Relevant bibliographies by topics / Streptozotocin model

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Academic literature on the topic 'Streptozotocin model'

Author: Grafiati
Published: 28 June 2021
Last updated: 8 February 2022

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Journal articles on the topic "Streptozotocin model"

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Skaletskaya, G. N., N. N. Skaletskiy, E. A. Volkova, and V. I. Sevastyanov. "Streptozotocin model of stable diabetes mellitus." Russian Journal of Transplantology and Artificial Organs 20, no. 4 (January 31, 2019): 83–88. http://dx.doi.org/10.15825/1995-1191-2018-4-83-88.

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Aim:to create a model of stable experimental diabetes mellitus (DM) in laboratory rats using streptozotocin (STZ).Materials and methods.The dynamics of changes in glycemia and survival in 60 Wistar rats was determined. STZ at a dosage of 70 mg/kg was administered to these rats in two ways: once and fractionally (within 5 days).Results.After a single injection of the STZ, 6 out of 30 rats (20%) died, in 7 cases (23.3%) a spontaneous reversion of the diabetic status occurred and in 17 animals (56.6%) the DM remained stable throughout the observation period (8 weeks). After the fractional administration of the STZ no mortality was observed. Spontaneous reversal of DM occurred only in 2 of 30 rats (6.6% of cases). In other 28 animals hyperglycemia was stable until the end of the experiment. It is important to note that in all rats with a stable course of DM, the level of glycemia after 2 weeks after the injection of the STZ was at least 20 mmol/l.Conclusion.Fractional intraperitoneal injection of STZ has an obvious advantage compared with a single injection, providing 100% survival and stable course of DM in 93.4%. The main criterion for a stable course of experimental DM is the level of hyperglycemia not less than 20 mmol/l after 2 weeks after intraperitoneal administration of STZ.
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Miao, Ming San, Bo Lin Cheng, and Na Jiang. "Effect of Sophora Japonica Total Flavonoids on Mouse Models of Hyperglycemia and Diabetes Model." Applied Mechanics and Materials 664 (October 2014): 397–401. http://dx.doi.org/10.4028/www.scientific.net/amm.664.397.

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Objective: To investigate the effects of Sophora japonica total flavonoids hyperglycemia and diabetes in mice models. Methods: intraperitoneal injection of epinephrine, intravenous injection of freshly prepared alloxan or intravenous injection of streptozotocin, alloxan build adrenaline or hyperglycemia model streptozotocin diabetic model. Glucose values ​​were selected for each experiment> 11.1mmol / L, with a significantly more drinking, eating, and more urinary symptoms in mice 60, according to blood glucose levels were randomly divided into six groups, namely large, medium and small doses of Sophora japonica total flavonoids group, metformin group, the control group and model group. And were fed the appropriate medication, model group and the control group fed with the same volume of saline solution. Results: Sophora japonica total flavonoids can significantly reduce the adrenaline and alloxan mice with high blood sugar glucose levels, improve liver glycogen content; can significantly reduce the streptozotocin-diabetic mouse model of blood glucose levels and improve hepatic glycogen,can significantly improve the streptozotocin-induced islet cell damage. Conclusion: Sophora japonica total flavonoids mouse model of hyperglycemia and diabetes mellitus have a better hypoglycemic effect of its hypoglycemic effect and promote glycogen synthesis, reduce islet cell damage.
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Malaisse, Willy J., Marie-Hélène Giroix, Dagmar Zähner, Greta Marynissen, Abdullah Sener, and Bernard Portha. "Neonatal streptozotocin injection: A model of glucotoxicity?" Metabolism 40, no. 10 (October 1991): 1101–5. http://dx.doi.org/10.1016/0026-0495(91)90137-l.

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Botolin, Sergiu, and Laura R. McCabe. "Bone Loss and Increased Bone Adiposity in Spontaneous and Pharmacologically Induced Diabetic Mice." Endocrinology 148, no. 1 (January 1, 2007): 198–205. http://dx.doi.org/10.1210/en.2006-1006.

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Insulin-dependent diabetes mellitus (IDDM) is associated with increased risk of osteopenia/osteoporosis in humans. The mechanisms accounting for diabetic bone loss remain unclear. Pharmacologic inducers of IDDM, such as streptozotocin, mimic key aspects of diabetes in rodents, allow analysis at the onset of diabetes, and induce diabetes in genetically modified mice. However, side effects of streptozotocin, unrelated to diabetes, can complicate data interpretation. The nonobese diabetic (NOD) mouse model develops diabetes spontaneously without external influences, negating side effects of inducing agents. Unfortunately, in this model the onset of diabetes is unpredictable, occurs in a minority of male mice, and can only be studied in a single mouse strain. To validate the relevance of the more flexible streptozotocin-induced diabetes model for studying diabetes-associated bone loss, we compared its phenotype to the spontaneously diabetic NOD model. Both models exhibited hyperglycemia and loss of body, fat pad, and muscle weight. Furthermore, these genetically different and distinct models of diabetes induction demonstrated similar bone phenotypes marked by significant trabecular bone loss and increased bone marrow adiposity. Correspondingly, both diabetic models exhibited decreased osteocalcin mRNA and increased adipocyte fatty acid-binding protein 2 mRNA levels in isolated tibias and calvaria. Taken together, multiple streptozotocin injection-induced diabetes is a valid model for understanding the acute and chronic pathophysiologic responses to diabetes and their mechanisms in bone.
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GAO, Yu, Jin-hui WU, and Lin LIU. "Streptozotocin-induced early diabetic retinopathy model in rats." Academic Journal of Second Military Medical University 30, no. 10 (December 1, 2010): 1053–59. http://dx.doi.org/10.3724/sp.j.1008.2010.01053.

