988 resultados para streptozotocin (STZ)-diabetic rat
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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
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INTRODUÇÃO: Modelos experimentais são desenvolvidos com propósito de ampliar o entendimento dos mecanismos fisiopatológicos envolvidos no diabete. Os achados experimentais levam ao desenvolvimento de tratamentos alternativos para a manutenção das condições metabólicas normais. Existem vários estudos sobre o diabete induzido por streptozotocin mimetizando o quadro clínico do DM2. No entanto, a interação entre os níveis de glicose, perfil lipídico e estresse oxidativo nestes animais são escassos. Portanto, o objetivo do trabalho foi avaliar estes parâmetros em ratas Wistar adultas com diabete induzido com streptozotocin no período neonatal. MÉTODOS: Fêmeas recém-nascidas receberam streptozotocin (70mg/Kg, ip) no 5º dia de vida (n5-STZ). A glicemia foi medida no terceiro e quarto meses de vida dos animais. No final do quarto mês de vida, amostras de sangue foram coletadas e processadas para a dosagem de lipídios e marcadores de estresse oxidativo. RESULTADOS: A glicemia das ratas do grupo n5-STZ foi significativamente maior comparada às ratas do grupo controle (p<0,05). Não houve alteração nos níveis de colesterol total e triglicérides, peroxidação lipídica (TBARS), atividade da SOD e determinação da GSH-t (p>0,05) nas ratas n5-STZ em relação às ratas do grupo controle. No entanto, houve diminuição significativa no HDL-colesterol (p<0,05). CONCLUSÃO: Este modelo de indução de diabete em ratas causou hiperglicemia (120-360mg/dL), caracterizando o diabete moderado. Essa glicemia levou a alterações no HDL-colesterol, a qual não foi suficiente para prejudicar a atividade das enzimas antioxidantes ou marcadores da peroxidação lipídica na vida adulta. Além disso, esta investigação experimental contribuiu para entender os diferentes resultados encontrados em outros modelos deindução do diabete moderado em animais de laboratório, como também para a melhor compreensão dos mecanismos fisiopatológicos do diabete moderado ou da hiperglicemia em humanos.
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This study aimed at evaluating glycemia and lipid profile of offspring from diabetic Wistar rats treated with Mentha piperita (peppermint) juice. Male offspring from nondiabetic dams (control group: 10 animals treated with water and 10 treated with peppermint juice) and from dams with streptozotocin-induced severe diabetes (diabetic group: 10 animals treated with water and 10 treated with peppermint juice) were used. They were treated during 30 days, and, after the treatment period, levels of glycemia, triglycerides, total cholesterol, and fractions were analyzed in the adult phase. The offspring from diabetic dams treated with peppermint showed significantly reduced levels of glucose, cholesterol, LDL-c, and triglycerides and significant increase in HDL-c levels. The use of the M. piperita juice has potential as culturally appropriate strategy to aid in the prevention of DM, dyslipidemia, and its complications.
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Knowing that maternal diabetes is related to hyperglycemia and fetal hyperinsulinemia, which affect the lipid metabolism, the aim of this study was to evaluate the effects of Malpighia emarginata (acerola) juice on the glycemic and lipid profile of offspring of diabetic and nondiabetic Wistar rats. The adult offspring of non-diabetic dams and of dams with severe streptozotocin-induced diabetes were divided into groups: G1, offspring (of control dams) treated with water, G2, offspring (of diabetic dams) treated with water, G3, male offspring (of control dams) treated with acerola juice, and G4, male offspring (of diabetic dams) treated with acerola juice. The offspring of diabetic dams treated with acerola juice showed significantly decreased levels of glucose, cholesterol, triglycerides, and increased HDL-c. The use of acerola juice is a potential strategy to aid in the prevention of DM and dyslipidemia and its complications or to act as an auxiliary in the treatment of these diseases.
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Several local factors that influence the healing process of replanted teeth have been investigated. However, it remains unclear how systemic alterations, such as diabetes mellitus, affect the prognosis of these cases. The purpose of this study was to evaluate the healing process of incisors of non-controlled diabetic rats replanted after storage in bovine long shelf-life (UHT) whole milk. Thirty-two rats were randomly assigned to receive an endovenous injection of either citrate buffer solution (group I - control; n = 16) or streptozotocin dissolved in citrate buffer solution to induce diabetes (group II; n = 16). After confirmation of the diabetic status by analysis of the glycemic levels, the maxillary right incisor of each animal was extracted and immersed in milk for 60 min. The root canals of teeth were then instrumented, and were filled with a calcium hydroxide-based dressing and replanted into their sockets. All animals received systemic antibiotic and were killed by anesthetic overdose 10 and 60 days after replantation. The specimens containing the replanted teeth were removed, fixed, decalcified, and embedded in paraffin. Semi-serial 6-mu m-thick sections were obtained and stained with hematoxylin and eosin for histologic and histometric analyses. The results showed that the connective tissue adjacent to the root surface was less organized in the diabetic animals than in the control animals in both periods; the root dentin was less severely affected by root resorption in the diabetic rats; there were no significant differences between the control and diabetic groups regarding the occurrence of replacement resorption and inflammatory resorption.
