-Development occurs in a proper rhythm as result of genetic inheritance and environment factors. This study had the aim to identify some environmental risk factors for the motor development in two groups of healthy children. 100 pre-school aged (five years children) from two day-care centers and a private school were evaluated, in Recife-PE. All the children underwent to a motor skills assessment and their parents answered a questionnaire. The children from the public nursery remained behind in fine motor skills. The results showed that the biologically healthy children development can suffer negative influence of the environmental risk factors. In this research these factors were: the father absence, improper toys use to the correct age, the place were the child was kept in the early childhood, the lack of pedagogical guidance and extra-parental socialization and low familiar socioeconomic status.KEY WORDS: motor development, environment stimulation, child.Influências do ambiente podem alterar a aquisição de habilidades motoras? Uma comparação entre Influências do ambiente podem alterar a aquisição de habilidades motoras? Uma comparação entre Influências do ambiente podem alterar a aquisição de habilidades motoras? Uma comparação entre Influências do ambiente podem alterar a aquisição de habilidades motoras? Uma comparação entre Influências do ambiente podem alterar a aquisição de habilidades motoras? Uma comparação entre pré-escolares de creches públicas e escolas privadas pré-escolares de creches públicas e escolas privadas pré-escolares de creches públicas e escolas privadas pré-escolares de creches públicas e escolas privadas pré-escolares de creches públicas e escolas privadas RESUMO -----O desenvolvimento ocorre num ritmo resultante da interação entre herança genética e fatores ambientais. Este estudo teve por objetivo identificar alguns fatores de risco ambientais para o desenvolvimento motor, em dois grupos de crianças saudáveis. Foram avaliadas 100 crianças (idade:5 anos) provenientes de duas creches públicas e uma escola particular, em Recife-PE. Todas as crianças foram submetidas a uma avaliação das habilidades motoras e seus pais responderam a um questionário. As crianças da creche pública mostraram atraso no campo das habilidades motoras finas. Os resultados indicaram que o desenvolvimento das crianças biologicamente saudáveis pode sofrer influência negativa dos fatores de risco ambientais. Os fatores encontrados foram: a ausência do pai; a utilização de brinquedos inadequados para faixa etária; o local onde a criança era mantida em idades precoces da infância; a falta de orientação pedagógica e de socialização extra-familiar precoce, e a baixa condição socioeconômica familiar.

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Early malnutrition has been associated with a high risk of developing obesity, diabetes and cardiovascular diseases in adulthood. In animals, poor perinatal nutrition produces hyperphagia and persistent increased levels of serotonin (5-HT) in the brain. Inasmuch as 5-HT is directly related to the negative regulation of food intake, here we have investigated whether the anorexic effects of 5-HT are altered by protein malnutrition. Pregnant Sprague-Dawley rats were fed ad libitum either a control (20% protein) or a low-protein (8% protein) diet throughout pregnancy and lactation. At weaning, pups received a standard diet and at 35 days their feeding behaviour was evaluated after the administration of DL-fenfluramine (DL-FEN), an anorexic compound that blocks the reuptake of 5-HT and stimulates its release. Male offspring born to protein-restricted dams exhibited significantly decreased body weight and hyperphagia compared with controls. DL-FEN dose-dependently reduced the 1 h chow intake at the onset of the dark cycle in both control and undernourished rats. However, the hypophagic effects of DL-FEN were significantly attenuated in animals submitted perinatally to protein restriction. The stimulatory action of DL-FEN on c-fos immunoreactivity within the paraventricular nucleus of the hypothalamus was also decreased in low-protein-fed rats. Further pharmacological analysis with selective 5-HT(1B) and 5-HT(2C) receptor agonist showed that the reduced anorexic effects of 5-HT in malnourished animals were coupled to a desensitization of 5-HT(1B) receptors. These observations indicate that the hyperphagia associated with metabolic programming is at least partially related to a reduced regulatory function of 5-HT on food intake.

BackgroundNutrient deficiency during perinatal development is associated with an increased risk to develop obesity, diabetes and hypertension in the adulthood. However, the molecular mechanisms underlying the developmental programming of the metabolic syndrome remain largely unknown.Methodology/Principal FindingsGiven the essential role of the hypothalamus in the integration of nutritional, endocrine and neuronal cues, here we have analyzed the profile of the hypothalamus transcriptome in 180 days-old rats born to dams fed either a control (200 g/kg) or a low-protein (80 g/kg) diet through pregnancy and lactation. From a total of 26 209 examined genes, 688 were up-regulated and 309 down-regulated (P<0.003) by early protein restriction. Further bioinformatic analysis of the data revealed that perinatal protein restriction permanently alters the expression of two gene clusters regulating common cellular processes. The first one includes several gate keeper genes regulating insulin signaling and nutrient sensing. The second cluster encompasses a functional network of nuclear receptors and co-regulators of transcription involved in the detection and use of lipid nutrients as fuel which, in addition, link temporal and nutritional cues to metabolism through their tight interaction with the circadian clock.Conclusions/SignificanceCollectively, these results indicate that the programming of the hypothalamic circuits regulating energy homeostasis is a key step in the development of obesity associated with malnutrition in early life and provide a valuable resource for further investigating the role of the hypothalamus in the programming of the metabolic syndrome.

