Restrição proteica materna e alteração do desenvolvimento das artérias coronárias em camundongos

• Autor(a) principal: Silva Junior, Geraldo de Oliveira
• Data de Publicação: 2011
• Tipo de documento: Tese
• Idioma: por
• Título da fonte: Biblioteca Digital de Teses e Dissertações da UERJ
• Texto Completo: http://www.bdtd.uerj.br/handle/1/7765
• topic: Coronary artery development; Nutritional programming; Cardiovascular risk; Embryo; Mice; Coronary arteries; Diet with protein restriction; Fetal development; Fetus - Development; Diseases of the coronary arteries; Coronary arteries - Development; Nutritional status; Rat as laboratory animal; Desenvolvimento da artéria coronária; Programação nutricional; Risco cardiovascular; Embrião; Camundongo; Artérias coronárias; Dieta com restrição de proteínas; Desenvolvimento fetal; Feto Desenvolvimento; Doenças das coronárias; Artérias coronárias - Desenvolvimento; Estado nutricional; Rato como animal de laboratório; CNPQ::CIENCIAS BIOLOGICAS::MORFOLOGIA

Programming of fetal development is considered to be an important risk factor for non-communicable diseases of adulthood, including coronary heart disease (CHD). Aiming to investigate the association between maternal nutrition and the development of the coronary arteries (CA) in staged mice embryos, C57BL/6 mice embryos from stages 16 to 23 were taken from mothers fed a normal protein (NP) or low protein (LP) diet, and the CA were studied. Although the LP embryos had lower masses, they had faster heart growth rates when compared to the NP embryos. The subepicardial plexuses were observed earlier in the NP embryos (stage 20) than in the LP ones (stage 22) (P<0.01). Apoptotic nuclei were seen around the aortic peritruncal ring beginning at stage 18 in the NP and LP embryos. FLK1+ (fetal liver kinase 1 = VEGFr2 or vascular endothelial growth factor receptor 2) cells had a homogeneous distribution in the NP embryos as early as stage 18, whereas a similar distribution in the LP embryos was only seen at stages 22 and 23. Maternal protein restriction in mice leads to a delay in the growth of the heart in the embryonic period modifying the development of the subepicardial peritruncal plexus and the apoptosis in the future coronary orifice region.