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Diabetes Induction (diabetes + induction)
Selected AbstractsIn vivo astaxanthin treatment partially prevents antioxidant alterations in dental pulp from alloxan-induced diabetic ratsINTERNATIONAL ENDODONTIC JOURNAL, Issue 11 2010M. F. Leite Leite MF, de Lima A, Massuyama MM, Otton R.In vivo astaxanthin treatment partially prevents antioxidant alterations in dental pulp from alloxan-induced diabetic rats. International Endodontic Journal, 43, 959,967, 2010. Abstract Aim, To evaluate the effect of astaxanthin on antioxidant parameters of dental pulp from diabetic rats. The hypothesis tested was that supplementation of diabetic rats with astaxanthin might eliminate, or at least attenuate, the defect in their antioxidative status. Methodology, Wistar rats (n = 32) were divided into four groups: untreated control, treated control, untreated diabetic and treated diabetic rats. A prophylactic dose of astaxanthin (20 mg kg,1 body weight) was administered daily by gavage for 30 days. On day 23, diabetes was induced by injection of alloxan (60 mg kg,1 body weight). After 7 days of diabetes induction, the rats were killed, and pulp tissue from incisor teeth removed. Superoxide dismutase (SOD), catalase, glutathione peroxidase (GPx) and reductase activities were determined. Data were compared by anova and the Newman,Keuls test (P < 0.05). Results, Diabetes caused a reduction in SOD, GPx and reductase activity in dental pulp tissue. Astaxanthin had no effect on SOD and catalase activities; however, it stimulated GPx in control and diabetic rats. Conclusions, Diabetes altered the antioxidant system in dental pulp tissue; astaxanthin partially improved the diabetic complications. [source] External urethral sphincter activity in diabetic ratsNEUROUROLOGY AND URODYNAMICS, Issue 5 2008Guiming Liu Abstract Aim To examine the temporal effects of diabetes on the bladder and the external urethral sphincter (EUS) activity in rats. Methods Female Sprague-Dawley rats (n,=,24) were divided into two groups: streptozotocin-induced diabetic rats and age-matched controls. Cystometrograms (CMGs) were taken under urethane anesthesia and electromyograms (EMG) of the EUS were evaluated in all rats at 6 and 20 weeks after diabetes induction. After EMG assessment, the tissues of the urethra were harvested for morphological examination. Results Diabetes caused reduction of body weight, but an increase in bladder weight. CMG measurements showed diabetes increased threshold volume, contraction duration, high-frequency oscillations (HFO), and residual volume. Peak contraction amplitude increased in 6-week but not 20-week diabetic rats. EUS-EMG measurements showed increased frequency of EUS-EMG bursting discharge during voiding in 6-week diabetic rats (8.1,±,0.2 vs. 6.9,±,0.6/sec) but not in 20-week (5.8,±,0.3 vs. 6.0,±,0.2/sec) diabetic rats compared with controls. EUS-EMG bursting periods were also increased in both 6-week and 20-week diabetic rats compared with controls. EUS-EMG silent periods were reduced in 6-week diabetic rats, but were not changed in 20-week diabetic rats compared with controls. Active periods did not change in 20-week diabetic rats, but increased in 6-week diabetic rats compared with controls. Morphometric analysis showed atrophy of the EUS after 20 week but not 6 weeks of DM induction. Conclusions Our data indicates diabetes causes functional and anatomical abnormalities of the EUS. These abnormalities may contribute to the time-dependent bladder dysfunction in diabetic rats. Neurourol. Urodynam. 27:429,434, 2008. © 2008 Wiley-Liss, Inc. [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] 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] Novel role of curcumin in the prevention of cytokine-induced islet death in vitro and diabetogenesis in vivoBRITISH JOURNAL OF PHARMACOLOGY, Issue 5 2008M Kanitkar Background and purpose: Oxidative stress caused by cytokine exposure is a major cause of pancreatic islet death in vitro and of diabetogenesis. Antioxidant compounds may prevent cytokine-induced damage to islet cells. Hence, we studied the potential of curcumin, an antioxidant and anti-inflammatory compound, in vitro to protect islets against pro-inflammatory cytokines and in vivo to prevent the progression of diabetes induced by multiple low doses of streptozotocin (MLD-STZ). Experimental approach: Pancreatic islets from C57/BL6J mice were pretreated with curcumin (10 ,M) and then exposed to a combination of cytokines. Islet viability, reactive oxygen species (ROS), NO, inducible NO synthase and