Información del artículo
Cambios metabólicos in utero establecen patrones fisiológicos y estructurales a largo plazo que pueden “programar” la salud durante la vida adulta, teoría popularmente conocida como “hipótesis de Barker”. La programación fetal implica que durante los períodos críticos del crecimiento prenatal, ciertos cambios en el entorno hormonal y nutricional del embrión, pueden alterar la expresión del genoma fetal, en tejidos con funciones fisiológicas y metabólicas en la etapa adulta. La evidencia sugiere que patologías como enfermedad vascular (por ejemplo, hipertensión), síndrome metabólico y diabetes mellitus tipo 2, pueden “programarse” durante las primeras etapas del desarrollo fetal y manifestarse en etapas tardías, al interactuar con el estilo de vida y otros factores de riesgo adquiridos convencionales con el medio ambiente. El objetivo de esta revisión es presentar evidencia adicional que apoye la asociación entre el bajo peso al nacer, con el aumento en la prevalencia de la hipertensión arterial en la edad adulta. Se revisan la función endotelial, el estrés oxidativo, la resistencia a la insulina y la función mitocondrial, como posibles mecanismos celulares y moleculares.
Palabras clave:
programación fetal
enfermedad cardiovascular
hipertensión arterial
Keywords:
fetal programming
cardiovascular disease
hypertension
Metabolic changes in utero establish long-term physiological and structural patterns which can “program” health in adulthood, theory popularly known as “Barker hypothesis”. The fetal programming implies that during critical periods of prenatal growth, some changes in hormonal and nutritional environment of the embryo can alter fetal genome expression in tissues with physiological and metabolic functions in adulthood. Evidence suggests that pathologies like vascular disease (eg, hypertension), metabolic syndrome and type 2 diabetes mellitus, may “be programmed” during the early stages of fetal development and manifest in later stages, when interacting with lifestyle and other conventional acquired risk factors with the environment. The aim of this review is to present additional evidence to support the association between low birth weight with the increased prevalence of arterial hypertension in adulthood. We review endothelial function, oxidative stress, insulin resistance and mitochondrial function, as possible cellular and molecular mechanisms.
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