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Mahata, Liganda Endo, Hirowati Ali, and Arina Widya Murni. "Effect of Streptozotocin on Liver Histology Damage in Rats Model of Gestational Diabetes Mellitus." International Journal of Research and Review 8, no. 9 (September 4, 2021): 18–22. http://dx.doi.org/10.52403/ijrr.20210904.

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Background: Gestational Diabetes Mellitus (GDM) is a disorder of carbohydrate metabolism that causes hyperglycemia, insulin resistance and failure of organs especially the liver. There is great interest in understanding the pathophysiology and treatment of GDM. Due to ethical issues involving human studies, it is necessary to use animal models to understand pathophysiology and potential treatment for GDM. Streptozotocin-induced diabetes mellitus in pregnant rats was commonly used by several author. Aims: The aim of this study is to investigate the effect of streptozotocin (STZ) on liver histology in pregnant rats. Methods: Pregnant rats were divided into two groups; 1) Negative control, 2) Positive control. Positive control were pregnant rats induced with a single intraperitoneal injection of streptozotocin 40 mg/Kg b.w. Fourteen days after induction, rats were sacrificed to evaluate the histopathological effect of STZ on the liver using hematoxylin Eosin staining and calculate the presentation of degraded cell and sinusoidal area with ImageJ 1.49v software, National Institute of Health, Bethesda, MD, USA. Data were processed statistically using SPSS with T-Test. Results: Microscopic examination of the liver of STZ-induced rats showed histologic changes in the form of an increase in the number of degenerated cells and a significant expansion of the sinusoidal area (p < 0.000). The percentage of degenerated cells in the healthy group was 9.3%, increased to 70% in the STZ-induced group. In addition, the percentage of the sinusoidal area, which was 19.98% in the healthy group, increased to 49.5%. Conclusions: Streptozotocin induces liver damage in the pregnant rats model. Keywords: Gestational Diabetes Mellitus, Streptozotocin, Liver, Histology
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Vastyanov, R. S., and O. V. Chekhlova. "Pathophysiological model of indirect revascularization in rats with microangiopathy of limbs caused by experimental streptozocin diabetes." Reports of Morphology 25, no. 4 (December 19, 2019): 24–29. http://dx.doi.org/10.31393/morphology-journal-2019-25(4)-04.

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Despite the large number of publications, the model of experimental diabetes after the introduction of streptozotocin remains a subject of lively scientific debate. The purpose of this study was to develop a pathophysiological model of indirect revascularization in rats with microangiopathy of limbs caused by experimental streptozotocin diabetes. Experimental studies were carried out in a chronic experiment on 100 sexually mature Wistar rats weighing 180-250 g. The streptozotocin diabetes model used. After culling animals from increased resistance to pancreatotropic toxicity by the criterion of the absence of hyperglycemia, three experimental groups were formed: Group I (control) – rats with streptozotocin-induced angiopathy without treatment (n=10); II group – rats with streptozotocin-induced angiopathy treated with pentoxifylline (100 mg/kg IP for 10 days) for therapeutic purposes (n=25); III group – rats with streptozotocin-induced angiopathy, which together with the treatment were injected with platelet-rich plasma (in the right hind limb, once, with a volume of 0.2 ml, linearly, retrogradely, from two points) and pentoxifylline (100 mg/kg IP for 10 days) (n=25). The duration of the experiment was 110 days. We studied the level of glycemia, the state of microcirculation, and the degree of pathomorphological changes in the various study groups. Statistical processing was performed by non-parametric methods using software Statistica 10.0. The developed pathophysiological model of indirect revascularization with the introduction of pentoxifylline and plasma enriched with platelets in diabetic angiopathy is adequate to the needs of clinical physiology. It has been shown that the isolated administration of pentoxifylline is inferior to combined therapy by revascularizing activity. The results of the work may be an experimental justification for the feasibility of clinical application of the combination of pentoxifylline and platelets rich plasma in the treatment of diabetic angiopathy, as well as its use in prophylactic purposes in patients with diabetes mellitus.
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Zhu, Lei, Zhen Zhang, Xiao-jie Hou, Yong-feng Wang, Jing-yu Yang, and Chun-fu Wu. "Inhibition of PDE5 attenuates streptozotocin-induced neuroinflammation and tau hyperphosphorylation in a streptozotocin-treated rat model." Brain Research 1722 (November 2019): 146344. http://dx.doi.org/10.1016/j.brainres.2019.146344.

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Gvazava, I. G., A. V. Kosykh, O. S. Rogovaya, O. P. Popova, K. A. Sobyanin, A. K. Khrushchev, A. V. Timofeev, and E. A. Vorotelyak. "A Simplified Streptozotocin-Induced Diabetes Model in Nude Mice." Acta Naturae 12, no. 4 (December 22, 2020): 98–104. http://dx.doi.org/10.32607/actanaturae.11202.

