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.
Highlights
Diabetes mellitus (DM) is a syndrome that is a growing health problem, accounting for 10.4% of global mortality
The feed intake was increased, and water intake was decreased compared with non-diabetic rats receiving high-fat/high-sugar diet (NDHF/HS) and DS groups; and the DHF/HS group had the gravid uterus weight decrease compared with the NDHF/HS rats and a higher positive obesity rate compared with the DS group
The streptozotocin-induced mild diabetes in rat offspring after birth caused a diabetic status. This was confirmed by oral glucose tolerance test (OGTT) and higher area under curve (AUC) data
Summary
Diabetes mellitus (DM) is a syndrome that is a growing health problem, accounting for 10.4% of global mortality. Fetal programming is a theory that suggests that the environment around the developing fetus plays an important role in determining the risk of disease in childhood and adulthood (Entringer et al, 2012) In this sense, factors such as overweight, obesity, and maternal diabetes during pregnancy are known to be effective agents leading to chronic-disease development in offspring (Yessoufou and Moutairou, 2011), showing the relevance of intrauterine environment for health of descendants in the future. To reproduce maternal hyperglycemia found in Type 2 DM in animal models, streptozotocin (STZ) induction can be performed in the neonatal period of rats (Tsuji et al, 1988; Jawerbaum and White, 2010; Santos et al, 2015; Bequer et al, 2018; Bueno et al, 2020) This type of experimental diabetes is termed as “mild diabetes” (Hauschildt et al, 2018; Machado et al, 2020). Considering that pregnancy is a critical period, where maternal conditions and habits can lead to persistent changes in offspring (Fleming et al, 2015), it is important that the studies are conducted in a manner where new care strategies can be taken
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