The effect of maternal obesity on fatty acid transporter expression and lipid metabolism in the full‐term placenta of lean breed swine

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Obesity and obesity‐associated hyperlipidemia have been demonstrated to provoke a reproductive disorder in human beings and some animal species like pigs (Brewer & Balen, 2010; Metwally, Ledger, & Li, 2008; Ratky et al., 2005). In pigs, negative relationships of growth rate (GR) or back‐fat thickness (BF) with the subsequent sow reproductive performance were observed in several studies (Amaral Filha, Bernardi, Wentz, & Bortolozzo, 2010; Rozeboom, Pettigrew, Moser, Cornelius, & el Kandelgy, 1996). Additionally, a high occurrence of intrauterine growth restriction (IUGR) is common and widely described for lean or obese breed swine (Foxcroft et al., 2006; Gonzalez‐Anover et al., 2011). Although the connection between offspring outcomes and maternal obesity is established in pigs, the molecular mechanisms connecting maternal obesity to foetal development remain elusive.
As a critical transport interface between the maternal and foetal environment, the placenta sensitizes the developing foetus to environmental disturbances. Studies have shown that maternal obesity promotes a lipotoxic placental environment characterized by lipid accumulation, inflammation and oxidative stress (Challier et al., 2008; Roberts et al., 2009). A lipotoxic milieu within the placenta has been linked to dysregulation of placental lipid transport and metabolism, thus resulting in an aberrant foetal development (Dube et al., 2012; Saben et al., 2014; Zhu, Ma, Long, Du, & Ford, 2010). Essential fatty acids (EFA) are crucial for foetal growth and development (Haggarty, 2002), especially during the late gestation when the foetus intensifies its nutrient demand for exponential growth. To satisfy its need for fatty acids (FA), the foetus depends on the maternal diet as well as on placental transport and metabolism (Haggarty, 2010). Because triglyceride (TG) is not transported across the placenta, their hydrolysis by placental lipoprotein lipase (LPL) to non‐esterified fatty acids (NEFA) provides a vital source of EFA for both the placenta and foetus (Herrera, Amusquivar, Lopez‐Soldado, & Ortega, 2006). FA can be transferred to the foetus by simple diffusion or though transport proteins. Several transmembrane FA transport proteins have been identified in human or animal placenta, including fatty acid transport proteins 1‐6 (FATPs/SLC27As), intracellular FA binding proteins (FABPs) and FA translocase (FAT/CD36). Considering the importance of placental lipid transport and metabolism in weight control of the newborn either by promoting or by limiting FA transfer to the foetus, we hypothesized that maternal lipid profile influences FA transport and metabolism in the placenta of pigs. Therefore, this study was designed to characterize the effects of obese pregnancy in sows with high BF on maternal and newborn circulating lipids, expression of several FA carriers, and on lipid accumulation in placenta.

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