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Preclinical studies of human cellular and tissue-based products (HCT/Ps) for transplantation therapy of type 1 diabetes mellitus (T1DM) necessarily involve animal models, particularly mouse models of diabetes induced by streptozotocin (STZ). These models should mimic the clinical and metabolic manifestations of T1DM in humans (face validity) and be similar to T1DM in terms of the pathogenetic mechanism (construct validity). Furthermore, since HCT/Ps contain human cells, modeling of diabetes in immune-deficient animals is obligatory. Here we describe the most simplified diabetes model in Nude mice. Diabetes was induced in 31 males by a single intraperitoneal injection of STZ in normal saline at a medium-to-high dose of 150 mg/kg body weight. Fourteen control animals received only saline. Non-fasting plasma glucose (PG) levels were measured periodically for 50 days. All STZ-treated mice survived beyond 50 days. By day 15 after STZ administration, 22 of 31 (71%) mice developed stable diabetes based on the following criteria: (1) non-fasting PG 15 mmol/L on consecutive measurements up until day 50; (2) no diabetes remission. The mean non-fasting PG in mice with stable diabetes over the period of 35 days was equal to 25.7 mmol/L. On day 50, mean plasma insulin concentration, mean pancreatic insulin content, and the average number of -cells in pancreatic islets were 2.6, 8.4, and 50 times lower, respectively, than in the control animals. We consider that our Nude mouse model of diabetes meets face validity and construct validity criteria and can be used in preclinical studies of HCT/Ps.
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Baig, Mirza Anwar, and Shital Sharad Panchal. "Streptozotocin-Induced Diabetes Mellitus in Neonatal Rats: An Insight into its Applications to Induce Diabetic Complications." Current Diabetes Reviews 16, no. 1 (December 13, 2019): 26–39. http://dx.doi.org/10.2174/1573399815666190411115829.

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Background: Diabetic complications are the major contributor in the mortality of diabetic patients despite controlling blood glucose level. In the journey of new drug discovery, animal models have to play a major role. A large number of chemical-induced and genetically modified animal models have been investigated to induce diabetic complications but none of them was found to be mimicking the pathophysiology of the human. Therefore, the search and identification of the appropriate animal model become essential. Objective: In the present review, we have made an attempt to understand the pathophysiology of diabetic complication in the neonatal streptozotocin-diabetic rat model and tried to identify the targets for therapeutic agents. The review will help the researchers to explore the animal model to induce diabetic complications, to identify targets and further to find lead molecules for treatment or prevention of diabetic complications. Methods: We have compiled the available research work from 1974 by using prominent databases, organized the available information and analyzed the data to improve the understanding of the pathophysiology of streptozotocin-induced diabetic complications in neonates of rats. Results: The neonatal streptozotocin-diabetic rat model is frequently used and well-established animal model for type 2 diabetes mellitus. We have found that this model has been used to study the pathogenesis of various micro and macrovascular diabetic complications and also investigated for its effects on the liver, thymus gland, and brain. The underlying pathophysiology for complications had a resemblance to the human. Conclusion: The neonatal streptozotocin-diabetic rat model may demonstrate symptomatic diabetic complications due to persistent hyperglycemia at the age of approximately 18-24 weeks. Critical interpretations of available research work showed that the researcher can explore split dose STZ (90- 100mg/kg b.w) model to induce Type 2 DM in neonates of rats at 2nd or 3rd postnatal day.
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Dissertations / Theses on the topic "Streptozotocin model"

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Shamsaldeen, Yousif. "Endothelial TRPV4 dysfunction in a streptozotocin-diabetic Rat Model." Thesis, University of Hertfordshire, 2016. http://hdl.handle.net/2299/17622.

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Diabetes mellitus is a complex disease characterised by chronic hyperglycaemia due to compromised insulin synthesis and secretion, or decreased tissue sensitivity to insulin, if not all three conditions. Endothelial dysfunction is a common complication in diabetes in which endothelium-dependent vasodilation is impaired. The aim of this study was to examine the involvement of TRPV4 in diabetes endothelial dysfunction. Male Charles River Wistar rats (350-450 g) were injected with 65mg/kg streptozotocin (STZ) intraperitoneally. STZ-injected rats were compared with naïve rats (not injected with STZ) or control rats (injected with 10ml/kg of 20mM citrate buffer, pH 4.0-4.5), if not both. Rats with blood glucose concentrations greater than 16mmol/L were considered to be diabetic. As the results revealed, STZ-diabetic rats showed significant endothelial dysfunction characterised by impaired muscarinic-induced vasodilation, as well as significant impairment in TRPV4-induced vasodilation in aortic rings and mesenteric arteries. Furthermore, STZ-diabetic primary aortic endothelial cells (ECs) showed a significant reduction in TRPV4-induced intracellular calcium ([Ca2+]i) elevation. TRPV4, endothelial nitric oxide synthase (eNOS), and caveolin-1 (CAV-1) were also significantly downregulated in STZ-diabetic primary aortic ECs and were later significantly restored by in vitro insulin treatment. Methylglyoxal (MGO) was significantly elevated in STZ-diabetic rat serum, and nondiabetic aortic rings incubated with MGO (100μM) for 12 hours showed significant endothelial dysfunction. Moreover, nondiabetic primary aortic ECs treated with MGO (100μM) for 5 days showed significant TRPV4 downregulation and significant suppression of 4-α-PDD-induced [Ca2+]i elevation, which was later restored by L-arginine (100μM) co-incubation. Incubating nondiabetic aortic rings with MGO (100μM) for 2 hours induced a spontaneous loss of noradrenaline-induced contractility persistence. Moreover, MGO induced significant [Ca2+]i elevation in Chinese hamster ovary cells expressing rat TRPM8 channels (rTRPM8), which was significantly inhibited by AMTB (1-5μM). Taken together, TRPV4, CAV-1, and eNOS can form a functional complex that is downregulated in STZ-diabetic aortic ECs and restored by insulin treatment. MGO elevation might furthermore contribute to diabetes endothelial dysfunction and TRPV4 downregulation. By contrast, MGO induced the loss of contractility persistence, possibly due to MGO's acting as a TRPM8 agonist.
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Bahremand, Saeid. "Blood Glucose Management Streptozotocin-Induced Diabetic Rats by Artificial Neural Network Based Model Predictive Control." Thesis, Southern Illinois University at Edwardsville, 2017. http://pqdtopen.proquest.com/#viewpdf?dispub=10249804.