NF-,B translocation were studied. Curcumin pretreated (7.5 mg kg,1 day,1) C57/BL6J mice were given MLD-STZ (40 mg kg,1), and various parameters of diabetes induction and progression were monitored. Key results: Curcumin protected islets from cytokine-induced islet death in vitro by scavenging ROS and normalized cytokine-induced NF-,B translocation by inhibiting phosphorylation of inhibitor of kappa B alpha (I,B,). In vivo, curcumin also prevented MLD-STZ, as revealed by sustained normoglycaemia, normal glucose clearance and maintained pancreatic GLUT2 levels. Pro-inflammatory cytokine concentrations in the serum and pancreas were raised in STZ-treated animals, but not in animals pretreated with curcumin before STZ. Conclusions and implications: Here, we have demonstrated for the first time that curcumin in vitro protects pancreatic islets against cytokine-induced death and dysfunction and in vivo prevents STZ-induced diabetes. British Journal of Pharmacology (2008) 155, 702,713; doi:10.1038/bjp.2008.311; published online 11 August 2008 [source] Alteration of Ca2+ -ATPase activity in the homogenate, plasma membrane and microsomes of the salivary glands of streptozotocin-induced diabetic ratsCELL BIOCHEMISTRY AND FUNCTION, Issue 3 2009José Nicolau Abstract Diabetes has been implicated in the dryness of the mouth, loss of taste sensation, sialosis, and other disorders of the oral cavity, by impairment of the salivary glands. The aim of the present study was to examine the plasma membrane, microsomal, and homogenate Ca2+ -ATPase activity in the rat submandibular and parotid salivary glands of streptozotocin-induced diabetes. We have also examined the influence of the acidosis state on this parameter. Diabetes was induced by an intraperitoneal injection of streptozotocin and acidosis was induced by daily injection of NH4Cl. At 15 and 30 days after diabetes induction, the animals were euthanized and the submandibular and parotid salivary glands were removed and analyzed. Ca2+ -ATPase (total, independent, and dependent) was determined in the homogenate, microsomal, and plasma membranes of the salivary glands of diabetic and control rats. Calcium concentration was also determined in the glands and showed to be higher in the diabetic animals. Ca2+ -ATPase activity was found to be reduced in all cell fractions studied in the diabetic animals compared with control. Similar results were obtained for the submandibular salivary glands of acidotic animals; however in the parotid salivary glands it was found an increase in the enzyme activity. Copyright © 2009 John Wiley & Sons, Ltd. [source] THERAPEUTIC EFFECT OF GREEN TEA EXTRACT ON ADVANCED GLYCATION AND CROSS-LINKING OF COLLAGEN IN THE AORTA OF STREPTOZOTOCIN DIABETIC RATSCLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 4 2006Pon Velayutham Anandh Babu SUMMARY 1The therapeutic effect of green tea extract (GTE) on the aortic collagen content and its characteristics were investigated in streptozotocin diabetic rats. 2Diabetes was induced in rats by a single intra peritoneal injection of streptozotocin (60 mg/kg bodyweight). Six weeks after diabetes induction, GTE was administered orally for four weeks (300 mg/kg bodyweight daily). Systolic blood pressure, blood glucose, anti-oxidant status, collagen content, extent of glycation, collagen linked fluorescence and aortic collagen solubility pattern were determined in experimental rats. 3At the end of the experimental period, there was a significant increase in the systolic blood pressure and blood glucose in diabetic rats. The lipid peroxides increased whereas glutathione and vitamin C levels were decreased in the serum of diabetic rats. The collagen content, extent of glycation, the advanced glycation end products (AGEs) and degree of cross-linking were increased in the aorta of diabetic rats. 4The oral administration of GTE to diabetic rats significantly reduced the systolic blood pressure and blood glucose. The level of lipid peroxides reduced and the content of glutathione and vitamin C increased in the serum of GTE treated diabetic rats. Green tea extract also impede the accumulation of aortic collagen, extent of glycation, formation of AGEs and cross-linking of collagen in diabetic rats. The antihyperglycemic, anti-oxidant and antiglycating effects of GTE ascribed for these beneficial effects. In conclusion, green tea may have therapeutic effect in the treatment of cardiovascular complications characterized by increased AGE accumulation and protein cross-linking associated with diabetes. 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