Decidual abnormalities in the prepubertal period and day 9 of pregnancy in diabetic rat offspring
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Keywords

diabetes gestacional – útero - programación fetal

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Decidual abnormalities in the prepubertal period and day 9 of pregnancy in diabetic rat offspring. (2020). Universitas Medica. https://revistas.javeriana.edu.co/index.php/vnimedica/article/view/31046
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Abstract

Decidual abnormalities in the prepubertal period and day 9 of pregnancy in diabetic rat offspring.

Lic. Cintia Gatti* 1, Lic. Sabrina Roberti* 1, Ph D. Evangelina Capobianco 1, Bioq. Dalmiro Gómez Ribot 1, Ph D. Alicia Jawerbaum 1

1 Laboratorio de Reproducción y metabolismo, CEFYBO - CONICET, Facultad de Medicina, Universidad de Buenos Aires, Argentina.

Introduction: Maternal diabetes induces an intrauterine prooxidant/proinflammatory environment, associated to impaired PPAR pathways, which could alter the offspring’s uterus. Objectives: To evaluate, in control and diabetic rat offspring, the uterine weight (decidualized or not) in the prepubertal period, and decidual PPARs protein expression on day 9 of pregnancy. Methods: Diabetes was induced in F0 rats by neonatal administration of streptozotocin (90 mg/kg sc). Females were mated with healthy males to study the offspring’s uterus a) on postnatal day 30, with or without induction of decidualization (PMSG/hCG, 50 IU) and b) on day 9 of pregnancy. Uteri were weighed at the prepubertal stage and decidual PPAR levels were evaluated on day 9 of pregnancy. Results: In the prepubertal stage, the uterus of the offspring of diabetic rats showed reduced weight (p<0.05 vs Control), and the induction with PMSG/hCG increased its weight to values similar to controls. In pregnancy, number of implantations and resorptions did not change in the studied groups. Protein expression of PPARalpha, PPARgamma and PPARdelta were found reduced (p<0.05 vs Control). Conclusions: Maternal diabetes alters the offspring’s uterus at prepuberty and leads to reduced expression of decidual PPARs in pregnancy, possibly contributing to an F1 prooxidant/proinflammatory intrauterine environment.

 

Keywords: gestational diabetes - uteri - fetal programming

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