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Diabetes is a group of metabolic diseases where the body’s pancreas does not produce enough insulin or does not properly respond to insulin produced, resulting in high blood sugar levels over a prolonged period. There are several different types of diabetes, but the most common forms are type 1 and type 2 diabetes. Type 1 diabetes Mellitus (T1DM) can occur at any age, but is most commonly diagnosed from infancy to late 30s. If a person is diagnosed with type 1 diabetes, their pancreas produces little to no insulin, and the body’s immune system destroys the insulin-producing cells in the pancreas. Those diagnosed with type 1 diabetes must inject insulin several times every day or continually infuse insulin through a pump, as well as manage their diet and exercise habits. If not treated appropriately, it can cause serious complications such as cardiovascular disease, stroke, kidney failure, foot ulcers, and damage to eyes.

During the past decade, researchers have developed artificial pancreas (AP) to ease management of diabetes. AP has three components: continuous glucose monitor (CGM), insulin pump, and closed-loop control algorithm. Researchers have developed algorithms based on control techniques such as Proportional Integral Derivative (PID) and Model Predictive Control (MPC) for blood glucose level (BGL) control; however, variability in metabolism between or within individuals hinders reliable control.

This study aims to develop an adaptive algorithm using Artificial Neural Networks (ANN) based Model Predictive Control (NN-MPC) to perform proper insulin injections according to BGL predictions in diabetic rats. This study is a ground work to implement NN-MPC algorithm on real subjects. BGL data collected from diabetic rats using CGM are used with other inputs such as insulin injection and meal information to develop a virtual plant model based on a mathematical model of glucose–insulin homeostasis proposed by Lombarte et al. Since this model is proposed for healthy rats; a revised version on this model with three additional equations representing diabetic rats is used to generate data for training ANN which is applicable for the identi?cation of dynamics and the glycemic regulation of rats. The trained ANN is coupled with MPC algorithm to control BGL of the plant model within the normal range of 100 to 130 mg/dl by injecting appropriate amount of insulin. The ANN performed well with less than 5 mg/dl error (2%) for 5-minute prediction and about 15 mg/dl error (7%) for 30-minute prediction. In ¬¬addition, the NN-MPC algorithm kept BGL of diabetic rats more than 90 percent of the time within the normal range without hyper/hypo-glycaemia.

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Kekatpure, Avantika. "Gender differences in aortic endothelial function in a rat model of streptozotocin-induced diabetes : possible role of superoxide and cyclooxygenase." Scholarly Commons, 2009. https://scholarlycommons.pacific.edu/uop_etds/737.

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Objectives: To date little is known of the interaction between diabetes and sex hormones in the vasculature. A number of studies suggest that premenopausal diabetic women loose their gender based cardiovascular protection. However, there is insufficient evidence to explain the mechanism underlying the loss of this gender based cardioprotection in premenopausal diabetic women. The objectives of this study were to investigate whether there is a gender difference in the aortic endothelial function in · streptozotocin (STZ, 58 mg/kg, iv)-induced diabetic rats, and the potential role of superoxide and cyclooxygenase (COX) metabolites in diabetes-induced vascular dysfunction.
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Thomas, Adam J. "Characterization of cAMP-Specific Phosphodiesterase-4 (R)-[11C]Rolipram Small Animal Positron Emission Tomography and Application in a Streptozotocin-Induced Model of Hyperglycemia." Thèse, Université d'Ottawa / University of Ottawa, 2011. http://hdl.handle.net/10393/19877.

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Elevated sympathetic nervous system (SNS) tone contributes to excess cardiac mortality associated with type 2 diabetes mellitus (T2DM). Chronic SNS stimulation has detrimental effects to the heart, in particular, with its cell signaling abilities. (R)-[11C]Rolipram small animal positron emission tomography (PET), an noninvasive nuclear imaging modality, was used to assess phosphodiesterase-4 (PDE4) alterations in a high fat diet (HFD), streptozotocin (STZ) induced model of hyperglycemia in rats. Prior to investigation in the animal model, characterization of (R)-[11C]rolipram small animal PET was completed. (R)-[11C]Rolipram binds specifically to PDE4 in the rat heart demonstrated by competitive blockade with (R)-rolipram with the PDE4 enzyme susceptible to saturation with increasing injected masses of unlabeled rolipram. (R)-[11C]Rolipram cardiac retention was elevated by acute norepinephrine stimulation via desipramine pharmacologic challenge. Quantitative (R)-[11C]rolipram PET was highly reproducible in the heart and presents an ideal avenue to investigate PDE4 alterations. (R)-[11C]rolipram small animal PET did not reveal changes in PDE4 expression and activity in STZ-treated hyperglycemic animals compared to STZ-treated euglycemic and control groups. In vitro measures of PDE4 enzyme expression and activity, with or without desipramine, were also not altered between treatment groups. Although (R)-[11C]rolipram small animal PET does not reveal PDE4 alterations in this animal model of diabetes, its utility to assess PDE4 alterations in other over active SNS pathologies, such as heart failure and obesity, remains.
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Ayeleso, Ademola Olabode. "Influence of two plant products (red palm oil and rooibos) on streptozotocin-induced hyperglycaemia and its implications on antioxidant status and other biochemical parameters in an animal model." Thesis, Cape Peninsula University of Technology, 2012. http://hdl.handle.net/20.500.11838/1517.

