Non-diabetic individuals use hormones like insulin to improve muscle strength and performance. However, as insulin also leads the liver and the adipose tissue to an anabolic state, the purpose of this study was to investigate the effects of insulin on liver metabolism in trained non-diabetic Swiss mice. The mice were divided into four groups: sedentary treated with saline (SS) or insulin (SI) and trained treated with saline (TS) or insulin (TI). Training was made in a vertical stair, at 90% of the maximum load, three times per week. Insulin (0.3 U/kg body weight) or saline were given intraperitoneally five times per week. After eight weeks, tissue and blood were collected and in situ liver perfusion with glycerol+lactate or alanine+glutamine (4 mM each) was carried out. The trained animals increased their muscle strength (+100%) and decreased body weight gain (–11%), subcutaneous fat (–42%), mesenteric fat (–45%), and peritoneal adipocyte size (–33%) compared with the sedentary groups. Insulin prevented the adipose effects of training (TI). The gastrocnemius muscle had greater density of muscle fibers (+60%) and less connective tissue in the trained groups. Liver glycogen was increased by insulin (SI +40% and TI +117%), as well as liver basal glucose release (TI +40%). Lactate and pyruvate release were reduced to a half by training. The greater gluconeogenesis from alanine+glutamine induced by training (TS +50%) was reversed by insulin (TI). Insulin administration had no additional effect on muscle strength and reversed some of the lipolytic and gluconeogenic effects of the resistance training. Therefore, insulin administration does not complement training in improving liver glucose metabolism.
Hypertriglyceridemia is a predisposing factor for several metabolic diseases in the worldtoday. Their cause is multifactorial, several factors are directly linked to the modification ofplasma lipid metabolism, among them are genetics and exercise. The genic overexpression ofapoCIII makes the animal hypertriglyceridemic and high levels of blood cholesterol, enablingfurther studies to be done on its metabolic profile. This study investigates how apoCIIIoverexpression and exercise modify the metabolism of genetically modified mice, especiallytheir energy expenditure. We used 15-month-old male C57Bl/6 mice, subdivided into 4groups: 2 NTG groups (non-transgenic mice that were submitted to training and theircontrols) and 2 CIII groups (transgenic Mice with basal triglyceridemia above 300mg/dL thatwere submitted to training and their controls). The exercised groups underwent for 8 weeks amoderate intensity training for 40 minutes 3 times a week. All animals were submitted to astress test to evaluate performance and energy expenditure. The trained animals had higherenergy expenditure during all stages of the test (p<0.01) and the area under curve of the EEshowed that the trained animals had higher caloric consumption (p<0.001), while the animalCIII sed had a much higher energy expenditure than its control NTG sed (p<0.001). Weconclude that dyslipidemia makes the CIII animal less fit for exercise, and trained animalshave lower energy expenditure independent of dyslipidemia and produced more work.
O aprimoramento genético de aves tem sido usado com o objetivo de maximizar a produção de carne de frango. Assim, técnicas de manejo têm se destacado, pois melhoram a rentabilidade e reduzem os custos de produção, uma vez que otimizam o ganho de peso das aves e aceleram o abate. Todavia, o acelerado ganho de peso pode tornar os animais suscetíveis a transtornos metabólicos em decorrência da falta de adaptação do aparelho cardiorrespiratório cujo funcionamento se relaciona à temperatura ambiente e à inervação cardíaca. Desta forma, o objetivo deste estudo foi avaliar a influência do estresse térmico agudo sobre o coração de frangos de granja, avaliando o epicárdio, os vasos epicárdicos e os aspectos quantitativos, morfológicos, morfométricos e histopatológicos do plexo cardíaco. Para tanto, foram utilizados 14 animais machos divididos em dois grupos (n=7): animais mantidos em ambiente de conforto térmico (18oC) e animais em ambiente de estresse térmico (mantidos a 32o C nas 12 horas prévias ao abate). Os resultados mostraram que o estresse térmico diminuiu a área dos adipócitos, a área e o comprimento dos gânglios cardíacos, aumentou o colágeno total dos adipócitos e diminuiu o colágeno total dos vasos e gânglios do coração. Pode-se concluir que de fato o estresse térmico agudo interferiu nos parâmetros avaliados, pois várias alterações histopatológicas foram identificadas tais como a presença de infiltrados linfocitários nos adipócitos do tecido epicárdico, edema, congestão vascular, infiltração de fibrina nos gânglios do plexo cardíaco e ganglionite.
Estresse é uma resposta não específica do organismo a condições adversas, podendo, quando aplicado de maneira constante durante a infância, gerar consequências graves e duradouras. Assim, o objetivo deste estudo foi avaliar os efeitos do estresse psicológico aplicado na fase juvenil do desenvolvimento sobre o plexo cardíaco de ratos machos da linhagem Wistar. Os animais foram distribuídos em dois grupos: Controle (GC; n=3) e Estresse Psicológico (EP; n=4). Os procedimentos de estresse foram aplicados durante três dias consecutivos a partir dos 25 dias de vida pós-natal. O grupo EP foi submetido à exposição ao predador (gato) durante duas sessões de 10 minutos com intervalo de 5 minutos. A eutanásia foi realizada aos 64 dias de idade e os corações coletados, fixados e processados histologicamente. Cortes de 5 µm foram corados pelas técnicas de Giemsa, Hematoxilina-Eosina e Picro-sirius a fim de que análises morfométricas, morfológicas e quantitativas dos neurônios e de fibras colágenas associadas ao plexo cardíaco fossem realizadas. Os resultados demonstraram que o estresse psicológico por exposição ao predador provocou diminuição da área neuronal e do número de neurônios, aumento do peso corporal e predispôs deposição de fibras colágenas do tipo I no plexo cardíaco.
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