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It is known that adverse stimuli, such as altered diets during pregnancy and lactation, can result in deleterious effects on the progeny. The aim of this study was to evaluate the possible gastrointestinal repercussions in the offspring of Wistar rats exposed to high-fat diets. Pregnant rats were divided into three groups: normolipidic diet (3.5% lipids), a diet containing 28% lipids, and a diet with 40% lipids. Body weight and food, water, daily caloric, and macronutrient intake were evaluated in the pregnant rats. Structural and functional gastrointestinal parameters were assessed in 30-day-old male pups. Depending on the lipid content of the maternal diet, the pups may exhibit gastric mucosal thickening, an increase in the relative weight of the small intestine, a reduction in the jejunal and ileal mucosa, and a decrease in the total thickness of the ileum. Additionally, there may be a reduction in the number of villi per area in these organs and a thinning of the muscular layer in the large intestine. The structural changes induced by the maternal high-fat diet seem to reduce the stomach’s sensitivity to ethanol-induced ulcers, which is the only functional alteration observed. Therefore, the offspring of dams exposed to high-fat diets during pregnancy and lactation exhibits impaired gastrointestinal development, with alterations depending on dietary fat content and specific gastrointestinal regions. Structural changes did not always result in functional abnormalities and, in some cases, appeared protective. The long-term consequences of the observed morphological alterations require further investigation.
Accumulating evidence suggests that maternal overnutrition can result in a higher development risk of obesity and renal disease in the offspring’s adulthood. The present study tested different lipid levels in the maternal diet during pregnancy and lactation and its repercussions on the offspring of Wistar rats. Offspring of 1, 7, 30 and 90-d-old were divided into the following groups: Control (CNT) – offspring of dams that consumed a standard chow diet (3.5% of lipids); Experimental 1 (EXP1) – offspring of dams exposed to a high-fat diet (HFD) (28% of lipids); and Experimental 2 (EXP2) – offspring of dams exposed to a HFD (40% of lipids). Regarding maternal data, there was a decrease in the amount of diet ingested by EXP2. Daily caloric intake was higher in EXP1, while protein and carbohydrate intakes were lower in EXP2. While lipid intake was higher in the experimental groups, EXP1 consumed more lipids than EXP2, despite the body weight gain being higher in EXP2. Adult offspring from EXP1 presented higher blood glucose. Regarding morphometric analysis, in both experimental groups, there was an increase in the glomerular tuft and renal corpuscle areas, but an increase in the capsular space area only in EXP1. There was a decrease in the glomerular filtration rate (GFR) in EXP1, in contrast to an increase in GFR of EXP2, along with an increase in urinary protein excretion. In conclusion, the maternal HFDs caused significant kidney damage in offspring, but had different repercussions on the type and magnitude of recorded change.
Alterations in the maternal environment may impact on the fetal development. The objective of this study was to investigate the gastrointestinal consequences of maternal hypothyroidism for the male offspring from Wistar rats. The pregnant rats were divided into three groups: control (C – received water), experimental 1 [E1 – received methimazole (MMI) solution] during gestation and lactation, and experimental 2 (E2 – received MMI solution) during gestation. Maternal parameters evaluated: free T3 and T4, bodyweight variation, and water/food intake. Offspring parameters evaluated: litter size, number of male/female, free T3 and T4, stomach area, gastric ulcer susceptibility, small intestine length and weight, small intestine and distal colon motility, the stomach and intestinal weight–body weight ratio (SW/BW–IW/BW), and the accumulation of intestinal fluid. Maternal T3 and T4 from E1 were decreased when compared to the other groups. There were no differences for maternal water/food intake and weight gain, litter size, and number of males and females. Regarding to offspring, free T3, SW/BW, IW/BW, and intestinal fluid accumulation were not different between the groups, but T4 was decreased in E1. However, 30-day-old pups from E1 and E2 were smaller with lower stomach and small intestine. Even more, E1 presented a lower ulcer index when compared to the C, while E2 had a higher distal colon transit. It can be concluded that maternal hypothyroidism impaired the total body development, as well as gastric and intestinal development, besides interfering with the susceptibility to the ulcer and intestinal transit of male offspring from Wistar rats.
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