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Thesis submitted in fulfilment of the requirements for the Doctor of Technology: Biomedical Technology In the Faculty of Health and Wellness At the CAPE PENINSULA UNIVERSITY OF TECHNOLOGY, 2012
Diabetes mellitus is a major health problem not only in urban, but also in the rural areas and is diagnosed by the presence of high glucose levels in the blood. Oxidative stress is known to be actively involved in the onset and progression of diabetes and its complications. Antioxidants have important roles in biological systems by scavenging free radicals which may result in oxidative damage of biological molecules such as lipids, proteins and DNA. Red palm oil, originally from the tropical area of Africa, generally consumed as cooking oil, is known to have some beneficial health effects due to the presence of lipid soluble antioxidants such as carotenoids, tocopherols and tocotrienols. It also contains almost an equal proportion of both saturated and unsaturated fatty acids which makes it distinctive from other vegetable oils. Rooibos, on the other hand, is grown in the Cederberg area of the Western Cape in South Africa and it is commonly consumed as a beverage. It contains a complex profile of water soluble antioxidants (flavonoids) and its health promoting potentials have been reported extensively. Some of the flavonoids present in rooibos include aspalathin, nothofagin, quercetin, rutin and orientin. The objective of this research project was to examine the potential beneficial effects of the dietary intake of red palm oil and rooibos on streptozotocin-induced hyperglycaemia and its influence on the antioxidant status and some biochemical parameters in male Wistar rats. The preliminary phase of this study was designed to investigate the biochemical effects of these two plant products at different dosages following consumption for a period of 7 weeks. The preliminary study did not reveal any adverse effects of the different dosages of red palm oil (1 ml, 2 ml and 4 ml) and rooibos (2%, 4% and 6%) on the experimental rats following dietary intake for 7 weeks. However, these natural products showed an improvement in the antioxidant status of the rats at the different doses. Using a single dose each of both plant products from the preliminary study, the main study was performed to investigate the influence of these two plant products singly and in combination on the blood and liver of streptozotocin-induced hyperglycaemic male Wistar rats. In the main study, streptozotocin (50 mg/kg) dissolved in 0.1 M citrate buffer (pH 4.5) through intramuscular injection was used for the induction of diabetes which was confirmed by the presence of high blood glucose after 72 hours. Red palm oil or rooibos extract alone did not have any effect on the control of blood glucose in the diabetic rats. The dietary intake of the combined treatment with red palm and rooibos had more health promoting effects on the diabetic rats which included a decrease in blood glucose, glycosylated haemoglobin, fructosamine and increased insulin levels. There was a marked increase in liver glycogen levels in all the diabetic groups. Treatment with rooibos alone showed a decrease in glycogen levels in the diabetic rats. The presence of liver enzymes in the serum, commonly used as indicators of liver damage was increased in all the diabetic rats. However, the combined treatment of diabetic rats with red palm oil and rooibos protected the liver from injury. Red palm oil improved high density lipoprotein cholesterol levels (HDL-cholesterol) in the diabetic rats. There was no effect on the activity of glucokinase, the first enzyme in the the glycolytic pathway in both the untreated and treated diabetic rats. However, the activity of pyruvate kinase, the last enzyme in the glycolytic pathway was reduced in all the diabetic groups. The combined treatment with both red palm and rooibos increased the activity of pyruvate kinase. Oxidative stress was confirmed in the diabetic rats with an increase in the plasma thiobarbituric acid reactive substances (TBARS), an indicator of lipid peroxidation. Treatment of diabetic rats with rooibos and the combination of red palm oil and rooibos brought plasma TBARS to a level that was not significantly different from the normal control group. There was a non-significant reduction of total glutathione in the non-treated and treated diabetic groups. A non-significant increase in the activity of liver catalase was observed in all the treated diabetic groups. The activity of superoxide dismutase was significantly decreased in the liver of diabetic rats. Diabetic rats treated with red palm oil, rooibos and the combined treatment showed an increased activity of superoxide dismutase in the liver. Red palm oil and the combined treatment increased the activity of glutathione peroxidase in both the red blood cells and liver of diabetic rats. Red palm oil, rooibos and their combined treatments also improved the plasma antioxidant capacity such as ferric reducing antioxidant power (FRAP) and oxygen reducing absorbance capacity (ORAC) in the diabetic rats. In conclusion, oxidative stress is actively involved in the progression of diabetes mellitus. Red palm oil and rooibos, most especially their combined treatment showed significant beneficial health promoting effects in the diabetic rats. The remarkable effects of the combined treatment of red palm oil and rooibos in the diabetic rats could be due to their antioxidant profiles. Based on the findings from this study, it can be adduced that these plant products could help in the management of diabetes and its complications and therefore, suggested the need for further research studies on antioxidant therapy in the management of diabetes mellitus.
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Sakai, Takeru. "Leptin restores the insulinotropic effect of exenatide in a mouse model of type 2 diabetes with increased adiposity induced by streptozotocin and high-fat diet." Kyoto University, 2015. http://hdl.handle.net/2433/195969.

