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Fumonisins are naturally occurring mycotoxins that contaminate food for human and animal consumption. They have neurotoxic effects, but the mechanisms by which these toxins affect the nervous system are not fully known. In the present study, male Wistar rats were fed between 21 and 63 days of age with diets that contained fumonisins B1+B2 at 0, 1, and 4 mg/kg. The following variables were assessed: food consumption, growth, body weight gain, and blood parameters. Morphoquantitave analyses of the most metabolically active myenteric neurons were performed, detected by NADH-diaphorase activity. Nitrergic neurons were detected by NADPH-diaphorase activity. The fumonisin-containing diets did not significantly alter food consumption or the body or plasma parameters. These diets decreased the metabolic activity of jejunal myenteric neurons, reducing neuronal density of the most metabolic active neurons by 30.8% and the cell body area by 4.3%. The diets also decreased the cell body area of nitrergic neurons by 22.1%. The effects of fumonisin B1 on the respiratory metabolism of isolated mitochondria in the brain and liver were also assessed. A decrease in oxygen consumption up to a 29% in the brain and 38% in the liver was observed in mitochondrial isolates to which 50 µM fumonisin B1 was added. The decrease in respiratory activity that was triggered by exposure to fumonisins was related to the lower metabolic activity of myenteric neurons, which had a negative impact on neuroplasticity of the enteric nervous system.

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The impact of oral supplementation with an effervescent glutamine formulation on the beneficial effects of antiretroviral therapies was evaluated in people living with HIV/AIDS. For this purpose, 12 HIV/AIDS carrier patients with CD4+ T cell counts <500, and who had received the same antiretroviral therapy for at least 1 year before starting this investigation were selected. The patients were required to dissolve the effervescent glutamine formulation (supplied in sachets) in water immediately before oral ingestion (12.4 g), once a day, after lunch or after dinner during 30 days. CD4+ T cell counts, complete blood cell counts, serum cytokines, and amino acids levels were quantified; biochemical and toxicological measurements were performed. The numbers of CD4+ T cells were increased (P < .05), and the serum C-reactive protein levels decreased (P < .01) after the administration of effervescent glutamine formulation. Serum levels of interferon-gamma inducible protein-10, RANTES, and macrophage inflammatory protein-1ß were decreased after the treatment with effervescent glutamine formulation. No changes were observed in the serum levels of amino acids, hematological, toxicological, and biochemical parameters. In conclusion, the treatment during 30 days with effervescent glutamine formulation was well tolerated, promoted reduction of inflammation, and improved the beneficial effects of antiretroviral therapies in HIV/AIDS carrier patients.

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ABSTRACT We developed a pre-clinical model in which to evaluate the impact of orally administered carbohydrates on postprandial blood glucose levels. For this purpose, we compared the effects of different carbohydrates with well-established glycemic indexes. We orally administered (gavage) increasing amounts (0.2, 0.4, 0.6, 0.8, and 1.0 g/kg) of sucrose and lactose to rats which had been fasted for 6 h or 15 h, respectively. In part of the experiments we administered frutose (gavagem). Three different models were compared for measuring postprandial blood glucose levels: a) evaluation of interstitial glucose concentrations by using a real time continuous glucose monitoring system; b) evaluation of glucose levels in blood obtained from the rat tail; c) evaluation of serum glucose levels in blood collected after decapitation. Our results showed that blood obtained from the tails of 15-h fasted rats was the best model in which to evaluate the effect of carbohydrates on postprandial blood glucose levels.

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ABSTRACT The effect of glutamine dipeptide (GDP) supplementation in patients with diabetic foot syndrome was evaluated. A total of 22 patients took part in the study. GDP was supplied in 10 g sachets, and was dissolved in water immediately before use, with ingestion once a day, after lunch or after dinner (20 g/day) over a period of 30 days. Quantification of foot insensitive areas, oxidative stress, blood cytokines, and biochemical, hematological and toxicological parameters was performed before and after GDP supplementation. We observed an increase in blood levels of interferon-α (P=0.023), interferon-γ (P=0.038), interleukin-4 (P=0.003), interleukin-6 (P=0.0025), interleukin-7 (P=0.028), interleukin-12 p40 (P=0.017), interleukin-13 (P=0.001), leukocytes (P=0.037), eosinophils (P=0.049), and typical lymphocytes (P<0.001) due to GDP administration. In addition, we observed a reduced number (P=0.048) of insensitive areas on the foot, and reduction (P=0.047) of fasting hyperglycemia. Patients also showed increased blood high density lipoprotein (P<0.01) and protein thiol groups (P=0.004). These favorable results were associated with the absence of renal and hepatic toxicity. These results are of clinical relevance, since supplementation with GDP over 30 days improved clinical responses in patients with diabetic foot syndrome.

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AIMS: Liver glycogen catabolism was evaluated in male Swiss mice fed a high-fat diet rich in saturated fatty acids (HFD) or normal fat diet (NFD) during one week. MAIN METHODS: Liver glycogenolysis (LG) and liver glucose production (LGP) were measured either under basal or stimulated conditions (infusion of glycogenolytic agents). Thus, isolated perfused livers from HFD and NFD mice were infused with glycogenolytic agents, i.e., glucagon, epinephrine, phenylephrine, isoproterenol, adenosine-3'-5'-cyclic monophosphate (cAMP), N(6),2'-O-dibutyryl-cAMP (DB-cAMP), 8-bromoadenosine-cAMP (8-Br-cAMP) or N(6)-monobutyryl-cAMP (N6-MB-cAMP). Moreover, glycemia and liver glycogen content were measured. KEY FINDINGS: Glycemia, liver glycogen content and basal rate of LGP and LG were not influenced by the HFD. However, LGP and LG were lower (p<0.05) in HFD mice during the infusions of glucagon (1 nM), epinephrine (20 µM) or phenylephrine (20 µM). In contrast, the activation of LGP and LG during the infusion of isoproterenol (20 µM) was not different (HFD vs. NFD). Because glucagon showed the most prominent response, the effect of cAMP, its intracellular mediator, on LGP and LG was investigated. cAMP (150 µM) showed lower activation of LGP and LG in the HFD group. However, the activation of LGP and LG was not influenced by HFD whether DB-cAMP (3 µM), 8-Br-cAMP (3 µM) or N6-MB-cAMP (3 µM) were used. SIGNIFICANCE: The activation of LGP and LG depends on the intracellular availability of cAMP. It can be concluded that cAMP played a pivotal role on the activation of LG in high-fat diet fed mice.

