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Morphofunctional renal alterations in rats induced by intrauterine hyperglycemic environment

INTRODUCTION: The renal development of rats begins in intrauterine life, finishing by 15 days after birth. Diabetes and other diseases during pregnancy can cause systemic changes in the offspring. We evaluated the structural and functional renal alterations of the offspring from diabetic mothers. MA...

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Detalles Bibliográficos
Autores principales: França-Silva, Nathane, Oliveira, Natácia Dreyce Gonçalves, Balbi, Ana Paula Coelho
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Termedia Publishing House 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4848350/
https://www.ncbi.nlm.nih.gov/pubmed/27186167
http://dx.doi.org/10.5114/aoms.2015.48220
Descripción
Sumario:INTRODUCTION: The renal development of rats begins in intrauterine life, finishing by 15 days after birth. Diabetes and other diseases during pregnancy can cause systemic changes in the offspring. We evaluated the structural and functional renal alterations of the offspring from diabetic mothers. MATERIAL AND METHODS: Pregnant rats were separated and 1, 7, 30 and 90 days-old (DO) pups were divided into groups according to the treatment that the mothers received: G1: control, G2: untreated diabetic and G3: insulin-treated diabetic. The kidneys from offspring at 1, 7 and 30 DO were removed for immunohistochemical and histological studies. Furthermore, blood and urine samples were collected from animals at 30 DO to determine the glomerular filtration rate (GFR) by creatinine clearance, and the animals at 90 DO were subjected to blood pressure measurement by plethysmography. RESULTS: Our results show an increase of PCNA(+) glomerular cells at 7 DO and a reduction in 30 DO animals as well as increased α-smooth muscle actin (α-SMA) tubulointerstitial expression at 1 and 7 DO in animals from G2, when compared with controls. The adult offspring from G2 showed reduced GFR and increased blood pressure. CONCLUSIONS: Maternal diabetes may have induced programming of renal damage in offspring of hyperglycemic mothers, which may have contributed to the impairment of renal function.