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Quantification of fetal organ volume and fat deposition following in utero exposure to maternal Western Diet using MRI.

ABSTRACT: To examine the feasibility of using MRI to identify differences in liver size and fat deposition in fetal guinea pigs exposed to an in utero environment influenced by maternal consumption of a Western diet.Female guinea pigs fed either an energy-dense Western Diet (WD), comprised of increased saturated fats and simple sugars, or a Control Diet (CD) from weaning through pregnancy, underwent MR scanning near term (~ 60 days; term ~ 69 days). Maternal weights were collected at mating and at MR scanning. T1-weighted, T2-weighted, and IDEAL water-fat images were acquired at 3 Tesla. The images were used to segment maternal adipose tissue, fetal liver, fetal brain, fetal adipose tissue, and total fetal volumes and to measure maternal and fetal hepatic fat fractions.Weights of WD sows were lower prior to pregnancy (P = .04), however their weight gain over pregnancy did not differ from the CD group (P = .98). The WD sows had less total adipose tissue (TAT) at MR scanning (P = .04), while hepatic fat content was significantly elevated (P = .04). When controlling for litter size, WD fetuses had larger livers (P = .02), smaller brains (P = .01), and increased total adipose tissue volume (P = .01) when normalized by fetal volume. The WD fetuses also had increased hepatic fat fractions compared to CD fetal livers (P < .001).Maternal Western Diet consumption prior to and during pregnancy induces differences in maternal liver fat content, fetal liver volume and liver fat storage, as well as changes in fetal adipose tissue deposition that can be measured in utero using MRI.

SUBMITTER: Sinclair KJ

PROVIDER: S-EPMC5814025 | biostudies-literature | 2018

REPOSITORIES: biostudies-literature

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Quantification of fetal organ volume and fat deposition following in utero exposure to maternal Western Diet using MRI.

Sinclair Kevin J KJ Friesen-Waldner Lanette J LJ McCurdy Colin M CM Wiens Curtis N CN Wade Trevor P TP de Vrijer Barbra B Regnault Timothy R H TRH McKenzie Charles A CA

PloS one 20180215 2

<h4>Purpose</h4>To examine the feasibility of using MRI to identify differences in liver size and fat deposition in fetal guinea pigs exposed to an in utero environment influenced by maternal consumption of a Western diet.<h4>Materials and methods</h4>Female guinea pigs fed either an energy-dense Western Diet (WD), comprised of increased saturated fats and simple sugars, or a Control Diet (CD) from weaning through pregnancy, underwent MR scanning near term (~ 60 days; term ~ 69 days). Maternal w ...[more]

PMID: 29447203

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Project description:OBJECTIVE:Recent evidence indicates that the adult hematopoietic system is susceptible to diet-induced lineage skewing. It is not known whether the developing hematopoietic system is subject to metabolic programming via in utero high-fat diet (HFD) exposure, an established mechanism of adult disease in several organ systems. We previously reported substantial losses in offspring liver size with prenatal HFD. As the liver is the main hematopoietic organ in the fetus, we asked whether the developmental expansion of the hematopoietic stem and progenitor cell (HSPC) pool is compromised by prenatal HFD and/or maternal obesity. METHODS:We used quantitative assays, progenitor colony formation, flow cytometry, transplantation, and gene expression assays with a series of dietary manipulations to test the effects of gestational high-fat diet and maternal obesity on the day 14.5 fetal liver hematopoietic system. RESULTS:Maternal obesity, particularly when paired with gestational HFD, restricts physiological expansion of fetal HSPCs while promoting the opposing cell fate of differentiation. Importantly, these effects are only partially ameliorated by gestational dietary adjustments for obese dams. Competitive transplantation reveals compromised repopulation and myeloid-biased differentiation of HFD-programmed HSPCs to be a niche-dependent defect, apparent in HFD-conditioned male recipients. Fetal HSPC deficiencies coincide with perturbations in genes regulating metabolism, immune and inflammatory processes, and stress response, along with downregulation of genes critical for hematopoietic stem cell self-renewal and activation of pathways regulating cell migration. CONCLUSIONS:Our data reveal a previously unrecognized susceptibility to nutritional and metabolic developmental programming in the fetal HSPC compartment, which is a partially reversible and microenvironment-dependent defect perturbing stem and progenitor cell expansion and hematopoietic lineage commitment.

Dataset Information

Quantification of fetal organ volume and fat deposition following in utero exposure to maternal Western Diet using MRI.

Publications

Quantification of fetal organ volume and fat deposition following in utero exposure to maternal Western Diet using MRI.

Similar Datasets

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