Early exposure to distinct sources of lipids affects differently the development and hepatic inflammatory profiles of 21-day-old rat offspring

Abstract

IntroductionMaternal diet composition of fatty acids during pregnancy and lactation seems to modify the fetal programming, epigenetic pattern and offspring phenotype.AimHerein, we investigated the effects of maternal consumption of normal-fat diets with distinct lipid sources during pregnancy and lactation on the somatic development and proinflammatory status of 21-day-old rat offspring.Materials and MethodsOn the first day of pregnancy, female Wistar rats were divided into four groups as follows: soybean oil (M-SO), lard (M-L), hydrogenated vegetable fat (M-HVF) and fish oil (M-FO). Diets were maintained during pregnancy and lactation. Male offspring constituted the SO, L, HVF and FO groups. Pups were weighed and measured weekly. Lipopolysaccharide serum concentration was determined. Tumor necrosis factor alpha, interleukin (IL)-6 and IL-10 in the liver were evaluated by enzyme-linked immunosorbent assay. Liver gene expressions were determined by real-time polymerase chain reaction. Protein expressions in the liver were analyzed by Western blotting.ResultsWe observed an increase in body weight and adiposity in L and HVF groups. Moreover, HVF group showed an increase in the toll-like receptor 4 mRNA levels, IL10Rα and phosphorylated form of IκB kinase (IKK; p-IKKα+β) protein expression. The FO group presented a decrease in body weight, relative weight of retroperitoneal adipose tissue, ADIPOR2 gene expression, lipopolysaccharide and p-IKKα+β and phosphorylated form of nuclear transcription factor kappa B (NFκB) p50 (p-NFκB p50) protein expression.ConclusionSummarily, whereas maternal intake of normal-fat diets based on L and HVF appear to affect the somatic development negatively, only early exposure to HVF impairs the pups’ proinflammatory status. In contrast, maternal diets based on FO during pregnancy and lactation have been more beneficial to the adiposity and toll-like receptor 4 signaling pathway of the 21-day-old rat offspring, particularly when compared to L or HVF diets.

Interactive effects of maternal and weaning high linoleic acid intake on hepatic lipid metabolism, oxylipins profile and hepatic steatosis in offspring

“…During the pregnancy and/or lactation period, diet represents one of the essential environmental factors that can have beneficial or adverse consequences on phenotype and health of offspring [1]. Evidence that the quantity but also the type of dietary fatty acids (FA) in maternal diet during this period could influence the fetal programming has emerged [3][4][5]. Essential polyunsaturated FA (PUFA) and their long-chain derivatives (LC-PUFA) are central nutrients required for cell membrane structure and bioactive molecule synthesis.…”

“…Because fetus and newborn have a limited capacity to synthesize LC-PUFA, their intake mainly depends on the maternal availability and hepatic conversion from precursors. Several reports suggested that maternal LC-PUFA precursor's intake during the early stages of fetal development can influence lipid metabolism and signaling pathways leading to the development of later disorders in offspring [3,5,6].…”

“…Several reports suggested that the maternal quantity of fat intake plays a major role in the offspring development by showing that offspring of obese or high fat diet (HFD) fed mothers are more susceptible to develop the features of NAFLD [2,[17][18][19]. However, the importance of maternal dietary type of fat has also been highlighted in the development of hepatic inflammation and steatosis independently from an excess of caloric consumption [3,20]. The hepatic FA analysis of NAFLD patients have shown an imbalance of n-6/n-3 PUFA in patients but the link with their diet has not been reported and the mechanisms remain unclear.…”

Proinflammatory State in the Odontogenesis of Fetuses Exposed to Different Types of Fatty Acids during Pregnancy

“…Odontogenesis is characterized by the following stages: dental lamina, button, cap, bell, crown, and rizinogenesis phases [ 20 ]. The harmful effects of maternal consumption of SFAs and TFAs, especially when consumed during pregnancy and/or lactation, are already known [ 17 , 18 ]. Previous studies have shown that the increased consumption of SFAs can lead to an increase in the levels of glucose, insulin, leptin, TNF-α, MCP-1, IL-6, NF-κB, and activation of TLR4 [ 21 ].…”

“…The addition of 10 g of soybean oil to every 1 kg of diet, except for diet C, was made to meet the minimum requirement of essential FAs. The experimental design was established in previous studies conducted by our group [ 17 , 18 ].…”