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Kusakabe, Toru. "Beneficial effects of leptin on glycaemic and lipid control in a mouse model of type 2 diabetes with increased adiposity induced by streptozotocin and a high-fat diet." Kyoto University, 2009. http://hdl.handle.net/2433/124316.

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Haley, James M. "Ex Vivo Evaluation of Myocardial Beta-Adrenergic Receptors in High-Fat Fed STZ and ZDF Models of Diabetes Using [3H]-CGP12177." Thesis, Université d'Ottawa / University of Ottawa, 2013. http://hdl.handle.net/10393/30363.

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Diabetes mellitus (DM) and hyperglycemia contribute to sympathetic nervous system (SNS) activation and cardiovascular dysfunction. SNS activation and increased norepinephrine levels downregulate cardiac β-adrenergic receptors (β-AR). The ADMIRE-HF trial identified reduced cardiac SNS innervation as an independent prognostic marker in heart failure. The β-AR antagonist [3H]-CGP12177 was used to quantify cardiac β-AR in ex vivo biodistribution studies in streptozotocin (STZ)-treated rats after 8 weeks of sustained hyperglycemia, and in the Zucker Diabetic Fatty (ZDF) rat model of type-2 diabetes at the onset of hyperglycemia (10 weeks of age) and after a sustained period of hyperglycemia (16 weeks of age). In some STZ rats, insulin was provided at the onset of hyperglycemia, or after a sustained period of hyperglycemia. Insulin treatment at both time points prevented reduced [3H]-CGP12177 binding (33-38% compared to controls) observed in STZ hyperglycemics. ZDF β-ARs were intact at 10 weeks but became reduced (16-25% relative to the Zucker leans) following 6 weeks of hyperglycemia. This work supports that cardiac β-AR are reduced in models of DM and that restoring insulin signalling to maintain glycemic control can normalize β-AR density whether provided early or after a period of sustained hyperglycemia.
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Wong, Ching-keung, and 黃靜強. "The effects of streptozotocin-diabetes on adrenomedullin gene expression and peptide levels in the gastrointestinal system of therat." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2006. http://hub.hku.hk/bib/B45011503.

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Esteves, Ingrid de Miranda. "Caracterização das alterações na via hipocampo-córtex pré-frontal medial em modelo farmacológico da doença de Alzheimer." Universidade de São Paulo, 2016. http://www.teses.usp.br/teses/disponiveis/17/17140/tde-26082016-110343/.

