Maternal obesity has been associated with shifts in intestinal microbiota which may contribute to impaired barrier function Impaired barrierfunction may expose the placenta and fetus to pro-inflammatory mediators.
We investigated the impacts of diet-induced obesity in mice on maternal and fetalintestinal structure and placental vascularization Diet-induced obesity decreased maternal intestinal short chain fatty acids, their receptors, impaired gutbarrier integrity and was associated with fetalintestinal inflammation. Placenta from obese mothers showed blood vessel immaturity, hypoxia, increased transcript levels of inflammation, autophagy and ER stress markers.
These data suggest that maternalintestinal changes likely contribute to adverse placentaladaptations and, via alterations in fetalgut development, impart increased risk of obesity in the offspring ABSTRACT: Shifts in maternalintestinal microbiota have been implicated in metabolic adaptations to pregnancy.
In this study we generated cohorts of female C57BL/6J mice fed a control (17% kcal fat, n = 10-14) or a high-fatdiet (HFD 60% kcal from fat, n = 10-14; ad libitum) to investigate impacts on the maternal gut microbiota, intestinal inflammation and gutbarrier integrity, placental inflammation, and fetalintestinal development at E18.5.
HFD was associated with decreased relative abundances of SCFA producing genera during pregnancy. These diet-induced shifts paralleled decreased maternalintestinal mRNA levels of SCFA receptor Gpr41, modestly decreased cecal butyrate, and altered mRNA levels of inflammatory cytokines and immune cell markers in the maternal intestine.
Maternal HFD resulted in impaired gutbarrier integrity, with corresponding increases in circulating maternal levels of LPS and TNF. Placenta from HFD dams demonstrated blood vessel immaturity and hypoxia, decreased free carnitine, acylcarnitine derivatives, TMAO, as well as altered mRNA levels of inflammation, autophagy and ER stress markers. HFD exposed fetuses had increased activation of NF-κB and inhibition of the unfolded protein response in the developing intestine.
Together, these data suggest that HFD intake prior to and during pregnancy shifts the composition of the maternalgut microbiota and impairs gutbarrier integrity, resulting in increased maternal circulating LPS, which may ultimate contribute to changes in placental vascularization and fetalgut development.
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