A protocol of physical exercise, based on maximal oxygen uptake (V O 2 max ), for female rats before and during pregnancy was developed to evaluate the impact of a low-protein diet on oxygen consumption during gestation and growth rate of the offspring. Virgin female Wistar rats were divided into four groups as follows: untrained (NT, n = 5); trained (T, n = 5); untrained with low-protein diet (NT+LP, n = 5); and trained with low-protein diet (T+LP, n = 5). Trained rats were submitted to a protocol of moderate physical training on a treadmill over a period of 4 weeks (5 days week −1 and 60 min day −1 , at 65% ofV O 2 max ). At confirmation of pregnancy, the intensity and duration of the exercise was reduced. Low-protein groups received an 8% casein diet, and their peers received a 17% casein diet. The birth weight and growth rate of the pups up to the 90th day were recorded. Oxygen consumption (V O 2 ), CO 2 production and respiratory exchange ratio (RER) were determined using an indirect open-circuit calorimeter. Exercise training increaseḋ V O 2 max by about 20% when compared with the initial values (45.6 ± 1.0 ml kg −1 min −1 ). During gestation, all groups showed a progressive reduction in the restingV O 2 values. Dams in the NT+LP group showed lower values of restingV O 2 than those in the NT group. The growth rate of pups from low-protein-fed mothers was around 50% lower than that of their respective controls. The T group showed an increase in body weight from the 60th day onwards, while the NT+LP group presented a reduced body weight from weaning onwards. In conclusion, physical training attenuated the impact of the low-protein diet on oxygen consumption during gestation and on the growth rate of the offspring.

The effects of maternal moderate -low physical training on postnatal development, glucose homeostasis and leptin concentration in adult offspring subjected to a low-protein diet during the perinatal period were investigated. Male Wistar rats (aged 150 d old) were divided into four groups according to maternal group: untrained (NT p , n 8); trained (T p , n 8); untrained with a low-protein diet (NT þ LP p , n 8); trained with a low-protein diet (T þ LP p , n 8). The trained mothers were subjected to a protocol of moderate physical training over a period of 4 weeks (treadmill, 5 d/week, 60 min/d, at 65 % VO 2max ) before mating. At pregnancy, the intensity and duration of exercise was progressively reduced (50 -20 min/d, at 65 -30 % VO 2max ). The low-protein diet groups received an 8 % casein diet, and their peers received a 17 % casein diet during gestation and lactation. The pups' birth weight and somatic growth were recorded weekly up to the 150th day. Fasting blood glucose, cholesterol, serum leptin concentration, glucose and insulin tolerance tests were evaluated. The T p animals showed no changes in somatic and biochemical parameters, while the NT þ LP p group showed a greater abdominal circumference, hyperglycaemia, hypercholesterolaemia, glucose intolerance and lower plasma leptin. In the T þ LP p animals, all of those alterations were reversed except for plasma leptin concentration. In conclusion, the effects of a perinatal low-protein diet on growth and development, glucose homeostasis and serum leptin concentration in the offspring were attenuated in pups from trained mothers.

Objective: Several lines of evidence indicate that nutrient restriction during perinatal development sensitizes the offspring to the development of obesity, insulin resistance and cardiovascular disease in adulthood via the programming of hyperphagia and reduced energy expenditure. Given the link between the circadian clock and energy metabolism, and the resetting action of food on the circadian clock, in this study, we have investigated whether perinatal undernutrition affects the circadian expression rhythms of genes regulating food intake in the hypothalamus and energy metabolism in the liver. Design: Pregnant Sprague-Dawley rats were fed ad libitum either a control (20% protein) or a low-protein (8% protein) diet throughout pregnancy and lactation. At weaning, pups received a standard diet and at 17 and 35 days of age, their daily patterns of gene expression were analyzed by real-time quantitative PCR experiments. Results: 17-day-old pups exposed to perinatal undernutrition exhibited significant alterations in the circadian expression profile of the transcripts encoding diverse genes regulating food intake, the metabolic enzymes fatty acid synthase and glucokinase as well as the clock genes BMAL1 and Period1. These effects persisted after weaning, were associated with hyperphagia and mirrored the results of the behavioral analysis of feeding. Thus, perinatally undernourished rats exhibited an increased hypothalamic expression of the orexigenic peptides agouti-related protein and neuropeptide Y. Conversely, the mRNA levels of the anorexigenic peptides pro-opiomelanocortin and cocaine and amphetamine-related transcripts were decreased. Conclusion: These observations indicate that the circadian clock undergoes nutritional programming. The programming of the circadian clock may contribute to the alterations in feeding and energy metabolism associated with malnutrition in early life, which might promote the development of metabolic disorders in adulthood.

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