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Search Results: 1 - 10 of 8490 matches for " Yuri Karen Sinzato "
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Neonatally Induced Mild Diabetes in Rats and Its Effect on Maternal, Placental, and Fetal Parameters
Yuri Karen Sinzato,Gustavo Tadeu Volpato,Isabela Lovizutto Iessi,Aline Bueno,Iracema de Mattos Paranhos Calderon,Marilza Vieira Cunha Rudge,Débora Cristina Damasceno
Experimental Diabetes Research , 2012, DOI: 10.1155/2012/108163
Abstract: The aim of this study was to assess placental changes and reproductive outcomes in neonatally induced mild diabetic dams and fetal development in their offspring. At birth, female rats were assigned either to control or diabetic group (100 mg of streptozotocin/Kg, subcutaneously). At adulthood, the female rats were mated. During pregnancy, the blood glucose levels and glucose and insulin tolerance tests were performed. At term, maternal reproductive outcomes, fetal and placental weight, and placental morphology were analyzed. Diabetic rats had smaller number of living fetuses, implantations and corpora lutea, and increased rate of embryonic loss. Placenta showed morphometric alterations in decidua area. Our results showed that mild diabetes was sufficient to trigger alterations in maternal organism leading to impaired decidua development contributing to failure in embryonic implantation and early embryonic losses. Regardless placental decidua alteration, the labyrinth, which is responsible for the maternal-fetal exchanges, showed no morphometric changes contributing to an appropriate fetal development, which was able to maintain normal fetal weight at term in mild diabetic rats. Thus, this experimental model of diabetes induction at the day of birth was more effective to reproduce the reproductive alterations of diabetic women.
Association of diabetes and cigarette smoke exposure on the glycemia and liver glycogen of pregnant Wistar rats
Sinzato, Yuri Karen;Lima, Paula Helena Ortiz;Santos, Carlos Eduardo Meirelles dos;Campos, Kleber Eduardo de;Rudge, Marilza Vieira Cunha;Damasceno, Débora Cristina;
Acta Cirurgica Brasileira , 2008, DOI: 10.1590/S0102-86502008000600002
Abstract: purpose: to evaluate cigarette smoke exposure and/or diabetes association effects on the glycemia and liver glycogen levels of pregnant wistar rats. methods: 60 adult rats were randomly distributed into (n=10/group): non-diabetic exposed to filtered air (g1); non-diabetic exposed to cigarette smoke only before pregnancy (g2); non-diabetic exposed to cigarette smoke before and during pregnancy (g3); diabetic exposed to filtered air (g4); diabetic exposed to cigarette smoke only before pregnancy (g5), and diabetic exposed to cigarette smoke before and during pregnancy (g6). glycemia was determined at days 0 and 21 of pregnancy. liver samples were collected for liver glycogen determinations. results: at day 21 of pregnancy, glycemia was higher in g5 and g6 compared to g4 group. g2 (2.43±0.43), g3 (3.20±0.49), g4 (2.62±0.34), g5 (2.65±0.27) and g6 groups (1.94±0.35) presented decreased liver glycogen concentrations compared to g1 (4.20±0.18 mg/100mg liver tissue) (p<0.05). g5 and g6 groups presented decreased maternal weight gain and litter weight. conclusions: severe diabetes and cigarette smoke exposure, alone or associated, caused impairment in liver glycogen storage at term pregnancy. due to the fact that liver glycogen storages were considered determinant for glucose tolerance, it is relevant to point out a rigid clinical glycemic control and to stop smoking so earlier in pregnancy programming.
