglycemia and hyperlipidemia related to the risk of diabetes mellitus. © 2010 Wiley Periodicals, Inc. J Biochem Mol Toxicol 24:95,101, 2010; Published online in Wiley InterScience (www.interscience.wiley.com). DOI 10.1002/jbt.20317 [source] Correction of protein kinase C activity and macrophage migration in peripheral nerve by pioglitazone, peroxisome proliferator activated-,-ligand, in insulin-deficient diabetic ratsJOURNAL OF NEUROCHEMISTRY, Issue 2 2008Shin-Ichiro Yamagishi Abstract Pioglitazone, one of thiazolidinediones, a peroxisome proliferator-activated receptor (PPAR)-, ligand, is known to have beneficial effects on macrovascular complications in diabetes, but the effect on diabetic neuropathy is not well addressed. We demonstrated the expression of PPAR-, in Schwann cells and vascular walls in peripheral nerve and then evaluated the effect of pioglitazone treatment for 12 weeks (10 mg/kg/day, orally) on neuropathy in streptozotocin-diabetic rats. At end, pioglitazone treatment improved nerve conduction delay in diabetic rats without affecting the expression of PPAR-,. Diabetic rats showed suppressed protein kinase C (PKC) activity of endoneurial membrane fraction with decreased expression of PKC-,. These alterations were normalized in the treated group. Enhanced expression of phosphorylated extracellular signal-regulated kinase detected in diabetic rats was inhibited by the treatment. Increased numbers of macrophages positive for ED-1 and 8-hydroxydeoxyguanosine-positive Schwann cells in diabetic rats were also corrected by the treatment. Pioglitazone lowered blood lipid levels of diabetic rats, but blood glucose and nerve sorbitol levels were not affected by the treatment. In conclusion, our study showed that pioglitazone was beneficial for experimental diabetic neuropathy via correction of impaired PKC pathway and proinflammatory process, independent of polyol pathway. [source] Early, Selective, and Marked Loss of Sympathetic Nerves from the Islets of Biobreeder Diabetic RatsJOURNAL OF THE PERIPHERAL NERVOUS SYSTEM, Issue 2 2003Q Mei To discover whether islet sympathetic nerves are damaged during the autoimmune destruction of islet B-cells, we immunostained sections of pancreas from Bio-Breeder (BB) diabetic rats, using antibodies against vesicular monoamine transporter 2 (VMAT2), a marker of sympathetic nerve terminals. We found a marked decrease in the VMAT2-positive fiber area in the islets of BB rats that had been diabetic for only 1,2 weeks compared with their nondiabetic controls. In contrast, there was no significant decrease in the VMAT2-positive fiber area in the exocrine pancreas in these early diabetic BB rats. Furthermore, streptozotocin-diabetic rats showed no decrease in VMAT2-positive fiber area in their islets compared with controls. The classical diabetic autonomic neuropathy (DAN) that eventually occurs in the heart was not present in BB diabetic rats at this early stage as evidenced by normal cardiac VMAT2 immunostaining and normal cardiac norepinephrine content. Also, in contrast to DAN, this islet neuropathy did not worsen with duration of diabetes. These data provide evidence of a heretofore unrecognized early sympathetic islet neuropathy (eSIN). Because eSIN occurs selectively in the islet, is rapid in onset, and is associated with autoimmune but not chemically induced diabetes, it is distinct from DAN in location, time course, and mechanism. [source] The effects of chard,(Beta vulgaris L. var. cicla) extract on the kidney tissue, serum urea and Creatinine levels of diabetic ratsPHYTOTHERAPY RESEARCH, Issue 8 2002R. Yanarda Abstract The aim of this work was to investigate the effects of chard (Beta vulgaris L. var. cicla) extract on serum urea and creatinine concentrations and on kidney tissue in normal and streptozotocin-diabetic rats. The extract was administered to rats at a dose of 2,g/kg every day for 28 days, 14 days after animals were made diabetic. On day 42, kidney tissue and blood samples were examined. Significant degenerative changes in kidney tissue of diabetic rats were observed, but in the group given chard extract, the morphology of kidney tissue was found to be nearly the same as the controls. Serum urea and creatinine levels significantly increased in the diabetic groups, but the chard extracts significantly reduced serum urea and creatinine levels. It is concluded that the extract of this plant may reduce serum urea and creatinine levels and confer a protective effect on the kidney of diabetic rats. Copyright © 2002 John Wiley & Sons, Ltd. [source] Induction of Indoleamine 2,3-Dioxygenase by Gene Delivery in Allogeneic Islets Prolongs Allograft SurvivalAMERICAN JOURNAL OF TRANSPLANTATION, Issue 8 2010H. Dellê Indoleamine 2,3-dioxygenase (IDO), an enzyme that plays a critical role in fetomaternal tolerance, exerts immunoregulatory functions suppressing T-cell responses. The aims of this study were to promote IDO expression in rat islets using a nonviral gene transfer approach, and to analyze the effect of the in vivo induction of IDO in a model of allogeneic islet transplantation. The IDO cDNA was isolated from rat placenta, subcloned into a plasmid and transfected into rat islets using Lipofectamine. The efficiency of transfection was confirmed by qRT-PCR and functional analysis. The in vivo effect of IDO expression was analyzed in streptozotocin-induced diabetic Lewis rats