METABOLIC IMPRINTING: CAUSES AND CONSEQUENCES

A programação metabólica é um fenômeno desencadeado por alterações nutricionais e/ou hormonais que modulam fases críticas do desenvolvimento. O objetivo inicial da programação metabólica é melhorar a sobrevivência da prole pela regulação do balanço energético, de modo a utilizar os nutrientes disponíveis da forma mais eficiente. Os mecanismos através dos quais o fenômeno de programação metabólica pode ocorrer são: indução de variações na estrutura de alguns órgãos, com alterações na vascularização, na inervação ou na justaposição das diferentes células do órgão; alterações no número de células e diferenciação metabólica, modificações na expressão de certos genes, acarretando variações na síntese de enzimas, hormônios, receptores hormonais e transportadores. Estes eventos desencadeiam ao longo da vida doenças crônicas, em especial obesidade e suas co-morbidades, como o Diabetes Mellitus tipo 2 e Doenças Cardiovasculares

Risk factors associated with growth failure in the follow-up of very low birth weight newborns

Abstract Objective: To determine risk factors during neonatal hospital stay and follow-up associated with failure to thrive in the first year of life of very low birth weight newborns. Methods: Study of preterm very low birth weight newborns followed from 2006 to 2013 in a public institutional hospital program. The study included newborns that attended at least one appointment in each of the three periods: Period I, up to 3 months of corrected age (CA); Period II, 4-6 months of CA; and Period III, 7-12 months of CA. The variables were analyzed by logistic regression with XLSTAT 2014 software (Microsoft®, WA, USA). Failure to thrive (Z-score below -2 SD) was classified as a dichotomous dependent variable (0 - failure/1 - success), while the other variables were classified as explanatory variables for the hospitalization periods and for each of the follow-up periods (I, II, and III). Results: Children born adequate for gestational age increased the chance of Z-score for weight at discharge > -2 SD (OR = 10.217; 95% CI: 1.117-93.436). Metabolic bone disease and retinopathy of prematurity in Period I, as well as hospital readmissions in Periods II and III during follow-up increased the chance of Z-score < -2 SD. Conclusion: Failure to thrive is influenced by intrauterine factors and, subsequently, by several morbidities, both in the birth and hospitalization period, as well as in the post-discharge period and thus, such variables should be prioritized in the follow-up

Swim training restores glucagon-like peptide-1 insulinotropic action in pancreatic islets from monosodium glutamate-obese rats

Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)Aims: Glucagon-like peptide-1 (GLP-1) is an important modulator of insulin secretion by endocrine pancreas. In the present study, we investigated the effect of swim training on GLP-1 insulinotropic action in pancreatic islets from monosodium glutamate (MSG)-obese rats. Methods: Obesity was induced by neonatal MSG administration. MSG-obese and control (CON) exercised rats swam for 30 min (3 times week(-1)) for 10 weeks. Pancreatic islets were isolated by colagenase technique and incubated with low (5.6 mM) or high (16.7 mM) glucose concentrations in the presence or absence of GLP-1 (10 nM). In addition, GLP-1 gene expression in ileum was quantified in fasting and glucose conditions. Results: Exercise reduced obesity and hyperinsulinemia in MSG-obese rats. Swim training also inhibited glucose-induced insulin secretion in islets from both groups. Islets from MSG-obese rats maintained GLP-1 insulinotropic response in low glucose concentration. In contrast, in the presence of high glucose concentration, GLP-1 insulinotropic action was absent in islets from MSG-obese rats. Islets from MSG-exercised rats showed reduced GLP-1 insulinotropic action in the presence of low glucose. However, in high glucose concentration swim training restored GLP-1 insulinotropic response in islets from MSG-obese rats. In all groups, glucose intake increased GLP-1immunoreactivity and gene expression in ileum cells in relation to fasting conditions. Swim training reduced these parameters only in ileum cells from CON-exercised rats. Neither MSG treatment nor exercise affected GLP-1 expression in the ileum. Conclusions: Exercise avoids insulin hypersecretion restoring GLP-1's insulinotropic action in pancreatic islets from MSG-obese rats.20913444Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)Fundacao Araucaria (Fundacao Araucaria de Apoio ao Desenvolvimento Cientifico e Tecnologico do Estado do Parana)Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)SETI/UGF (Secretaria de Estado da Ciencia, Tecnologia e Ensino Superior/Unidade Gestora do Fundo do Parana)Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq

Supplementary Material for: Glycolytic and Mitochondrial Metabolism in Pancreatic Islets from MSG-Treated Obese Rats Subjected to Swimming Training

<b><i>Backgrounds/Aims: </i></b>Obese rats obtained by neonatal monosodium glutamate (MSG) administration present insulin hypersecretion. The metabolic mechanism by which glucose catabolism is coupled to insulin secretion in the pancreatic β-cells from MSG-treated rats is understood. The purpose of this study was to evaluate glucose metabolism in pancreatic islets from MSG-treated rats subjected to swimming training. <b><i>Methods: </i></b>MSG-treated and control (CON) rats swam for 30 minutes (3 times/week) over a period of 10 weeks. Pancreatic islets were isolated and incubated with glucose in the presence of glycolytic or mitochondrial inhibitors. <b><i>Results: </i></b>Swimming training attenuated fat pad accumulation, avoiding changes in the plasma levels of lipids, glucose and insulin in MSG-treated rats. Adipocyte and islet hypertrophy observed in MSG-treated rats were attenuated by exercise. Pancreatic islets from MSG-treated obese rats also showed insulin hypersecretion, greater glucose transporter 2 (GLUT2) expression, increased glycolytic flux and reduced mitochondrial complex III activity. <b><i>Conclusion: </i></b>Swimming training attenuated islet hypertrophy and normalised GLUT2 expression, contributing to a reduction in the glucose responsiveness of pancreatic islets from MSG-treated rats without altering glycolytic flux. However, physical training increased the activity of mitochondrial complex III in pancreatic islets from MSG-treated rats without a subsequent increase in glucose-induced insulin secretion