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Ginecología y obstetricia de México

versão impressa ISSN 0300-9041

Resumo

BEQUER, Leticia et al. Diabetic embryopathy and disorders in maternal reproductive development in rats with pregestational diabetes. Ginecol. obstet. Méx. [online]. 2023, vol.91, n.1, pp.21-31.  Epub 14-Abr-2023. ISSN 0300-9041.  https://doi.org/10.24245/gom.v91i1.8339.

OBJECTIVES:

Diabetes mellitus is one of the most frequent disorders of pregnancy with adverse consequences for the mother and a high risk of diabetic embryopathy in the offspring. The objective of the research was to determine the effect of pregestational diabetes with moderate hyperglycemia on maternal reproductive performance, growth, development and embryonic morphology in Wistar rats.

MATERIALS AND METHODS:

Longitudinal, prospective and experimental study carried out at the Biomedical Research Unit of the University of Medical Sciences of Villa Clara, Cuba. A model of neonatally induced moderate diabetes was used in female Wistar rat pups two days old, by subcutaneous administration of 100 mg/kg of body weight of streptozotocin in a single dose. At 120 days after birth, rats from both experimental groups (diabetic and control) were mated with healthy males. Weight and glycemia were determined during pregnancy and at 11,5 days the cesarean section was performed. The variables of maternal reproductive performance and of growth, development and external morphology in the embryos were analyzed. According to the results, non-parametric tests were used for the analysis of the quantitative variables and the Chi-square test for the qualitative variables.

RESULTS:

Moderate pregestational diabetes caused changes in maternal weight gain, number of resorptions, implantation sites, preimplantation loss, and implantation efficiency, as well as in morphology, size, and number of somites in embryos.

CONCLUSIONS:

Moderate pregestational diabetes altered maternal reproductive performance and intrauterine growth and development of embryonic offspring. Diabetic embryopathy was also manifested by malformations of the central nervous system.

Palavras-chave : Diabetes mellitus; Experimental; Rats; Streptozotocin; Hyperglycemia; Embryon.

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