transplanted with allogeneic islets under the renal capsule. Transplantation of IDO-allogeneic islets reversed diabetes and maintained metabolic control, in contrast to transplantation of allogeneic nontransfected islets, which failed shortly after transplantation in all animals. Graft survival of allograft islets transfected with IDO transplanted without any immunosuppression was superior to that observed in diabetic rats receiving nontransfected islets. These data demonstrated that IDO expression induced in islets by lipofection improved metabolic control of streptozotocin-diabetic rats and prolonged allograft survival. [source] The effect of sorbinil, an aldose reductase inhibitor, on aortic function in control and streptozotocin-induced diabetic ratsAUTONOMIC & AUTACOID PHARMACOLOGY, Issue 1 2000D. J. Sellers 1 The present study investigates the effect of treatment of 14-day streptozotocin-diabetic rats with the aldose reductase inhibitor, sorbinil, on changes ex vivo in aortic vasoconstriction and vasodilation. 2 Maximum contractile responses and aortic sensitivity to phenylephrine were significantly enhanced in aortae from 14-day diabetic rats, in accordance with our previous data. 3 Endothelium-dependent relaxations to carbachol were, in contrast, depressed, although endothelium-independent relaxations to forskolin and sodium nitroprusside were unaltered. 4 Sorbinil treatment of diabetic animals failed to prevent any of these diabetes-induced alterations in aortic function, and indeed exacerbated some of these alterations. In addition, sorbinil treatment caused altered aortic responses in control animals, which sometimes mirrored those found in diabetic animals. 5 It can be concluded that sorbinil may have actions in addition to, and independent of, polyol pathway inhibition. Thus, sorbinil may not be an effective tool for the investigation of aldose reductase inhibition within the vascular system of the rat. [source] Effects of antioxidant stobadine on protein carbonylation, advanced oxidation protein products and reductive capacity of liver in streptozotocin-diabetic rats: Role of oxidative/nitrosative stressBIOFACTORS, Issue 3 2007Ahmet Cumao Background: Increased oxidative/nitrosative stress is important in the pathogenesis of diabetic complications, and the protective effects of antioxidants are a topic of intense research. The purpose of this study was to investigate whether a pyridoindole antioxidant stobadine (STB) have a protective effect on tissue oxidative protein damage represented by the parameters such as protein carbonylation (PC), protein thiol (P-SH), total thiol (T-SH) and non-protein thiol (Np-SH), nitrotyrosine (3-NT), and advanced oxidation protein products (AOPP) in streptozotocin-diabetic rats. Methods: Diabetes was induced in male Wistar rats by intraperitonal injection of streptozotocin (55 mg/kg). Some of the non-diabetic (control) and diabetic rats treated with STB (24.7 mg/kg/day) during 16 weeks, and the effects on blood glucose, PC, AOPP, 3-NT, P-SH, T-SH and Np-SH were studied. Biomarkers were assayed by enzyme-linked immunosorbent assay (ELISA) or by colorimetric methods. Results: Administration of stobadine to diabetic animals lowered elevated blood glucose levels by ,16% relative to untreated diabetic rats. Although stobadine decreased blood glucose, poor glycemic control was maintained in stobadine treated diabetic rats during the treatment period. Biochemical analyses of liver proteins showed significant diminution of sulfhydryl groups, P-SH, T-SH, Np-SH, and elevation of carbonyl groups in diabetic animals in comparison to healthy controls. As a biomarker of nitrosative stress, 3-NT levels did not significantly change by diabetes induction or by stobadine treatment when compared to control animals. However, the treatment with stobadine resulted in a significant decrease in PC, AOPP levels and normalized P-SH, T-SH, Np-SH groups in liver of diabetic animals. [source] DOSE-DEPENDENT EFFECT OF CAPTOPRIL ON AORTIC REACTIVITY OF STREPTOZOTOCIN-DIABETIC RATSCLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 5-6 2004Tourandokht Baluchnejadmojarad Summary 1.,Diabetes mellitus is a primary risk factor for cardiovascular disorders. Strategies that interrupt the renin,angiotensin system have been known to reduce cardiovascular disease. The present study was performed to investigate the effect of sub-chronic administration of captopril on the aortic reactivity of streptozotocin-diabetic rats. 2.,Streptozotocin-diabetic rats received captopril (30 and 50 mg/kg per day) for 2 months. Contractile responses to phenylephrine (PE) and relaxation responses to acetylcholine (ACh) and isosorbide dinitrate (ISD) were obtained from aortic rings. 3.,Concentration,response curves from captopril-treated diabetic rats to PE were attenuated compared with vehicle (Saline)-treated diabetic rats, especially at a dose of 50 mg/kg captopril. In addition, endothelium-dependent relaxation responses induced by ACh were significantly higher in captopril-treated diabetic rats compared with diabetic rats. The endothelium-independent relaxation responses for ISD were found not to be significantly different among the groups. 4.,Therefore, sub-chronic treatment of diabetic rats with captopril in a dose-dependent manner could prevent the functional changes in vascular reactivity in diabetic rats. [source] | |||||||||||||