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Severas altera¸c~oes no metabolismo energ´etico, no consumo de glicose e na sinaliza¸c~ao de insulina cerebral est~ao presentes na doen¸ca de Alzheimer (DA). O modelo animal da DA obtido pela administra¸c~ao intracerebroventricular de estreptozotocina (STZ-icv) em ratos induz um estado de resist^encia `a insulina no c´erebro associado `a disfun¸c~oes colin´ergicas e a d´eficits cognitivos, tornando-o um dos poucos modelos experimentais da forma espor´adica da DA. Este trabalho tem como objetivo caracterizar, neste modelo, as disfun¸c~oes sin´apticas na via hipocampo - c´ortex pr´e-frontal medial (CA1-CPFm) e testar se o tratamento com nicotina ´e capaz de prevenir as disfun¸c~oes sin´apticas e reverter os preju´?zos cognitivos induzido pelo STZ-icv. Para isso, ratos Wistar receberam STZ e foram submetidos a 20 dias de tratamento com nicotina. Dois dias depois, foram realizados nos animais teste de campo aberto e de reconhecimento de objeto. Em seguida os animais foram anestesiados com uretana para que os registros eletrofisiol´ogicos fossem realizados. Um eletrodo foi utilizado para estimular CA1 com pulso pareado e potenciais de campo p´os-sin´apticos (fPSP1) e sua facilita¸c~ao (fPSP2) foram registradas por um eletrodo no CPFm. Ap´os 30 minutos de linha de base, uma estimula¸c~ao em alta frequ^encia foi aplicada para induzir a potencia¸c~ao de longa dura¸c~ao (LTP), seguido de mais quatro horas de registro. Outro grupo experimental foi realizado para avaliar o efeito de longo prazo da STZ-icv e do tratamento com nicotina. Neste grupo, testes comportamentais e eletrofisiol´ogicos foram realizados 60 dias ap´os o fim do tratamento. Independentemente do tempo, os resultados indicam que a STZ produziu uma redu¸c~ao na indu¸c~ao e na manuten¸c~ao da LTP, mas a facilita¸c~ao por pulso pareado (PPF = fPSP2 / fPSP1) mostra que a STZ prejudica a plasticidade pr´e-sin´aptica apenas a curto prazo. O tratamento com nicotina atenua a disfun¸c~ao na LTP induzida pela STZ. Al´em disso, apenas o tratamento de nicotina tamb´em ´e capaz de reduzir a plasticidade pr´e-sin´aptica no grupo controle dois dias ap´os o fim do tratamento. Estes resultados tamb´em est~ao associados com os dados comportamentais, uma vez que a nicotina reverteu os d´eficits de mem´oria de reconhecimento nos animais STZ mas manteve o comportamento explorat´orio reduzido. Sugerimos com isso que o sistema colin´ergico, que desempenha um papel importante em fun¸c~oes cognitivas e na LTP, est´a afetado nos animais injetados com STZ e o tratamento cr^onico com nicotina consegue reduzir os danos na plasticidade sin´aptica e comportamentais, induzidos pela STZ.
Severe abnormalities in brain glucose/energy metabolism and insulin signaling have been documented to play an important role in early stage of alzheimer disease (AD) pathology. Intracerebroventricular administration (icv) of streptozotocin (STZ) in rats can induce an insulin-resistant brain state associated with cholinergic dysfunctions and memory impairments, which make it a suitable experimental model of the sporadic form of AD. The present work aimed to extend the characterization of this model by probing synaptic plasticity dysfunctions in the medial prefrontal cortex (mPFC)- hippocampal (CA1) pathway and test if nicotine can prevent synaptic dysfunction and revert cognitive impairment induced by icv STZ. Here, Wistar rats received bilateral microinjection of STZ and were submitted to 20 days of nicotine treatment. After 2 days of withdrawing the subjects were submitted to open field and object recognition tests. After that, animals were anesthetized with urethane for electrophysiological tests. A twisted bipolar electrode was used to stimulate posterior-dorsal hippocampus (CA1/subiculum) with paired-pulse. Basal field post-synaptic potentials (fPSP1) and facilitated responses (fPSP2) were recorded by a monopolar electrode in the medial mPFC. After 30min of baseline, high frequency stimulation was applied to induce long-term potentiation (LTP) and additional four hours of electrophysiological recordings was performed. Another experimental group was performed to evaluate the long term effect of both icv STZ and nicotine treatment. In this group behavioral and electrophysiological tests were performed with 60 days after chronic treatment. Independently of time, our results indicate that STZ produced a significant decrease in the induction and maintenance of LTP, but paired pulse facilitation (PPF = fPSP2/fPSP1) shows that only the short-term pre-synaptic plasticity was impaired after STZ injection. The nicotine treatment attenuates the STZ-induced LTP dysfunction in the CA1-mPFC pathway. However, just the nicotine treatment (in control group) can reduce pre-synaptic plasticity two days after chronic treatment. These results are also associated with behavioral data, since nicotine treatment reversed the deficits in recognition memory of STZ animals but maintained the reduced exploratory behavior. We suggest that the brain cholinergic system, which plays a role in cognition function and LTP, is affected in STZ injected animals and chronic treatment with nicotine can attenuate the STZ-induced synaptic plasticity and behavioral dysfunctions.
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Book chapters on the topic "Streptozotocin model"

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Müller, Dorothea, Konstanze Plaschke, and Siegfried Hoyer. "Intracerebroventricular Injection of Streptozotocin — An Animal Model for Sporadic Alzheimer’s Disease?" In Alzheimer’s and Parkinson’s Diseases, 389–93. Boston, MA: Springer US, 1995. http://dx.doi.org/10.1007/978-1-4757-9145-7_58.

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Labak, M., T. Foniok, D. Kirk, D. Rushforth, B. Tomanek, A. Jasiński, and P. Grieb. "Metabolic Changes in Rat Brain Following Intracerebroventricular Injections of Streptozotocin: A Model of Sporadic Alzheimer’s Disease." In Brain Edema XIV, 177–81. Vienna: Springer Vienna, 2009. http://dx.doi.org/10.1007/978-3-211-98811-4_32.

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Rungger-Brändle, Elisabeth, and André A. Dosso. "Streptozotocin-Induced Diabetes — A Rat Model to Study Involvement of Retinal Cell Types in the Onset of Diabetic Retinopathy." In Advances in Experimental Medicine and Biology, 197–203. Boston, MA: Springer US, 2003. http://dx.doi.org/10.1007/978-1-4615-0067-4_25.

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King, Aileen J. F., Elisabet Estil·les, and Eduard Montanya. "Use of Streptozotocin in Rodent Models of Islet Transplantation." In Methods in Molecular Biology, 135–47. New York, NY: Springer US, 2020. http://dx.doi.org/10.1007/978-1-0716-0385-7_10.

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Meister, R., and K. Paul. "Investigations of Glucose Tolerance Following Pancreatic Transplantation in Rats with Streptozotocin-Induced Diabetes." In Microsurgical Models in Rats for Transplantation Research, 189–93. Berlin, Heidelberg: Springer Berlin Heidelberg, 1985. http://dx.doi.org/10.1007/978-3-642-61657-0_31.

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Kawaharada, Ritsuko, and Akio Nakamura. "Future Risks for Children Born to Mothers with Gestational Diabetes: Elucidation Using the Cell Model Approach." In Gestational Diabetes Mellitus - New Developments [Working Title]. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.100117.

