Consenso para las prácticas de alimentación complementaria en lactantes sanos

ResumenLa nutrición adecuada durante los primeros dos años de vida es fundamental para el desarrollo pleno del potencial de cada ser humano; actualmente se reconoce que este periodo es una ventana crítica para la promoción de un crecimiento y desarrollo óptimos y un buen estado de salud. Por tanto, cumplir con una alimentación adecuada en esta etapa de la vida tiene impacto sobre la salud, estado de nutrición, crecimiento y desarrollo de los niños; no sólo en el corto plazo, sino en el mediano y largo plazo. El presente trabajo ofrece recomendaciones de alimentación complementaria (AC) que se presentan en forma de preguntas o enunciados que consideran temas importantes para quienes atienden niños durante esta etapa de la vida; por ejemplo: inicio de la alimentación complementaria a los 4 o 6 meses de edad; exposición a alimentos potencialmente alergénicos; introducción de bebidas azucaradas; uso de edulcorantes artificiales y productos light; secuencia de introducción de alimentos; modificaciones de consistencia de alimentos de acuerdo a la maduración neurológica; número de días para probar aceptación y tolerancia a los alimentos nuevos; cantidades por cada tiempo de comida; prácticas inadecuadas de alimentación complementaria; mitos y realidades de la alimentación complementaria; hitos del desarrollo; práctica del “Baby Led Weaning” y práctica de vegetarianismo.AbstractA proper nutrition during the first two years of life is critical to reach the full potential of every human being; now, this period is recognized as a critical window for promoting optimal growth, development, and good health. Therefore, adequate feeding at this stage of life has an impact on health, nutritional status, growth and development of children; not only in the short term, but in the medium and long term. This paper provides recommendations on complementary feeding (CF) presented as questions or statements that are important for those who take care for children during this stage of life. For example: When to start complementary feedings: 4 or 6 months of age?; Exposure to potentially allergenic foods; Introduction of sweetened beverages; Use of artificial sweeteners and light products; Food introduction sequence; Food consistency changes according to neurological maturation; Number of days to test acceptance and tolerance to new foods; Amounts for each meal; Inadequate complementary feeding practices; Myths and realities of complementary feeding; Developmental milestones; Practice of “Baby Led Weaning” and practice of vegetarianism

Epsilon PKC Increases Brain Mitochondrial SIRT1 Protein Levels via Heat Shock Protein 90 following Ischemic Preconditioning in Rats

Ischemic preconditioning is a neuroprotective mechanism whereby a sublethal ischemic exposure is protective against a subsequent lethal ischemic attack. We previously demonstrated that SIRT1, a nuclear localized stress-activated deacetylase, is vital for ischemic preconditioning neuroprotection. However, a recent study demonstrated that SIRT1 can also localize to the mitochondria. Mitochondrial localized SIRT1 may allow for a direct protection of mitochondria following ischemic preconditioning. The objective of this study was to determine whether ischemic preconditioning increases brain mitochondrial SIRT1 protein levels and to determine the role of PKCɛ and HSP90 in targeting SIRT1 to the mitochondria. Here we report that preconditioning rats, with 2 min of global cerebral ischemia, induces a delayed increase in non-synaptic mitochondrial SIRT1 protein levels which was not observed in synaptic mitochondria. This increase in mitochondrial SIRT1 protein was found to occur only in neuronal cells and was mediated by PKCε activation. Inhibition of HSP90, a protein chaperone involved in mitochondrial protein import, prevented preconditioning induced increases in mitochondrial SIRT1 and PKCε protein. Our work provides new insights into a possible direct role of SIRT1 in modulating mitochondrial function under both normal and stress conditions, and to a possible role of mitochondrial SIRT1 in activating preconditioning induced ischemic tolerance