Study on experimental diabetes animal model in rats induced by streptozotocin
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Objective To study the experimental diabetes animal model in rats induced by streptozotocin and explore the difference in different ways. Methods The diabetic model of Wistar rats was duplicated with streptozotocin once introperitoneally or intratailvenously. The blood glucose and plasma insulin levels were detected. Results Blood glucose levels in streptozotocin groups were increased significantly as compared with control group (P 0. 01). Plasma insulin levels in streptozotocin groups were decreased significantly as compared with control group (P0. 01), while there was no significant difference between different ways(P0. 05). Conclusion The diabetic model of Wistar rats could be duplicated with streptozotocin once intrapertoneally or intratailvenously,while there was no significant difference between two ways.Keywords:
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Objective To explore the mechanism of diabetes of rats induced by streptozotocin(STZ).Methods The diabetic model of Wistar rats was duplicated with STZ once intraperitoneally.The changes of blood sugar and urine sugar were monitored.The tissue sections of pancreas were stained by HE and immunohistochemistry.Results 48 hours after injection,blood sugar exceeds the diabetes standard and diabetic symptoms appeared gradually in the rats.Morphological investigation on pancreas showed the reduction of islets,loss of β cells, nuclear pyknosis of β cells to varying degrees after 1,3,6 months injection of STZ.In DM6 group,there was yet fiber proliferation of pancreas.Conclusion β cells damaging is the mechanism of diabetes in rats induced by STZ.
Blood sugar
Intraperitoneal injection
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Objective To establish an ideal type 1 diabetes mellitus SD rats model.Methods SD rats were injected intraperitoneally with 65 mg/kg streptozotocin once to induce hyperglycemia.Results One week after induced by streptozotocin(STZ),the blood glucose of the experimental group were higher than 16.7 mmol/L.During the 8 weeks observation,the blood glucose of the experimental group were stably higher than 16.7 mmol/L.Morphological investigation on pancreas showed the reduction of islets, loss of β cells in the experimental group.Conclusion The experiment provided an ideal type 1 diabetes mellitus SD rats model.
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Pancreatic Islets
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Objective To establisk approriate method of diabetes rats model.Methods to establish type 1 diabetic rats model an animal Eight-week-old male Sprague-Dawley rats were intraperitionedl injected by a streptozotocin.Results Three days after injetion,the blood glucose of diabetes group were higher than 16.7 mmol/L.During the 8 weeks observation,the blood glucose values are always in the early hyperglycemia level fluctuation.Morphological investigation on pancreas showed the reduction of islets,loss of B cells in diabetes group.Conclusion The present experiment provided a type 1 diabetes rat model.
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Abstract Background This investigation is concentrated on how hematological and serum biochemical markers would change in streptozotocin-induced Insulin-Dependent diabetes mellitus(IDDM) in male adult wistar rats. Hematological parameters, serum protein electrophoresis parameters and hepatic transaminases level (SGOT-SGPT) were all measured in both control group rats (N=6) and diabetic group rats (N=6) and comparison between two groups was performed. Material and Method Single dose intraperitoneal injection of 60 mg/kg dose of streptozotocin(STZ) in male adult wistar rats, induces extensive necrosis in langerhans β-cell islets, because of its cytotoxicity. Experimental diabetes mellitus can be induced completely in less than 72 hours after STZ intraperitoneal injection. Streptozotocin(STZ) was purchased from Sigma company. Diabetic and control group rats were kept separately in different metabolic cages, and their blood glucose(BG), hematological parameters, serum protein electrophoretic pattern and hepatic transaminases level were analyzed and comparison was done. Results In our investigation, Insulin-Dependent Diabetes Mellitus(IDDM) was completely induced one week after single intraperitoneal injection of 60 mg/kg BW. Diabetes mellitus induction was verified by measuring fasting plasma glucose level in blood samples of rats. Level of blood glucose, hematological parameters, serum protein electrophoretic pattern and hepatic transaminase enzymes level, were all measured. In diabetic group rats level of blood glucose (BG), hepatic transaminase enzymes (SGOT & SGPT), serum α1-globulin and β-globulin were significantly increased but in albumin, albumin/globulin ratio (A/G ratio) and serum α2-globulin a significant decrease was observed in diabetic rats in comparison with normal rats. Conclusion Extensive inflammation and tissue necrosis induced following diabetes mellitus induction in rats. Significant alterations were observed in serum protein electrophoresis fractions and hepatic transaminase enzymes level due to streptozotocin cytotoxic impacts on some tissues specifically liver. Because of extensive β-cells necrosis and degeneration caused by streptozotocin exposure, high level of blood glucose(diabetic hyperglycemia) was observed in diabetic rats. This type of experimentally induced diabetes mellitus would highly affect hematological parameters. Insulin-Dependent Diabetes Mellitus induced by streptozotocin, can lead to anemia, neutrophilia and lymphocytosis and also has decreasing effects on red blood cell indices (HGB, MCV, MCH, MCHC) in diabetic group rats.
