Congenital Anomalies Programmed by Maternal Diabetes and Obesity on Offspring of Rats

Abstract

Embryo-fetal exposure to maternal disorders during intrauterine life programs long-term consequences for the health and illness of offspring. In this study, we evaluated whether mild diabetic rats that were given high-fat/high-sugar (HF/HS) diet presented maternal and fetal changes at term pregnancy. Female rats received citrate buffer (non-diabetic-ND) or streptozotocin (diabetic-D) after birth. According to the oral glucose tolerance test (OGTT), the experimental groups (n = 11 animals/group) were composed of non-diabetic and diabetic receiving standard diet (S) or HF/HS diet. High-fat/high-sugar diet (30% kcal of lard) in chow and water containing 5% sucrose and given 1 month before mating and during pregnancy. During and at the end of pregnancy, obesity and diabetes features were determined. After laparotomy, blood samples, periovarian fat, and uterine content were collected. The diabetic rats presented a higher glycemia and percentage of embryonic losses when compared with the NDS group. Rats DHF/HS presented increased obesogenic index, caloric intake, and periovarian fat weight and reduced gravid uterus weight in relation to the other groups. Besides, this association might lead to the inflammatory process, confirmed by leukocytosis. Obese rats (NDHF/HS and DHF/HS) showed higher triglyceride levels and their offspring with lower fetal weight and ossification sites, indicating intrauterine growth restriction. This finding may contribute to vascular alterations related to long-term hypertensive disorders in adult offspring. The fetuses from diabetic dams showed higher percentages of skeletal abnormalities, and DHF/HS dams still had a higher rate of anomalous fetuses. Thus, maternal diabetes and/or obesity induces maternal metabolic disorders that contribute to affect fetal development and growth.

Influence of maternal periuterine and periovarian fat on reproductive performance and fetal growth in rats

“…As evidenced in the present study, maternal HFD consumption caused a decreased percentage of AGA fetuses and an increased percentage of SGA fetuses, as seen in another laboratory study (Sinzato et al 2022). The increased percentage of SGA fetuses due to intrauterine growth restriction may be related to functional or morphological placental changes, contributing to decreased fetal weight (Araujo-Silva et al 2021). Due to intrauterine growth restriction and the increased number of SGA fetuses, there was a reduced litter weight.…”

Effects of female obesity on conception, pregnancy and the health of offspring

“…Meanwhile, obese pregnant women have a 30% higher risk for congenital anomalies of neural tube, heart and limb than normal-weight pregnant women ( 25 ). The precise mechanism by which maternal obesity impacts fetal development is not known.…”

Maternal and Fetal-Placental Effects of Etanercept Treatment During Rats’ Pregnancy

“…The pre-implantation loss percentage (embryo loss rate in the period prior to implantation) was calculated as follows: (Number of corpus luteum-Number of implantation/Number of corpus luteum) × 100. The percentage of post-implantation loss (death of embryos after implantation) was calculated as follows: (Number of implantations-Number of living fetuses/Number of implantations) × 100 (Araujo-Silva et al, 2021). The placental efficiency was calculated by the ratio between fetal weight and placental weight (Hayward et al, 2016).…”