Neonatally induced diabetes: liver glycogen storage in pregnant rats
Iessi, Isabela Lovizutto;Bueno, Aline;Sinzato, Yuri Karen;Spada, Ana Paula Machado;Rudge, Marilza Vieira Cunha;Heubel, Maricê Thereza Correa Domingues;Damasceno, Débora Cristina;
Brazilian Archives of Biology and Technology , 2012, DOI: 10.1590/S1516-89132012000200010
Abstract: the aim of this sstudy was to evaluate the liver glycogen storage in pregnant rats presenting neonatal streptozotocin-induced diabetes and to establish a relation with glycemia and insulin levels. wistar rats were divided in to two groups: 1) mild diabetes (stz) - received streptozotocin (glycemia from 120 to 300 mg/dl), 2) control - received vehicle (glycemia below 120 mg/dl). at days 0, 7, 14 and 21 of the pregnancy, body weight and glycemia were evaluated. at day 21 of the pregnancy, the rats were anesthetized for blood and liver collection so as to determine insulin and liver glycogen, which showed no changes in the stz group as compared to the controls. in the stz group, maternal weight gain were lower as compared to those in the control group. significantly increased glycemia was observed at days 0 and 14 of the pregnancy in the stz group. therefore, neonatally induced diabetes in the rats did not cause metabolic changes that impaired insulin and liver glycogen relation in these rats.
Neonatally-induced diabetes: lipid profile outcomes and oxidative stress status in adult rats
Sinzato, Yuri Karen;Lima, Paula Helena Ortiz;Campos, Kleber Eduardo de;Kiss, Ana Carolina Inhasz;Rudge, Marilza Vieira Cunha;Damasceno, Débora Cristina;
Revista da Associa??o Médica Brasileira , 2009, DOI: 10.1590/S0104-42302009000400010
Abstract: background: experimental models are developed for the purpose of enhancing the understanding of the pathophysiological mechanisms involved in diabetes. experimental findings lead to the development of treatment strategies to maintain metabolic conditions as close to normal as possible. there are several reports about streptozotocin induced mild diabetes to reproduce type 2 diabetes. however, studies about the interaction among glucose levels, lipid profile, and oxidative stress in these animals remain insufficient. therefore, this study evaluated these parameters in blood samples from adult wistar rats treated neonatally with streptozotocin. methods: female newborn wistar rats received streptozotocin (70 mg/kg, i.p.) on the 5th day of life (n5-stz). glycemia was measured in the 3rd and 4th month of life. at the end of the 4th month, blood samples were collected and processed for lipid profile and oxidative stress measurements. results: glycemia of n5-stz rats were significantly higher compared to those of control rats (p<0.05). there was no alteration in levels of total cholesterol, triglycerides, lipid peroxidation (tbars), sod activity and gsh-t determination (p>0.05) in the n5-stz animals when compared to control group. however n5-stz animals showed a significant decreased hdl-cholesterol rate (p<0.05). conclusion: this streptozotocin-induced diabetes model in rats caused hyperglycemia (120-360mg/dl), characterizing mild diabetes. this glycemic level led to hdl-lipoprotein alteration, which was not sufficient to impair antioxidant enzyme activities or determination of lipid peroxidation in adult life of rats. further this experimental investigation contributed to the understanding of different results found in other models for mild/moderate diabetes induction in laboratory animals as well as to a better comprehension of the pathophysiological mechanisms of mild diabetes or hyperglycemia in humans.
