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Antidepressants are among the most-prescribed class of drugs in the world and though weight gain is a common outcome of antidepressant treatment, that effect is not well understood. We employed an animal model comprised of 2 weeks of chronic restraint stress with antidepressant treatment, followed by diet-induced obesity. We showed that short-term antidepressant treatment had long-lasting effects, not only leading to weight gain, but also enhancing trabecular and cortical bone features in rats; therefore, weight gain in this model was different from that of the classic diet-induced obesity. Late in the post-restraint recovery period, antidepressant-treated animals were significantly heavier and had better bone features than saline-treated controls, when assessed in the distal femoral metaphysis. The propensity to gain weight might have influenced the rate of catch-up growth and bone allometry, as heavier animals treated with fluoxetine also had enhanced bone features when compared to non-stressed animals. Therefore, short-term antidepressant treatment ameliorated the long-term effects of stress on body growth and bone. Growth and bone structural features were associated with leptin levels, and the interaction between leptin levels and antidepressant was significant for bone mineral content, suggesting that short-term antidepressants in the context of long-term diet-induced obesity modified the role of leptin in bone formation. To our knowledge this is the first study reporting that short-term antidepressant treatment has long-lasting effects in restoring the effects of chronic stress in body weight and bone formation. Our findings may be relevant to the understanding and treatment of osteoporosis, a condition of increasing prevalence due to the aging population.

Background Catch up growth (CUG) motivated by under-nutrition can lead to insulin resistance (IR) and visceral fat over-accumulation. However, the precise mechanisms on IR induced by adipose tissue changes during CUG remain unresolved. Methods Experimental rats were divided into three groups: normal chow group, catch up growth group and resveratrol administrated group. The whole experiment was carried out in four stages: 4, 6, 8 and 12 weeks. Peroxisome-proliferator activated receptor gamma (PPAR-γ) and fat-specific protein 27 (FSP27) expression level in epididymal adipose tissues (EAT) and subcutaneous adipose tissues (SAT) were detected along with other IR indicators. Results Calorie restriction (CR) significantly increased PPAR-γ expression in EAT while decreased FSP27 expression. During re-feeding, both of the expression of PPAR-γ and FSP27 increased, even FSP27 returned to normal level when CUG for 4 weeks. Although PPAR-γ expression declined slightly at 8 weeks, it was still much stronger than normal chow groups. However, no changes were seen in SAT. Relative insufficiency of FSP27 expression in EAT results in a decrease in lipid storage capacity, causing a series of path physiological changes that led to the formation of IR. Resveratrol inhibited the expression of PPAR-γ and promoted FSP27 expression, thus fundamentally improving IR. Conclusions The imbalance between adipose synthesis and storage mediated by PPAR-γ / FSP27 in the EAT plays a pivotal role in the formation of IR during CUG. Resveratrol can correct fat formation and storage imbalance status by up-regulating FSP27 and down-regulating PPAR-γ expression level, ameliorating insulin sensitivity.

Studies in young mammals on the molecular effects of food restriction leading to prolong adult life are scares. Here, we used high-throughput quantitative proteomic analysis of whole rat livers to address the molecular basis for growth arrest and the apparent life-prolonging phenotype of the food restriction regimen. Over 1800 common proteins were significantly quantified in livers of ad libitum, restriction- and re-fed rats, which summed up into 92% of the total protein mass of the cells. Compared to restriction, ad libitum cells contained significantly less mitochondrial catabolic enzymes and more cytosolic and ER HSP90 and HSP70 chaperones, which are hallmarks of heat- and chemically-stressed tissues. Following re-feeding, levels of HSPs nearly reached ad libitum levels. The quantitative and qualitative protein values indicated that the restriction regimen was a least stressful condition that used minimal amounts of HSP-chaperones to maintain optimal protein homeostasis and sustain optimal life span. In contrast, the elevated levels of HSP-chaperones in ad libitum tissues were characteristic of a chronic stress, which in the long term could lead to early aging and shorter life span.

