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Comparação entre 2 protocolos para indução do DM2 e avaliação do efeito do exercício físico moderado sobre a lipotoxicidade e os eicosanóides / Comparison between 2 protocols for T2D induction and evaluation of the effect of moderate physical exercise on lipotoxicity and eicosanoidsLima, Kamila Lauany Lucas 26 October 2018 (has links)
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Previous issue date: 2018-10-26 / Conselho Nacional de Pesquisa e Desenvolvimento Científico e Tecnológico - CNPq / The present study aimed to test whether: 1) the high fat diet can induce T2D without the
administration of streptozotocin (STZ); 2) the high fat caloric intake causes metabolic,
behavioral and morphological changes, similar to t2D and; 3) the practice of moderate physical
exercise is effective to reverse the metabolic changes caused by T2D and of the high fat diet.
To test these hypotheses, we used 57 Wistar 8 week old rats. They were splited into the five
experimental groups: group D (N = 25) who received a single intraperitoneal dose of
streptozotocin (STZ diluted in citrate buffer, pH 4.5-25mg / kg body weight of the animal) and
were fed with high fat diet. To test the effect only of the high fat diet, the HL group (N = 8) was
fed with high fat diet but did not receive the STZ injection. Animals with similar ages were used
as control (CO, N = 24) and fed with a balanced diet. At the end of the third week, animals of
CO and D and HL groups were subdivided into two other groups: sedentary (SE) and exercised
(EF). EF groups were submitted to swimming for 6 weeks. The D-SE, D-EF and HL-SE groups
presented significant changes in body weight gain, abdominal fat gain, caloric intake, food
efficiency, lipid profile and fasting and capillary glucose levels, when compared to control
groups. There was no significant difference in the concentrations of arachidonic acid products
and the renal tissue did not present morphological alterations. Physical exercise increased high
density lipoproteins (HDL), but did not change others evaluated parameters. We conclude that
consumption of the high fat diet when associated with sedentary behavior may cause
metabolic alterations similar to T2D and that physical exercise was efficient to improve the lipid
profile. / Os objetivos do presente estudo foram investigar as seguintes hipóteses: 1) a dieta
hiperlipídica pode induzir o Diabetes Mellitus tipo 2 (DM2) sem a administração de
streptozotocina (STZ); a ingestão de dieta hiperlipídica e hipercalórica causam alterações
metabólicas, comportamentais e morfológicas, similares ao DM2 e; 3) a prática de exercício
físico moderado tem potencial sobre as alterações metabólicas causadas pelo DM2 e pela dietahiperlipídica. Para testarmos essas hipóteses foram utilizados 57 ratos Wistar com 8 semanas
de idade, distribuídos nos seguintes grupos experimentais: grupo D (N=25) que receberam
uma única injeção intraperitoneal de estreptozotocina (STZ diluído em tampão de citrato, pH
4,5 - 25mg/kg de peso corporal do animal) e foram alimentados com dieta hiperlipídica. Para
testar o efeito somente da dieta hiperlipídica, o grupo HL (N=8), recebeu uma dieta
hiperlipídica, mas não recebeu a injeção de STZ. Animais com idades similares foram utilizados
como controle (CO, N=24) e alimentados com dieta balanceada. No final da terceira semana,
animais dos grupos CO e D e HL foram subdivididos em dois grupos: sedentário (SE) e
exercitado (EF). Os grupos EF foram submetidos a um protocolo de natação durante 6
semanas. Após o protocolo experimental, os grupos D-SE, D-EF e HL-SE apresentaram
alterações significativas no ganho de massa, gordura abdominal, ingestão calórica, eficiência
alimentar, perfil lipídico e glicemia em jejum e capilar quando comparados aos animais
controles. Não houve diferença significativa nas concentrações dos produtos do ácido
araquidônico e o tecido renal não apresentou alterações morfológicas. O exercício físico
aumentou as lipoproteínas de alta densidade (HDL), mas não alterou os demais parâmetros
avaliados.
Concluímos
que
o
consumo
da
dieta
hiperlipídica
quando
associada
ao
comportamento sedentário pode causar alterações metabólicas similares ao DM2 e que o
exercício físico foi eficiente para melhorar o perfil lipídico.
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Développement et caractérisation d'un nouveau modèle expérimental de la maladie d'Alzheimer chez le rat non transgénique / Development and characterisation of a new experimental model of Alzheimer's disease in non-transgenic ratMaleysson, Vincent 06 January 2016 (has links)
La maladie d'Alzheimer (MA) est caractérisée par un déclin progressif des fonctions cognitives avec une détérioration de la mémoire, une atrophie cérébrale et deux lésions histologiques caractéristiques retrouvées lors d'examens post-mortem : les plaques extracellulaires de peptide β-amyloïde et les enchevêtrements intracellulaires de la protéine Tau anormalement phosphorylée. De nombreux modèles animaux de la MA ont été développés afin de comprendre et de tester différents traitements dirigés contre cette pathologie. Cependant, aucun modèle de rongeur non transgénique, développant à la fois les plaques amyloïdes et la pathologie neurofibrillaire, n'est disponible à ce jour. L'objectif de cette étude est de développer le premier modèle non transgénique, développant les deux lésions histologiques caractéristiques de la MA chez le rat. Le principe consiste à réaliser une injection concomitante et intrahippocampale d'un AAV (virus associé aux adénovirus) recombinant contenant le gène humain de la protéine Tau présentant la mutation P301L, et du peptide Aβ1-42 qui est le principal composant des plaques amyloïdes. Après plusieurs expériences, nous avons obtenu un modèle animal représentatif des stades précoces de la MA, c'est-à-dire avec des lésions focalisées dans l'une des premières structures du cerveau affectée par la MA : l'hippocampe. La présence des deux lésions histopathologiques caractéristiques de la maladie, accompagnée d'une astrocytose, a été observée par immunohistofluorescence. Une détérioration de la mémoire concernant plus particulièrement la mémoire de travail, ainsi que des anormalités de l'activité électrique cérébrale et notamment durant les phases de sommeil paradoxal, enregistrées par électroencéphalographie, ont également été mises en évidence. / Alzheimer's disease (AD) is characterized by a progressive decline in cognitive function with a memory impairment, a brain atrophy, and two histological hallmarks observed from post-mortem examination: extracellular β-amyloid plaques and intracellular tangles of the Tau protein abnormally phosphorylated. Numerous animal models of AD have been developed to understand and to test drugs against this pathology. However, any non-transgenic model of rodent developing amyloid plaques and the neurofibrilary pathology is currently available. The aim of this study is to develop the first non-transgenic model producing the two histopathological features of AD in the rat. The principle is to perform a concomitant intrahippocampal injection of a recombinant AAV (Adeno-Associated Virus) containing the human transgene tau with the P301L mutation, and of Aβ1-42 peptide, the main component of the amyloid plaques. After several experiments, we have obtained an animal model representative of the early steps of AD, i.e. with lesions focalized in one of the first affected brain structures in the AD: the hippocampus. The presence of the two histopathological hallmarks has been observed by immunohistofluorescence and associated with an astrogliosis. A memory impairment concerning more particulary the working memory, and abnormalities of the electrical activity of the brain and of the rapid eye movement sleep recorded by electroencephalography, are also characterized.
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