2 resultados para growth retardation
em Biblioteca Digital da Produção Intelectual da Universidade de São Paulo
Resumo:
Zinc is an essential micronutrient for growth and development. Its deficiency causes growth retardation in children and adolescents. The present study analyzes the effect of zinc on growth hormone (GH) secretion, insulin-like growth factor 1 (IGF1), and insulin-like growth factor-binding protein 3 (IGFBP3) in normal children before puberty. Thirty normal children were studied, 15 boys and 15 girls, aged 6-9 years. They were orally supplemented with 5 mg Zn/day for 3 months and 0.06537 mg Zn/kg body weight was injected before and after oral supplementation. Dietary intake and anthropometric measurements were assessed at baseline and end of study. Plasma GH levels increased during intravenous zinc administration and IGF1 and IGFBP3 increased after oral zinc supplementation. There was a positive correlation between the areas under the curves of GH and zinc after oral supplementation. Zinc supplementation was possibly effective in improving the body zinc status of the children, secretory levels of IGF1 and IGFBP3, GH potentialization, and height.
Resumo:
A previous study from our laboratory showed that maternal food restriction (MFR) delays thermoregulation in newborn rats. In neonates brown adipose tissue (BAT) is essential for thermogenesis due to the presence of uncoupling proteins (UCPs). The aim of this study was to evaluate the influence of MFR on the UCPs mRNA and protein expression in BAT and skeletal muscle (SM) of the newborn rat. Female Wistar EPM-1 control rats (CON) received chow ad libitum during pregnancy, whereas food-restricted dams (RES) received 50% of the amount ingested by CON. Fifteen hours after birth, the litters were weighed and sacrificed. Blood was collected for hormonal analysis. BAT and SM were used for determination of UCPs mRNA and protein expression, and Ca2+-ATPase sarcoplasmic reticulum (SERCA1). RES pups showed a significant reduction in body weight and fat content at birth. MFR caused a significant increase in the expression of UCP1 and UCP2 in BAT, without changes in UCP3 and SERCA1 expression in BAT and SM. No differences between groups were found for leptin, T4 and glucose levels. RES pups showed increased insulin and decreased T3 levels. The delay in development of thermoregulation previously described in RES animals appears not to result from impairment in thermogenesis, but from an increase in heat loss, since MFR caused low birth weight in pups, leading to greater surface/volume ratio. The higher expression of UCP1 and UCP2 in BAT suggests a compensatory mechanism to increased thermogenesis. (C) 2011 Elsevier Ltd. All rights reserved.