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Faecalibaculum rodentium as a key player in combating maternal obesity-induced labor disorders

ABSTRACT:

The global rise in maternal obesity increases the risk of adverse maternal and neonatal outcomes. This study demonstrates that both long- (12 weeks) and short-term (gestational) exposure to a high-fat diet (HFD) induces uterine labor disorders, elevates stillbirth rates, and alters gut microbiota composition. Fecal microbiota transplantation (FMT) reveals that HFD inhibits uterine AMPK phosphorylation and reduces COX4 expression via gut microbiota modulation, further contributing to labor dysfunction. Faecalibaculum rodentium, a dominant gut bacterium, shows a negative correlation with stillbirth incidence. Transplantation of Faecalibaculum rodentium mitigates HFD-induced labor disorders, restores uterine ATP levels, and reduces stillbirth rates. This intervention increases serum butyric and acetic acid levels, which inhibit ERK phosphorylation via the GPR41 receptor and activate AMPK phosphorylation, promoting Nrf1 and PGC1 expression. These findings highlight the pivotal role of Faecalibaculum rodentium in counteracting HFD-induced uterine mitochondrial dysfunction and stillbirth.

INSTRUMENT(S): Liquid Chromatography MS - alternating - reverse phase

PROVIDER: MTBLS12877 | MetaboLights | 2025-08-22

REPOSITORIES: MetaboLights

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			Action	DRS
	a_MTBLS12877_LC-MS_alternating_reverse-phase_metabolite_profiling.txt	Txt
	i_Investigation.txt	Txt
	m_MTBLS12877_LC-MS_alternating_reverse-phase_metabolite_profiling_v2_maf.tsv	Tabular
	s_MTBLS12877.txt	Txt

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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. Examination of differentially expressed genes between gestational day 15 (+/- 0.5 days) C57BL/6 mouse fetal livers from diet-induced (60% fat diet) obese or control female mice.

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Faecalibaculum rodentium as a key player in combating maternal obesity-induced labor disorders

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