Neonatally Induced Mild Diabetes in Rats and Its Effect on Maternal, Placental, and Fetal Parameters
Yuri Karen Sinzato,Gustavo Tadeu Volpato,Isabela Lovizutto Iessi,Aline Bueno,Iracema de Mattos Paranhos Calderon,Marilza Vieira Cunha Rudge,Débora Cristina Damasceno
Journal of Diabetes Research , 2012, DOI: 10.1155/2012/108163
Abstract: The aim of this study was to assess placental changes and reproductive outcomes in neonatally induced mild diabetic dams and fetal development in their offspring. At birth, female rats were assigned either to control or diabetic group (100?mg of streptozotocin/Kg, subcutaneously). At adulthood, the female rats were mated. During pregnancy, the blood glucose levels and glucose and insulin tolerance tests were performed. At term, maternal reproductive outcomes, fetal and placental weight, and placental morphology were analyzed. Diabetic rats had smaller number of living fetuses, implantations and corpora lutea, and increased rate of embryonic loss. Placenta showed morphometric alterations in decidua area. Our results showed that mild diabetes was sufficient to trigger alterations in maternal organism leading to impaired decidua development contributing to failure in embryonic implantation and early embryonic losses. Regardless placental decidua alteration, the labyrinth, which is responsible for the maternal-fetal exchanges, showed no morphometric changes contributing to an appropriate fetal development, which was able to maintain normal fetal weight at term in mild diabetic rats. Thus, this experimental model of diabetes induction at the day of birth was more effective to reproduce the reproductive alterations of diabetic women. 1. Background Pregnant women with type 1 or type 2 diabetes are at increased risk of miscarriage, stillbirth, congenital malformations, placental abnormalities, and intrauterine malprogramming. Despite current treatments, maternal diabetes is an unfavorable environment for embryonic and fetoplacental development [1–7]. These important aspects of human diabetic pregnancies can be studied using the appropriate animal models [8], not only by ethical reasons but also by the multiplicity of uncontrolled variables that may modify the intrauterine environment [9]. Experimental models of severe diabetes (glycemia > 300?mg/dL), which reproduce the clinical conditions of poorly controlled type-1 diabetes, have been widely used [10–14]. However, only a few studies have evaluated the repercussions of diabetes on pregnant rats and/or their offspring [9, 15–18] using models of mild diabetes (glycemia between 120 and 300?mg/dL). In a previous study conducted at our laboratory [19], experimental mild diabetes induced at 5 days of life was not effective in reproducing the reproductive outcomes (miscarriage, fetal viability, and morbidity) observed in diabetic pregnant women. Although glycemic levels were consistent with those reported elsewhere,
Comparison of methods for the identification of coagulase-negative staphylococci
Cunha, Maria de Lourdes RS;Sinzato, Yuri K;Silveira, Liciana VA;
Memórias do Instituto Oswaldo Cruz , 2004, DOI: 10.1590/S0074-02762004000800012
Abstract: coagulase-negative staphylococci (cns) species identification is still difficult for most clinical laboratories. the scheme proposed by kloos and schleifer and modified by bannerman is the reference method used for the identification of staphylococcal species and subspecies; however, this method is relatively laborious for routine use since it requires the utilization of a large number of biochemical tests. the objective of the present study was to compare four methods, i.e., the reference method, the api staph system (biomérieux) and two methods modified from the reference method in our laboratory (simplified method and disk method), in the identification of 100 cns strains. compared to the reference method, the simplified method and disk method correctly identified 100 and 99% of the cns species, respectively, while this rate was 84% for the api staph system. inaccurate identification by the api staph method was observed for staphylococcus epidermidis (2.2%), s. hominis (25%), s. haemolyticus (37.5%), and s. warneri (47.1%). the simplified method using the simple identification scheme proposed in the present study was found to be efficient for all strains tested, with 100% sensitivity and specificity and proved to be available alternative for the identification of staphylococci, offering, higher reliability and lower cost than the currently available commercial systems. this method would be very useful in clinical microbiology laboratory, especially in places with limited resources.
