Navegando por Palavras-chave "dietary"

Agora exibindo 1 - 2 de 2
  • Imagem de Miniatura
    Item
    Acesso aberto (Open Access)
    Deficiência de ferro nas afecções gastrointestinais da criança
    (Associação Brasileira de Hematologia e Hemoterapia e Terapia Celular, 2010-06-01) Morais, Mauro Batista de [UNIFESP]; Universidade Federal de São Paulo (UNIFESP)
    The relationships between iron deficiency, iron metabolism and the intestinal tract function can be analyzed from various perspectives: 1. the intestine as the site of iron absorption regulated by hepcidin produced in the liver; 2. the interaction between iron with other nutrients; 3. repercussions of iron deficiency in the intestine and 4. the intestine as the location of pathological loses that can cause or aggravate iron deficiency. The aim of this article is to cover these aspects of the interaction between iron and the intestinal tract. In iron deficiency, an increase in iron absorption has been observed, which in animals is accompanied by an increase in the height of the intestinal villosities. On the other hand, in humans with iron deficiency anemia, abnormalities of the intestinal physiology, different to those found in the laboratory, can occur. Poor intestinal iron absorption can occur in illnesses such as atrophy of the villosities as occurs in celiac disease and in illnesses associated with inflammation anemia such as cholestatic hepatic diseases. Nowadays blood loses from intestinal parasitosis are not a frequent cause of iron deficiency. Infants who have a high risk of developing iron deficiency anemia should be exclusively breast feed and a supplement of iron must be started from their sixth month of life. The use of cow milk is associated with lower iron absorption and blood loses that can aggravate iron deficiency. Infants who do not receive maternal milk must be fed with an infant formula fortified with iron.
  • Nenhuma Miniatura disponível
    Item
    Somente Metadadados
    Insulin resistance due to chronic salt restriction is corrected by alpha and beta blockade and by L-arginine
    (Elsevier B.V., 2006-07-30) Ruivo, Gilson Fernandes; Leandro, Sandra Marcia; Nascimento, Carlos Antonio do; Catanozi, Sergio; Rocha, Jussara Cordeiro; Furukawa, Luzia Naoko Shinohara; Dolnikoff, Miriam Sterman; Quintão, Eder Carlos Rocha [UNIFESP]; Heimann, Joel Claudio; Universidade de São Paulo (USP); Universidade Federal de São Paulo (UNIFESP)
    Dietary salt restriction is associated with evidence of low insulin sensitivity. the current study was undertaken to investigate whether sympathetic nervous system and L-arginine-nitric oxide pathway activities are linked to insulin resistance in rats under chronic low salt intake. Male Wistar rats were fed a low (LSD) or normal (NSD) salt diet from weaning to adulthood. A euglycemic hyperinsulinemic clamp was performed in 4 sub-groups on each diet: (1) sympathetic nervous system blockade (propranolol and prazosin), (2) vehicle, (3) L-arginine, and (4) D-arginine. Blood pressure, heart rate and metabolic measurements were done before and 45 min after drug infusion and at the end of the clamp. At baseline conditions, body weight, hematocrit, blood glucose, plasma insulin, cholesterol, and triacylglycerols were higher in LSD than in NSD rats. Systolic blood pressure was lower and heart rate was higher in rats on LSD than on NSD. Glucose uptake was lower on LSD compared to NSD. Sympathetic nervous system blockade and L-arginine did, and vehicle and D-arginine did not improve glucose uptake in LSD rats. On NSD there was no effect of any of the infused drugs. A positive correlation between plasma nitrate and nitrite at the end of clamp and glucose uptake was observed in L-arginine - but not in D-arginine-infused LSD rats. These results provide evidence that the sympathetic nervous system and the L-arginine-nitric oxide pathway are involved in the glucose uptake impairment induced by chronic dietary salt restriction. (c) 2006 Elsevier Inc. All rights reserved.