Childhood obesity by postnatal early overfeeding program permanent vascular dysfunction in female rats: role of the renin-angiotensin-aldosterone system

Childhood obesity by postnatal early overfeeding program permanent vascular dysfunction in female rats: role of the renin-angiotensin-aldosterone system

• Autor
• Moura, K. F.
• Co-autores
• Jezuino, J. S. , Gravena, R. C. , Stopa, L. R. , Uchoa, E. T. , Ceravolo, G. S.
• Resumo

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  Childhood obesity has increased in both developed and developing countries. In animal models, postnatal early overfeeding has helped to mimic childhood obesity. However, the vascular consequence of childhood obesity in female rats has not been investigated. The study aimed to evaluate the effects of postnatal overfeeding on aortic reactivity in prepubertal and adult female rats. At one day of life, litters of Wistar rats were distributed into normal litter (5 female and 5 male pups - NL) or small litter (2 male and 1 female pups - SL). At PND 30 and 120, female offspring were evaluated for body weight (g); retroperitoneal, and perigonadal adipose tissue (fat pad weight/100g of the body n=9-13), and in vitro thoracic aorta reactivity to phenylephrine (Pheny) in the presence or absence of endothelium, and acetylcholine (ACh). At PND 120, to understand the role of the renin-angiotensin-aldosterone system at alterations, new ACh curves were made using the blockers: apocynin, losartan, spironolactone, and s-methyl. Comparison between groups was made using the maximum response (maxR, grams or % relaxation) for the agonist. At PND 30, SL had a higher body weight [NL 76.56 ±2.12 vs SL 91.52±1.78], retroperitoneal [NL 0.09±0.01 vs SL 0.17±0.01] and perigonadal [NL 0.04±0.005 vs SL 0.09±0.009] adipose than NL. At PND 120, NL and SL have similar biometric parameters. At PND 30 and 120, maxR to Phenyl was similar between groups. The maxR to ACh of SL in PND 30 [NL 99.65±2.5 vs SL 90.92±2,4 n=9] and PND 120 [NL 94.05±1.5 vs SL 84.65±2.5 n=9] were decreased when compared with NL. In SL rats, LOS [ SL 79,15 vs LOS 90,67±1.05 n=5] increased maxR to ACh. The maxR for ACh with other blockers was similar between groups. In conclusion, postnatal overnutrition causes childhood obesity and endothelial dysfunction mediated by receptors for angiotensin II.

   

• Palavras-chave
• childhood obesity, angiotensin II, endothelium dysfunction
• Área Temática
• Apresentações Orais - Sessão VII

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