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Objective To explore an ideal establishment method of the diabetic animal model for studying the influence of diabetes mellitus on oral diseases.Methods Fifty Wistar rats were randomly divided into two groups:experimental group(n=40)and control group(n=10).Forty Wistar rats in experimental group were intravenously injected with streptozotocin(STZ)of 30 mg/kg once a week for four weeks to establish the diabetic model.The changes of blood sugar,urine sugar and histological damage were observed.Results The histological changes showed the delayed islet damage and autoimmune islet inflammation in experimental group.The urine sugar and blood sugar were significantly higher in experimental group than in control group(P0.05).Conclusion Diabetes mellitus(DM)animal model induced by intravenously injecting multiple low-dose of STZ can be used for studying oral diseases in patieats with diabetes and diabetes-related diseases.
Blood sugar
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Autoimmune diabetes
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Background: Diabetes mellitus is known to cause cognitive impairment that can be possibly attributed to deficient levels of leptin in diabetic animals. This study was undertaken to study the effect of administration of leptin on spatial learning, memory and blood glucose levels in diabetic rats.Methods: Rats were divided into three groups. The first group was the control group. Diabetes was induced in groups 2 and 3 by streptozotocin (STZ) injection (60 mg/kg) intraperitoneally. Group 2 received saline while group 3 received leptin (0.1 mg/kg) subcutaneously for 10 days from 4th day of STZ administration. Behavioural assessment was done in T maze after 21 days of the last injection of leptin. Blood glucose levels were also analysed.Results: The number of correct arm entries decreased while time spent being immobile and time spent to reach the correct arm increased in the diabetic group when compared to the control group and correct arm entries increased while time spent immobile and time spent to reach the correct arm decreased with leptin treatment when compared to the diabetic control rats. Blood glucose levels increased in the diabetic rats while leptin administration reduced blood glucose levels in the group 3.Conclusions: Our study suggests that leptin can improve learning and memory while also producing a slight reduction in the blood glucose levels in diabetic rats.
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To evaluate the effect of telmisartan on blood glucose levels and blood lipid levels in streptozotocin induced diabetic rats. Eighteen Wistar albino rats weighing 150-200gms of either sex were randomly selected from the central animal facility, and divided into 3 groups. Diabetes was induced by injecting Streptozotocin intraperitonelly. The control group received 1% Gum acacia (oral), standard group received 0.5 mg/kg Glibenclamide (oral) and the test group received Telmisartan 7.2mg/kg body weight (oral) from 0-28 days respectively. Body weight of the individual rats were measured on the respective days before blood glucose estimation on 0, 1, 3, 7, 14, 21 & 28th day and fasting blood glucose was estimated by (ACCUCHECK) glucometer. Estimation of fasting lipid profile by lipid screening strips on 1st and 28th day. When compared to control the capillary blood glucose (CBG) levels in the Telmisartan group was less at all the intervals but comparable with that of standard drug Glibenclamide in Streptozotocin induced diabetic rats. Improved lipid profile was seen with the Telmisartan group when compared to control group in Streptozotocin induced diabetic rats. Hypoglycemic activity and improved lipid profile action was seen with Telmisartan group which is comparable to standard drug glibenclamide in streptozotocin induced diabetic albino rats.
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The present study was conducted to see the effect of probucol on Streptozotocin diabetes in rats. After 2 weeks of a 1% probucol diet, 35 or 50 mg/kg of Streptozotocin were intravenously injected into male Wistar rats. All the rats became diabetic 2 days after treatment. Thereafter, in order to see the effect of probucol on spontaneous recovery from Streptozotocin diabetes, 25 mg/kg of Streptozotocin was injected into rats after two weeks of probucol diet and the diet was continued for additional two weeks. All the rats with a standard diet (group CS, n = 13) and 12 of 13 rats with probucol diet (group PS) became diabetic 2 days after Streptozotocin injection. One rat from group PS did not develop diabetes. Two weeks after injection, only 4 of 13 rats in groups CS showed recovery, while 11 of 12 rats in group PS showed recovery from Streptozotocin diabetes (p < 0.05). The average blood glucose levels in group PS were significantly lower than group CS (10.5±4.6 vs 18.5±0.6 mM, p < 0.05). In addition, the pancreatic insulin content of group PS was 8 times greater than that of group CS (0.75±0.24 vs 0.09±0.03 mmol/pancreas, p < 0.01). Thus, the in vivo diabetogenic action of Streptozotocin could not be reduced by pretreatment with probucol. However, recovery from Streptozotocin diabetes was induced by subsequent treatment with probucol. The precise mechanisms for this phenomenon were not known; but the present findings suggest the protective effect of probucol on β-cell damage induced by small dose of Streptozotocin.
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