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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
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Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
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Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
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Acarbose is a competitive inhibitor of the intestinal alpha-glycosidases, that can delay absorption of intestinal carbohydrates causing their malabsorption. In the present paper we studied the effects of insulin, acarbose and their association on glomerular basement membrane thickening in alloxan-diabetic rats. Twenty-five male and female Wistar rats, approximately 3 months old at the beginning of the experiment, were assigned randomly to each of five experimental groups: normal control rats, alloxan-diabetic control rats, alloxan-diabetic rats treated with acarbose, alloxan-diabetic rats treated with insulin, and alloxan-diabetic rats treated with insulin plus acarbose. Alloxan was administered in a single iv dose of 42 mg/kg body weight. Insulin was given subcutaneously at doses of 18 to 30 IU/kg corrected daily on the basis of glycosuria and ketonuria. Acarbose was given mixed with rat chow in a dose of 50 mg/100 g chow. Body weight, water and food intake and diuresis, as well as blood and urine glucose were determined after 1, 3, 6, 9, and 12 months of treatment. Glomerular basement membrane (GBM) thickening was determined by electron microscopy at the same times. Clear clinical and laboratory signs of severe diabetes, with blood glucose levels above 200 mg/dl and urine glucose above 3000 mg/dl, were observed in all alloxan-diabetic control rats, in all periods of follow-up, whereas administration of insulin or acarbose reduced the blood glucose levels of treated groups. The most satisfactory control of blood and urine glucose was observed in animals treated with both insulin and acarbose. However, diarrhea was observed in diabetic rats treated with acarbose associated or not with insulin. GBM thickening was correlated with age in all groups. Beginning at six months after diabetes induction, the GBM of untreated diabetic rats was significantly thicker (mean +/- SEM, 4.446 +/- 0.45 mm) than that of normal rats (2.977 +/- 0.63 mm). Both insulin and acarbose prevented GBM thickening and their combination induced thickening similar to the age-dependent thickening observed for normal rats of the same age. We conclude that acarbose when combined with insulin may be a good option in the control of diabetes and its renal complications.
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Objective: the aim of this work was to compare the effect of low-level laser therapy (LLLT) on the wound healing process in nondiabetic and diabetic rats. Background Data: Among the clinical symptoms caused by diabetes mellitus, a delay in wound healing is a potential risk for patients. It is suggested that LLLT can improve wound healing. Methods: the tissue used for this study was extracted from animals suffering from diabetes, which was induced by Streptozotocin (R), and from nondiabetic rats. Animals were assembled into two groups of 25 rats each (treated and control) and further subdivided into two groups: diabetic (n = 15) and nondiabetic (n = 10). A full-thickness skin wound was made on the dorsum. area, with a round 8-mm hole-punch. The treated group was irradiated by a HeNe laser at 632.8 nm, with the following parameters: 15 mW, exposition time of 17 sec, 0.025 cm(2) irradiated area, and energy density of 10 J/cm(2). Square full-thickness skin samples (18 mm each side, including both injured and noninjured tissues) were obtained at 4, 7, and 15 days after surgery and analyzed by qualitative and quantitative histological methods. Results: Quantitative histopathological analysis confirmed the results of the qualitative analysis through histological microscope slides. When comparing tissue components (inflammatory cells, vessels and fibroblast/area), we found that treated animals had a less intense inflammatory process than controls. Conclusion: Results obtained by both qualitative and quantitative analyses suggested that irradiation of rats with HeNe (632.8 nm), at the tested dose, promoted efficient wound healing in both nondiabetic and diabetic rats as, compared to the control group.
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These experiments were carried out to study the effects of acute cold exposure (0-2°C/4 hr) on rectal temperature, blood glucose and plasma free fatty acids (FFA) in alloxan-diabetic rats. Male Wistar rats weighing 170-190 g were used and diabetes was induced by i.v. alloxan injection (40 mg/kg body wt). Cold exposure produced severe hypothermia in diabetic rats. After 4 hr of cold, blood glucose of diabetic rats was reduced from 296±16 to 86t±12 mg/dl (P<0.01), and FFA increased slightly, but was not statistically different (P>0.05) from the initial value. As expected, interscapular brown adipose tissue (IBAT) and retroperitoneal and epididymal white adipose tissues were significantly lower in diabetic than in control rats. Cold exposure reduced total IBAT lipids in control but not in diabetic animals. The results of this experiment suggest that diabetic rats were unable to maintain body temperature in the cold, probably because of a failure to generate an adequate amount of heat by nonshivering thermogenesis in brown adipose tissue.
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1. 1. The aim of these experiments was to study the extent to which previous cold-acclimation improves the cold-tolerance of diabetic rats. 2. 2. Alloxan diabetic rats (fasting blood glucose higher than 200mg/dl) were used in the experiments. 3. 3. In Expt. 1, non-cold-acclimated control and diabetic rats were exposed to cold environment (7-9°C), and the percentage of survival calculated during a 12-day experimental period. In Expt. 2, the rats were previously cold-acelimated before alloxan or saline injection (diabetic and control cold-acclimated rats) and the survival rate was also assessed during a 12-day period in the cold. 4. 4. The percentage of survival of the non-cold-acclimated diabetic rats (Expt.l) was 19% compared with 79% of the diabetic cold-acclimated animals (Expt. 2). There were no deaths in the control groups. 5. 5. Cold-acclimated diabetic rats maintained a near-normal thermogenic response after noradrenaline injection. This response was impaired in non-cold-acclimated diabetic rats. 6. 6. The results of these experiments suggest that the enhanced cold-tolerance of diabetic cold-acclimated rats could be related to the increased sympathetic activity and enhanced insulin sensitivity in thermogenic tissues, such as brown fat. © 1987.