1000 resultados para experimental hyperthyroidism
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Aims. To analyze the influence of hyperthyroidism on the gene expression and serum concentration of leptin, resistin, and adiponectin in obese animals. Main Methods. Male Wistar rats were randomly divided into two groups: control (C)fed with commercial chow ad libitumand obese (OB)fed with a hypercaloric diet. After group characterization, the OB rats continued receiving a hypercaloric diet and were randomized into two groups: obese animals (OB) and obese with 25g triiodothyronine (T3)/100BW (OT). The T3 dose was administered every day for the last 2 weeks of the study. After 30 weeks the animals were euthanized. Samples of blood and adipose tissue were collected for biochemical and hormonal analyses as well as gene expression of leptin, resistin, and adiponectin. Results. T3 treatment was effective, increasing fT3 levels and decreasing fT4 and TSH serum concentration. Administration of T3 promotes weight loss, decreases all fat deposits, and diminishes serum levels of leptin, resistin, and adiponectin by reducing their gene expression. Conclusions. Our results suggest that T3 modulate serum and gene expression levels of leptin, resistin, and adiponectin in experimental model of obesity, providing new insights regarding the relationship between T3 and adipokines in obesity. Copyright © 2012 Renata de Azevedo Melo Luvizotto et al.
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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
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Role of reactive oxygen species (ROS)/nitric oxide (NO) balance and renin-angiotensin system in mediating cardiac hypertrophy in hyperthyroidism was evaluated in an in vivo and in vitro experimental model. Male Wistar rats were divided into four groups: control, thyroid hormone, vitamin E (or Trolox, its hydrosoluble analogue), thyroid hormone + vitamin E. Angiotensin II receptor (AT1/AT2) gene expression, immunocontent of AT1/AT2 receptors, angiotensinogen, NADPH oxidase (Nox2), and nitric oxide synthase isoforms, as well as ROS concentration (hydrogen peroxide and superoxide anion) were quantified in myocardium. Thyroid hormone increased ROS and NO metabolites, iNOS, nNOS and eNOS isoforms and it was accompanied by cardiac hypertrophy. AT1/AT2 expression and the immunocontent of angiotensinogen and Nox2 were enhanced by thyroid hormone. Antioxidants reduced ROS levels, Nox2, AT1/AT2, NOS isoforms and cardiac hypertrophy. In conclusion, ROS/NO balance may play a role in the control of thyroid hormone-induced cardiac hypertrophy mediated by renin-angiotensin system. (C) 2011 Elsevier Ireland Ltd. All rights reserved.
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In this study, we investigated the oxidative stress influence in some prosurvival and proapoptotic proteins after myocardial infarction (MI). Male Wistar rats were divided in two groups: Sham-operated (control) and MI. MI was induced by left coronary artery occlusion. 28-days after surgery, echocardiographic, morphometric, and hemodynamic parameters were evaluated. Redox status (reduced to oxidized glutathione ratio, GSH/GSSG) and hydrogen peroxide levels (H(2)O(2)) were measured in heart tissue. The p-ERK/ERK, p-Akt/Akt, p-mTOR/mTOR and p-GSK-3 beta/GSK-3 beta ratios, as well as apoptosis-inducing factor (AIF) myocardial protein expression were quantified by Western blot. MI group showed an increase in cardiac hypertrophy (23%) associated with a decrease in ejection fraction (38%) and increase in left ventricular end-diastolic pressure (82%) when compared to control, characterizing ventricular dysfunction. Redox status imbalance was seen in MI animals, as evidenced by the decrease in the GSH/GSSG ratio (30%) and increased levels of H(2)O(2) (45%). This group also showed an increase in the ERK phosphorylation and a reduction of Akt and mTOR phosphorylation when compared to control. Moreover, we showed a reduction in the GSK-3 beta phosphorylation and an increase in AIF protein expression in MI group. Taken together, our results show increased H(2)O(2) levels and cellular redox imbalance associated to a higher p-ERK and AIF immunocontent, which would contribute to a maladaptive hypertrophy phenotype.