Evaluation of neonatally-induced mild diabetes in rats: Maternal and fetal repercussions
Isabela L Iessi, Aline Bueno, Yuri K Sinzato, Kristin N Taylor, Marilza VC Rudge, Débora C Damasceno
Diabetology & Metabolic Syndrome , 2010, DOI: 10.1186/1758-5996-2-37
Abstract: Diabetes mellitus (DM) is a metabolic disorder characterized by hyperglycemia, insufficient insulin secretion, and receptor insensitivity to endogenous insulin. Its incidence is associated with high morbidity and mortality rates [1]. In pregnancies complicated by diabetes, hyperglycemia and alterations in lipid metabolism are associated with both maternal and fetal complications [2,3], causing reproductive abnormalities that enhance spontaneous abortion, congenital anomalies, and neonatal morbidity and mortality [4,5].Congenital anomalies are more common in infants of diabetic women than in children of nondiabetic women. The etiology, pathogenesis and prevention of diabetes-induced anomalies have spurred considerable clinical and basic research efforts. The infant of the diabetic mother also has increased risk for several neonatal complications, such as macrosomia, hypoglycemia, hypocalcemia, polycythemia and hyperbilirubinemia. Up to 25% of such offspring have been reported with these complications. It also appears that early detection and subsequent strict metabolic control of pregnant women with diabetes in pregnancy should decrease the frequency and severity of some of these short- and long-term complications in the offspring of the diabetic mother [4].Despite increased clinical efforts to improve glycemic control during diabetic pregnancy, however, the rate of congenital malformations remains increased in studies of Diabetes mellitus (DM) of type 1 [6-9], DM type 2 [9-12], and gestational diabetes (GDM) [10,13]. The prevalence of major congenital malformations is approximately three to five times higher in infants of diabetic mothers [14-17] and is presently the most common cause of perinatal death among these infants [18,19]. Diabetes is associated with a variety of anomalies, primarily cardiovascular, neurological, and musculoskeletal [20]. The malformation considered to be most pathognomic to the infants of diabetic mothers - caudal regression syndrome or sa
Histopathological placental lesions in mild gestational hyperglycemic and diabetic women
Marilza VC Rudge, César P Lima, Débora C Damasceno, Yuri K Sinzato, Gustavo Napoli, Cibele VC Rudge, Franciane Q Gallego, Iracema MP Calderon
Diabetology & Metabolic Syndrome , 2011, DOI: 10.1186/1758-5996-3-19
Abstract: One-hundred-and-thirty-one placental samples were collected from Diabetes mellitus (DM) positive screened patients. Two diagnostic tests, glycemic profile and 100 g oral glucose tolerance test (OGTT) in parallel identified 4 groups normoglycemic, mild gestational hyperglycemia (MGH), gestational DM (GDM) or overt DM (DM). Placental tissue specimens and sections from 4 groups were obtained by uniform random sampling and stained with hematoxylin-eosin.Placentas from MGH group presented 17 types of histopathological change and higher rates of syncytial nodes and endarteritis. GDM placentas presented only nine types of histopathological change, high rates of dysmaturity, low rates of calcification and no syncytial nodes. Overt DM placentas showed 22 types of histopathological change, 21 of which were present in the preterm period. There were histopathological similarities between MGH and DM placentas, but the former exhibited a higher incidence of endarteritis, which has been described as a "post-mortem" phenomenon.Our results confirmed that the distinct placental changes associated with DM and MGH depend on gestational period during which the diabetic insult occurs. It may reasonably be inferred that subclinical maternal hyperglycemia during pregnancy, as showed in MGH group, is responsible for increased placental endarteritis, a postmortem lesion in the live fetus.The placenta is a maternal-fetal organ that separates the maternal and fetal circulations and plays a central metabolic role in pregnancy. The placenta of diabetic women has attracted much interest, primarily because it is thought that placental damage may be partially responsible for the high incidence of fetal complications in pregnancies complicated by Diabetes mellitus [1]. Glucose is the main nutrient that passes to the fetus by facilitated diffusion. Thus, increased amounts of glucose may reach the fetus by facilitated transport through the placenta [2]. Therefore, adaptations in cells that are in cont
Effects of exposure to cigarette smoke prior to pregnancy in diabetic rats