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This paper provides an overview of insulin-induced hypoglycemia as a triggering factor of cognitive deficit in children with type 1 diabetes mellitus. For this purpose, databases from 1961 to 2013 were used with the objective of detecting the primary publications that address the impact of hypoglycemia on cognitive performance of diabetic children. The results obtained from experimental animals were excluded. The majority of studies demonstrated that the cognitive deficit in diabetic children involves multiple factors including duration, intensity, severity, and frequency of hypoglycemia episodes. Additionally, age at the onset of type 1 diabetes also influences the cognitive performance, considering that early inception of the disease is a predisposing factor for severe hypoglycemia. Furthermore, the results suggest that there is a strong correlation between brain damage caused by hypoglycemia and cognitive deterioration. Therefore, a more cautious follow-up and education are needed to impede and treat hypoglycemia in children with diabetes mellitus.

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This work was undertaken out to evaluate the effects of dietary phytase on pacu juvenile performance and mineral retention. One-hundred and sixty fish (16.42 ± 2 g) were fed diets containing 0; 500; 1,000 and 2,000 phytase units (PU)/kg of diet containing approximately 3,238 kcal of digestible energy, 30% of crude protein and 0.31% of available phosphorus. One-hundred and sixty fish were fed to apparent satiation for 60 days. No effects of the dietary phytase on survival, carcass humidity, crude protein and fat were observed. Increasing dietary phytase levels linearly increased weigh gain, carcass ash and bone ash, and a quadratic effect on feed conversion ratio, which the best values, were obtained using 433.33, 425, 1875 and 1833 PU/kg of diet respectively. It was concluded that the optimum phytase supplemental level in the diet of juvenile pacu is 433.33 PU/kg of diet.

Este trabalho foi realizado para avaliar os efeitos da utilização de fitase sobre o desempenho e retenção de minerais em juvenis de pacu. Foram utilizados 160 peixes (16,42 ± 2 g), que foram alimentados com rações contendo 0; 500; 1.000 e 2.000 unidades de fitase (UF)/kg e com aproximadamente 3.238 kcal de energia digestível, 30% de proteína bruta e 0,31% de fósforo disponível. Os peixes foram alimentados até saciedade aparente durante 60 dias. Não foi observado efeito dos níveis de fitase nas rações sobre as variáveis de sobrevivência, umidade, proteína bruta e gordura na carcaça. Foi observado aumento linear dos níveis de fitase nas dietas sobre o ganho de peso, cinzas da carcaça e dos ossos. Foi observado efeito quadrático dos níveis de fitase sobre a conversão alimentar, taxa de eficiência proteica e níveis de cálcio e fósforo nos ossos, em que os melhores valores foram estimados em 433,33; 425; 1875 e 1833 UF/kg dieta respectivamente. Concluiu-se que a suplementação ótima de fitase em rações para juvenis de pacu é de 433,33 UF/kg.

RESUMO

This work was undertaken out to evaluate the effects of dietary phytase on pacu juvenile performance and mineral retention. One-hundred and sixty fish (16.42 ± 2 g) were fed diets containing 0; 500; 1,000 and 2,000 phytase units (PU)/kg of diet containing approximately 3,238 kcal of digestible energy, 30% of crude protein and 0.31% of available phosphorus. One-hundred and sixty fish were fed to apparent satiation for 60 days. No effects of the dietary phytase on survival, carcass humidity, crude protein and fat were observed. Increasing dietary phytase levels linearly increased weigh gain, carcass ash and bone ash, and a quadratic effect on feed conversion ratio, which the best values, were obtained using 433.33, 425, 1875 and 1833 PU/kg of diet respectively. It was concluded that the optimum phytase supplemental level in the diet of juvenile pacu is 433.33 PU/kg of diet.

Este trabalho foi realizado para avaliar os efeitos da utilização de fitase sobre o desempenho e retenção de minerais em juvenis de pacu. Foram utilizados 160 peixes (16,42 ± 2 g), que foram alimentados com rações contendo 0; 500; 1.000 e 2.000 unidades de fitase (UF)/kg e com aproximadamente 3.238 kcal de energia digestível, 30% de proteína bruta e 0,31% de fósforo disponível. Os peixes foram alimentados até saciedade aparente durante 60 dias. Não foi observado efeito dos níveis de fitase nas rações sobre as variáveis de sobrevivência, umidade, proteína bruta e gordura na carcaça. Foi observado aumento linear dos níveis de fitase nas dietas sobre o ganho de peso, cinzas da carcaça e dos ossos. Foi observado efeito quadrático dos níveis de fitase sobre a conversão alimentar, taxa de eficiência proteica e níveis de cálcio e fósforo nos ossos, em que os melhores valores foram estimados em 433,33; 425; 1875 e 1833 UF/kg dieta respectivamente. Concluiu-se que a suplementação ótima de fitase em rações para juvenis de pacu é de 433,33 UF/kg.