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Há poucos estudos analisando a importante relação entre o exercício físico, agudo e crônico, e alterações metabólicas decorrentes do hipertireoidismo. O objetivo do presente estudo foi analisar o efeito de quatro semanas de treinamento aeróbio sobre o perfil lipídico de ratos com hipertireoidismo experimental. Foram utilizados 45 ratos da linhagem Wistar, divididos aleatoriamente em quatro grupos: Controle Sedentário (CS) - administrados com salina durante o período experimental, não praticaram exercício físico (n = 12); Controle Treinado (CT) - administrados com salina, participaram do treinamento (n = 11); Hipertireoidismo Sedentário (HS) - induzidos ao hipertireoidismo, não praticaram exercício físico (n = 12); e Hipertireoidismo Treinado (HT) - induzidos ao hipertireoidismo, participaram do treinamento (n = 10). O treinamento aeróbio teve duração de quatro semanas, cinco vezes na semana, com duração de uma hora por sessão. Após o término do período experimental todos os ratos foram anestesiados em câmara de CO2 até sua sedação. Coletaram-se amostras de sangue para dosagem de colesterol total, triglicerídeos, HDL-colesterol e LDL-colesterol e hormônio T3; e amostras do coração, fígado, músculo gastrocnêmio e tecido adiposo das regiões mesentérica, retroperitonial e subcutânea para pesagem e dosagem de triglicerídeos. Para análise estatística utilizou-se ANOVA two-way, seguida do post hoc LSD de Fischer. Observaram-se menores valores de AGL no grupo HS quando comparado ao CS. O grupo HS teve nível de triglicerídeos significativamente superior nas regiões mesentérica, do gastrocnêmio e retroperitonial quando comparado com os grupos CS e CT, e apenas o tecido adiposo da região retroperitonial apresentou diferenças significativas na qual o grupo HT apresentou menor peso quando comparado com o grupo CS. Pode-se concluir que os ratos hipertireoidicos apresentaram perfil lipídico diferente dos ratos controle, e o treinamento aeróbio em ratos Wistar pode ter alterado o perfil lipídico dos animais com hipertireoidismo experimental quando comparados com o grupo sedentário e grupos controle.
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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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Thyrotoxicosis, a condition in which there is an excessive amount of circulating thyroid hormones, leads to reduced glycogen content in different tissues. In this study we analyzed the effects of aerobic swimming training on liver, heart, and skeletal muscle glycogen content in experimentally induced thyrotoxicosis. Wistar male rats were divided into euthyroid sedentary (ES, n = 12), euthyroid trained (ET, n = 11), thyrotoxic sedentary (TS, n = 12), and thyrotoxic trained (TT, n = 10) groups. Thyrotoxic groups received daily i.p. doses of T4 (sodium levothyroxine, 25 mu g/100 g body mass) through the experimental period, and trained groups swam for 1 h at 80% of the aerobic-anaerobic transition intensity, 5 days/week for 4 weeks. Heart and liver glycogen stores were similar to 30% lower in T4 treated compared with nontreated groups, but were not changed by training status. on the other hand, glycogen content in mixed fiber type gastrocnemius of TT was 1.5- to 2.3-fold greater than those in other groups, whereas no significant differences were found for the slow soleus muscle. Increased gastrocnemius but not soleus, liver, or heart glycogen indicates that in mild long-term thyrotoxicosis chronic swimming affects glycogen stores in a tissue-specific manner.
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Hyperthyroidism can result in serious effects on the bone metabolism in humans as well as animals. For a better characterization of thyrotoxicosis effects, 16 cats were induced into thyrotoxicosis by intaking a dose of 150 μg/kg of sodium L-thyroxine every 24 hours during 42 days. The hormonal levels were evaluated by radioimmunoassay technique and the bone mineral density of the right distal radius extremity was measured through the radiographic optical densitometry. Was verified significant bone demineralization seven days of hormonal intake as weel as radius demineralization.
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Feline hyperthyroidism (thyrotoxicosis) is now recognised as the most common endocrine disease of the domestic cat. Feline hyperthyroidism cause multisystemic disorder associated with incresead circulating concentrations of the thyroid hormones, tri-iodothyronine (T3) and thyroxine (T4). Cardiovascular abnormalities in cats with spontaneous hyperthyroid have been described. Objective to determine heart size of progressing experimental thyrotoxicosis of 19 cats, using a vertebral scale system (VHS). The lateral, dorsoventral e ventrodorsal radiographs thoracic were measured using a vertebral scale system. Lateral radiographs thoracic to efficient develop that DV and VD. The VHS method is easy to use, allows objective assesment of heart size in cats hyperthyroid, and may be helpful to identify cardiomegaly and heart size progressing.
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Hyperthyroidism is and endocrinal dysfunction characterized by excessive serum concentrations of thyroid gland hormones, which can cause several effects on the bone tissue in humans and in animals. For a better characterization of thyrotoxicosis effects on bone metabolism, 16 cats were induced into hyperthyroid state. Results showed that, in some moments a major bone demineralization of the right distal radium estremity promoted an elevation of the serum levels of phosphorus and total alkaline phosphatase.
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Pós-graduação em Medicina Veterinária - FMVZ
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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)