Navegando por Palavras-chave "metabolismo energético"

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    Avaliação morfofuncional e estresse oxidativo no intestino de camundongos distróficos (mdx)
    (Universidade Federal de São Paulo (UNIFESP), 2014-12-17) Alves, Gabriel Andrade [UNIFESP]; Nouailhetas, Viviane Louise Andree Nouailhetas [UNIFESP]; Universidade Federal de São Paulo (UNIFESP)
    Dystrophin is a component of the complex of dystrophin-associated proteins, which connects the cytoskeleton to the plasma membrane and the extracellular matrix. Their lack causes Duchenne Muscular Dystrophy (DMD), characterized by a progressive degeneration of skeletal and cardiac muscle, leading to death in patients third decade of life. Although DMD patients had gastrointestinal symptoms such as diarrhea and pseudo obstruction, little is known of the role of dystrophin in the intestinal smooth muscle (MLI). We aim to understand what is the role of dystrophin protein in MLI: structurally and functionally, muscle contraction. Specifically studied animal model (mdx mice), and assess the structure and ultrastructure of the ILM, the resistance loss of contractile response of the MLI exposed stretch, a loss of contractile response in medium without Ca2 + (essential for contraction) and recovery contractile respota with the replacement of the ion in the presence or absence of nifedipine (blocker Cav1.2b). Observe surprising resistance to loss of response during stretch despite the animal gut dystrophic have structural mucosal deficit and have demonstrated loss of muscle layer (30%) compared to the control, present degenerate mitochondria and sarcoplasmic reticulum change. The response in medium without calcium, dystrophic animals was more resistant both to the loss of contraction in medium without Ca2 +, as the recovery of contractility with replacement ion. Dystrophin has a peculiar role in MLI, different from that of skeletal muscle, because despite the visible structural deficit, there was an increase in resistance to loss of contractility stretch. The dystrophic mdx mice also presents kinetics in response to varying external impaired calcium concentration (thus probably with changes in Cav1.2b), which may help to understand symptoms present in DMD patients.
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    Maternal obesity and late effects on offspring metabolism
    (Sociedade Brasileira de Endocrinologia e Metabologia, 2014-04-01) Vido, Daniele Sá; Nejm, Mariana Bocca; Silva, Neila Ribeiro; Silva, Sylvia Maria Affonso [UNIFESP]; Cravo, Sergio Luiz [UNIFESP]; Luz, Jacqueline [UNIFESP]; Universidade Federal de São Paulo (UNIFESP)
    Objective : The aim of this study was to evaluate the late effects of maternal obesity induced by lesion of the ventromedial hypothalamus on offspring metabolism.Materials and methods : Thirty days after the bilateral lesion of the ventromedial hypothalamus, female rats were mated and divided into 2 groups of pregnant animals: Control (C) – false lesion (sham) and Obese (OB) – lesion. Three months after that, with the groups of mothers, offspring were divided into control and obese animals that received a normocaloric diet (C-N and OB-N), and control and obese animals that received a hypercaloric diet (C-H and OB-H). At 120 days of age, the animals were euthanized and their carcasses, feces and food were submitted to calorimetric analysis to determine energy balance and body composition.Results : During the growth period, offspring from obese mothers showed higher values of body weight and food intake than controls. Obese animals showed higher body weight gain and gross food efficiency than control animals in adulthood. The hypercaloric diet led to increased metabolizable energy intake, percentage of absorbed energy and energy expenditure in both groups. Body composition was only affected by the association of hypercaloric diet and maternal obesity that led to increased body fat.Conclusions : Maternal obesity has led to the development of later overweight in offspring, suggesting fetal programming. According to the trend presented, it is believed that the prolonged intake of hypercaloric diets in adult animals may, as an additional effect, induce worsening of the overweight induced by maternal obesity. Arq Bras Endocrinol Metab. 2014;58(3):301-7