Débora C Damasceno, Yuri K Sinzato, Paula H Lima, Maricelma S de Souza, Kleber E Campos, Bruna Dallaqua, Iracema M Calderon, Marilza V Rudge, Gustavo T Volpato
Diabetology & Metabolic Syndrome , 2011, DOI: 10.1186/1758-5996-3-20
Abstract: Diabetes was induced by streptozotocin and cigarette smoke exposure was conducted by mainstream smoke generated by a mechanical smoking device and delivered into a chamber. Diabetic female Wistar rats were randomly distributed in four experimental groups (n minimum = 13/group): nondiabetic (ND) and diabetic rats exposed to filtered air (D), diabetic rats exposed to cigarette smoke prior to and into the pregnancy period (DS) and diabetic rats exposed to cigarette smoke prior to pregnancy period (DSPP). At day 21 of pregnancy, rats were killed for maternal biochemical determination and reproductive outcomes.The association of diabetes and cigarette smoke in DSPP group caused altered glycemia at term, reduced number of implantation and live fetuses, decreased litter and maternal weight, increased pre and postimplantation loss rates, reduced triglyceride and VLDL-c concentrations, increased levels of thiol groups and MDA. Besides, these dams presented increased SOD and GSH-Px activities. However, the increased antioxidant status was not sufficient to prevent the lipid peroxidation observed in these animals.Despite the benefits stemming from smoking interruption during the pregnancy of diabetic rats, such improvement was insufficient to avoid metabolic alterations and provide an adequate intrauterine environment for embryofetal development. Therefore, these results suggest that it is necessary to cease smoking extensive time before planning pregnancy, since stopping smoking only when pregnancy is detected may not contribute effectively to fully adequate embryofetal development.Diabetes mellitus (DM) is a group of diseases characterized by high blood glucose levels that result from defects in the body's ability to produce and/or use insulin [1]. In pregnancies complicated by diabetes, hyperglycemia and lipid metabolism alterations are associated with both maternal and fetal complications [2,3], causing reproductive abnormalities that enhance spontaneous abortion, congenit
Repercussions of mild diabetes on pregnancy in Wistar rats and on the fetal development
Felipe H Saito, Débora C Damasceno, Wilma G Kempinas, Glilciane Morceli, Yuri K Sinzato, Kristin N Taylor, Marilza VC Rudge
Diabetology & Metabolic Syndrome , 2010, DOI: 10.1186/1758-5996-2-26
Abstract: In the 1st induction, female offspring were distributed into two experimental groups: Group streptozotocin (STZ, n = 67): received the β-cytotoxic agent (100 mg STZ/kg body weight - sc) on the 1st day of the life; and Non-diabetic Group (ND, n = 14): received the vehicle in a similar time period. In the adult life, the animals were mated. After a positive diagnosis of pregnancy (0), female rats from group STZ presenting with lower glycemia than 120 mg/dL received more 20 mg STZ/kg (ip) at day 7 of pregnancy (2nd induction). The female rats with glycemia higher than 120 mg/dL were discarded because they reproduced results already found in the literature. In the mornings of days 0, 7, 14 and 21 of the pregnancy glycemia was determined. At day 21 of pregnancy (at term), the female rats were anesthetized and killed for maternal reproductive performance and fetal development analysis. The data were analyzed using Student-Newman-Keuls, Chi-square and Zero-inflated Poisson (ZIP) Tests (p < 0.05).STZ rats presented increased rates of pre (STZ = 22.0%; ND = 5.1%) and post-implantation losses (STZ = 26.1%; ND = 5.7%), reduced rates of fetuses with appropriate weight for gestational age (STZ = 66%; ND = 93%) and reduced degree of development (ossification sites).Mild diabetes led a negative impact on maternal reproductive performance and caused intrauterine growth restriction and impaired fetal development.Diabetes mellitus (DM) is characterized by disarrangement of the metabolism of carbohydrates, proteins and lipids caused by the complete or relative insufficiency of insulin secretion and/or insulin action [1]. DM is not a disease but rather a heterogeneous group of syndromes characterized by elevated glucose levels caused by the absolute or relative deficiency of insulin. DM can be classified into: type-1 diabetes (DM1), type-2 diabetes (DM2) and gestational diabetes (DMG). DM1 mainly affects children and young people and results in the destruction of beta (β)-pancreas cell
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