Introduction: Infant growth has not been studied in developing countries in relation to maternal factors related to malaria in pregnancy and maternal illiteracy. Objective: To describe growth patterns in infants with low and normal birthweight and determine maternal risk factors for infant undernutrition. Methods: Babies born in a rural district of southern Malawi were recruited. An infant cohort was selected on the basis of low or normal birthweight. Weight and length were recorded at birth and at 4-weekly intervals until at 52 weeks after birth. Maternal characteristics at first antenatal attendance and delivery were obtained. Odds ratios in univariate analysis were adjusted for birthweight. Factors included in the multivariate regression included maternal illiteracy, season of birth, maternal iron deficiency and number of infant illness episodes. Results: Low birthweight infants were shorter and lighter throughout infancy than either normal birthweight or international reference values. At 12 months, placental or peripheral malaria at delivery (adjusted odds 1.8; 1.0, 3.1), number of infant illness episodes (AOR = 2.1; 1.2, 3.6) and maternal illiteracy (AOR = 2.7; 1.5, 4.9) were independently associated with low weight for age. Maternal short stature (AOR = 1.8; 1.1. 3.2), male sex (AOR = 2.4; 1.4, 4.1), number of infant illness episodes (AOR = 2.6; 1.5, 4.4), and birth in the rainy season (2.1; 1.2, 3.7) were independently associated with stunting. Placental or peripheral malaria at delivery (AOR = 2.2; 1.1, 4.4) and number of illness episodes (AOR = 2.2; 1.1, 4.5) were independently associated with thinness. Conclusion: Malaria during pregnancy and maternal illiteracy are important maternal characteristics associated with infant undernutrition. Innovative health/literacy strategies are required to address malaria control in pregnancy in order to reduce the magnitude of its effects on infant undernutrition. © 2005 Elsevier Ireland Ltd. All rights reserved.

International audience; Intrauterine growth restriction (IUGR), along with postnatal growth trajectory, is closely linked with metabolic diseases and obesity at adulthood. The present study reports the time-dependent metabolomic response of male offspring of rat dams exposed to maternal adequate protein diet during pregnancy and lactation (CC) or protein deprivation during pregnancy only (IUGR with rapid catch-up growth, RC) or through pregnancy and lactation (IUGR with slow postnatal growth, RR). Plasma LC-HRMS metabolomic fingerprints for 8 male rats per group, combined with multivariate statistical analysis (PLS-DA and HCA), were used to study the impact of IUGR and postnatal growth velocity on the offspring metabolism in early life (until weaning) and once they reached adulthood (8 months). Compared with CC rats, RR pups had clear-cut alterations in plasma metabolome during suckling, but none at adulthood; in contrast, in RC pups, alterations in metabolome were minimal in early life but more pronounced in the long run. In particular, our results pinpoint transient alterations in proline, arginine, and histidine in RR rats, compared to CC rats, and persistent differences in tyrosine and carnitine, compared to RC rats at adulthood. These findings suggest that the long-term deregulation in feeding behavior and fatty acid metabolism in IUGR rats depends on postnatal growth velocity