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A number of studies have shown that foetal nutritional status significantly impacts an unborn child’s long-term health. The developmental origins of health and disease (DOHaD) hypothesis proposes that if a child is undernourished in the foetal period, the child will develop diabetes and hypertension in the future if adequate nutrition is given after birth. Moreover, hyperglycaemia (e.g. gestational diabetes mellitus [GDM]) experienced during foetal life can reportedly cause various complications in children. As diabetes is increasing worldwide, so is GDM, and many studies have been conducted using GDM animal models and GDM cell lines. We examined the effects of streptozotocin-induced diabetes, particularly on the heart of offspring, in rat GDM animal models. We also analysed primary cardiomyocyte cultures isolated from these GDM rats and found that insulin signalling was inhibited in GDM cells, as in the GDM animal models, by increased advanced glycation end products. Furthermore, the effect of eicosapentaenoic acid during pregnancy has been reported in GDM animal models and cells, and the findings indicated the importance of nutritional management for GDM during pregnancy.
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Bianchi, Maria Silvia, Veronica Calvo, Norma Alejandra Chasseing, Carlos Libertun, Alejandro Daniel Montaner, and Victoria Adela Lux-Lantos. "Effect of Oligonucleotide IMT504 in a Type I Diabetes Model Induced by Multiple Low Doses of Streptozotocin in Mice." In BASIC/TRANSLATIONAL - Type I Diabetes & Diabetic Complications, P1–502—P1–502. The Endocrine Society, 2011. http://dx.doi.org/10.1210/endo-meetings.2011.part2.p9.p1-502.

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Subramanian, Ramaswamy, and Kathleen M. MacLeod. "Vascular Reactivity in Streptozotocin-Induced Diabetes." In Experimental Models of Diabetes, 153–76. Routledge, 2018. http://dx.doi.org/10.1201/9780203756386-7.

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Battell, Mary L., Brian Rodrigues, Violet G. Yuen, and John H. McNeill. "Treatment and Pharmacological Interventions in Streptozotocin Diabetes." In Experimental Models of Diabetes, 195–216. Routledge, 2018. http://dx.doi.org/10.1201/9780203756386-9.

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Stanley, William C., Gary D. Lopaschuk, and Krista M. Kivilo. "Alterations in Myocardial Energy Metabolism in Streptozotocin Diabetes." In Experimental Models of Diabetes, 19–38. Routledge, 2018. http://dx.doi.org/10.1201/9780203756386-2.

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Conference papers on the topic "Streptozotocin model"

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Hendrawan, Thressia, Nurul Paramita, Dewi Irawati, and Ani Retno Prijanti. "Diabetes Sprague-Dawley Model Induced With Fat Diet And Streptozotocin." In Surabaya International Physiology Seminar. SCITEPRESS - Science and Technology Publications, 2017. http://dx.doi.org/10.5220/0007337902920293.

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Yuan, Hongping, Dongxu Zhao, and Boyin Zhang. "Minocycline Attenuates Kidney Injury in a Rat Model Of Streptozotocin-Induced Diabetic Nephropathy." In International Conference on Biomedical and Biological Engineering. Paris, France: Atlantis Press, 2016. http://dx.doi.org/10.2991/bbe-16.2016.41.

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Johnson, Kennita A., A. Gloria Nyankima, Paul A. Dayton, and Emily Chang. "Characterizing volumes of kidney segments in Streptozotocin induced diabetic rat model utilizing 4D contrast-enhanced ultrasound." In 2016 IEEE International Ultrasonics Symposium (IUS). IEEE, 2016. http://dx.doi.org/10.1109/ultsym.2016.7728850.

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Zangerolamo, Lucas, Helena Sampaio, Gabriela Soares, Jean Vettorazzi, Carina Solon, Daiane Engel, Licio Velloso, Antonio Boschero, and Everardo Carneiro. "The bile acid TUDCA reduces hypothalamic inflammation and food intake in streptozotocin-induced Alzheimer’s mice model." In Congresso de Iniciação Científica UNICAMP. Universidade Estadual de Campinas, 2019. http://dx.doi.org/10.20396/revpibic2720192769.

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Anapali, Merve. "Resveratrol and Vitamin D ameliorate liver fibrosis and apoptosis in fructose-fed diet and streptozotocin induced T2DM model." In European Microscopy Congress 2020. Royal Microscopical Society, 2021. http://dx.doi.org/10.22443/rms.emc2020.1144.

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Kerrigan, L., K. Edgar, A. Russell-Hallinan, D. Grieve, and C. Watson. "26 Using combination of high-fat diet and high-dose streptozotocin to develop an in vivo model of diabetic cardiomyopathy." In Irish Cardiac Society Annual Scientific Meeting & AGM, Thursday October 17th – Saturday October 19th 2019, Galway, Ireland. BMJ Publishing Group Ltd and British Cardiovascular Society, 2019. http://dx.doi.org/10.1136/heartjnl-2019-ics.26.

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Akarca Dizakar, Saadet Özen. "The effects of sunitinib on immunoreactivities of vimentin, E-cadherin and S100 in kidneys of the experimental Streptozotocin -induced mouse model." In 15th International Congress of Histochemistry and Cytochemistry. Istanbul: LookUs Scientific, 2017. http://dx.doi.org/10.5505/2017ichc.pp-235.

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Tuchina, Daria K., Alla B. Bucharskaya, and Valery V. Tuchin. "Pilot study of glycerol diffusion in ex vivo skin: a comparison of alloxan and streptozotocin diabetes models." In Saratov Fall Meeting 2019: Optical and Nano-Technologies for Biology and Medicine, edited by Valery V. Tuchin and Elina A. Genina. SPIE, 2020. http://dx.doi.org/10.1117/12.2563794.

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Reports on the topic "Streptozotocin model"

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Cook, Alonzo D. Realistic Murine Model for Streptozotocin-induced Diabetic Peripheral Neuropathy. Science Repository OÜ, August 2018. http://dx.doi.org/10.31487/j.rgm.2018.02.006.

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