OBJETIVO: Fornecer informações para pediatras e neonatologistas quanto à expectativa real da evolução destas crianças e, assim, auxiliar no planejamento de sua atuação. FONTES DOS DADOS: Pesquisa bibliográfica nas bases de dados da Cochrane Library, MEDLINE e Lilacs. SÍNTESE DOS DADOS: Para avaliação do crescimento e desenvolvimento nos primeiros 2-3 anos, deve-se corrigir a idade cronológica em função do grau de prematuridade. Prematuros pequenos para a idade gestacional e os com displasia broncopulmonar despertam maior preocupação quanto a seu prognóstico. Especial atenção deve ser dada à adequação da nutrição do prematuro de extremo baixo peso nos primeiros anos; estes prematuros geralmente evoluem com falha no catch-up, elevada morbidade e necessidade de reinternação nos primeiros 2 anos de vida. São crianças menores e mais leves no início da infância, mas podem apresentar catch-up tardio, entre 8-14 anos. Crianças nascidas de extremo baixo peso são de alto risco para anormalidades neurológicas e atraso no desenvolvimento nos primeiros anos de vida. Na idade escolar, são freqüentes os problemas educacionais, comportamentais e psicológicos. Adolescentes e adultos nascidos de extremo baixo peso ainda persistem com alguma diferença em seu desempenho, mas sua integração social não é prejudicada. CONCLUSÕES: O crescimento e desenvolvimento de todos os prematuros de extremo baixo peso devem ser cuidadosamente monitorizados após a alta hospitalar, para garantir que estas crianças e suas famílias recebam adequado suporte e intervenção, a fim de otimizar seu prognóstico. OBJETIVE: To provide information for pediatricians and neonatologists to create realistic outcome expectations and thus help plan their actions. DATA SOURCES: Searches were made of the Cochrane Library, MEDLINE, and Lilacs databases. SUMMARY OF FINDINGS: The assessment of growth and development over the first 2-3 years must adjust chronological age with respect of the degree of prematurity. There is special concern regarding the prognoses of small for gestational age preterm infants, and for those with bronchopulmonary dysplasia. Attention must be directed towards improving the nutrition of extremely low birth weight infants during their first years of life; these infants have high prevalence levels of failure to catch-up on growth, diseases and rehospitalizations during their first 2 years. They are frequently underweight and shorter than expected during early childhood, but delayed catch-up growth may occur between 8 and 14 years. Extremely low birth weight infants are at increased risk of neurological abnormalities and developmental delays during their first years of life. Educational, psychological, and behavioral problems are frequent during school years. Teenage and adult outcomes show that although some performance differences persist, social integration is not impaired. CONCLUSIONS: The growth and neurodevelopment of all ELBW infants must be carefully monitored after discharge, to ensure that children and their families receive adequate support and intervention to optimize prognoses.

Adiponectin is an adipocytokine with insulin-sensitizing and antiatherogenic properties. Reduced concentrations of adiponectin precede the onset of type 2 diabetes and the development of atherosclerosis. Our aim was to quantify adiponectin concentrations in small for gestational age (SGA) children. Fifty-one SGA children, 24 obese, and 17 short-normal children with birth weight appropriate for gestational age (short-AGA) were studied. The statures of the SGA children were corrected for their midparental height and subdivided into two groups according to their corrected height: catch-up growth group, children with corrected height of 0 z-score or greater (n = 17); and noncatch-up growth group, subjects with corrected height less than 0 z-score (n = 34). SGA children showed adiponectin levels significantly lower than short- normal children (35.2 +/- 3.5 vs. 80.4 +/- 26.6 micro g/ml; P < 0.0001) and obese children (77.5 +/- 39.4 micro g/ml; P < 0.0001). Catch-up growth children showed adiponectin levels significantly lower than noncatch-up growth subjects (29.4 +/- 10.3 vs. 38.1 +/- 11.5 micro g/ml; P = 0.01). Adiponectin concentrations were inversely related to height z-score, corrected stature, weight, and body mass index and were positively related to birth weight. Our results suggest that adiponectin levels are reduced in SGA children and are even lower in those with postnatal catch-up growth. Whether this finding implies a higher risk of developing type 2 diabetes and atherosclerosis remains to be established.

Background: There is a paucity of observational data from India on initial catch up growth in hypothyroid children started on thyroxine replacement therapy. Methods: We retrospectively studied 44 children and adolescents (32 girls) with a diagnosis of primary hypothyroidism i.e., (thyrotropin > 15 μIU/mL and thyroxine < 55ng/mL). All were started on treatment with oral thyroxine. The dose was adjusted to maintain thyrotropin between 0.5-5 μIU/mL. Height was measured at baseline and at each follow-up visit and height standard deviation scores (HtSDS) were calculated. We studied the therapeutic benefit of thyroxine replacement therapy on growth in the initial couple of years of treatment. Results: Dose of thyroxine required to restore euthyroidism was 4.1±2.5 μg/kg body weight. The dose fell from 9.7±2.4 μg/kg body weight in infants to 3.0±1.5 μg/kg body weight in adolescence (p