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Cesarean section-induced changes in the gut microbiota facilitate metabolic disease in high-fat diet-induced obese mice

ABSTRACT:

Growing evidence suggests that CS birth may alter the gut microbiota (i.e. dysbiosis), increasing the risk of immune and metabolic disorders. This study aims to investigate the causal relationship between caesarean section (CS)-induced gut dysbiosis and obesity in a high-fat diet mouse model. In this study, sera samples from male C57BL/6 mice were delivered via CS or vaginally (VD) at the age of 4 weeks were profiled for metabolomics by LC-MS. After preprocessing with XCMS, MS features showing significant difference in peak height between the two groups were annotated. The CS microbiome associated mice had higher levels of indoleactic acid, isovalerylcarnitine and pantothenic acid, the VD microbiome associated mice had higher levels of cholic acid and lysophosphatidylcholine 16:0.

INSTRUMENT(S): Liquid Chromatography MS - negative - reverse-phase, Liquid Chromatography MS - positive - reverse-phase

PROVIDER: MTBLS13792 | MetaboLights | 2026-02-03

REPOSITORIES: MetaboLights

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			Action	DRS
	a_MTBLS13792_LC-MS_negative_reverse-phase_metabolite_profiling.txt	Txt
	a_MTBLS13792_LC-MS_positive_reverse-phase_metabolite_profiling.txt	Txt
	i_Investigation.txt	Txt
	m_MTBLS13792_LC-MS_negative_reverse-phase_metabolite_profiling_v2_maf.tsv	Tabular
	m_MTBLS13792_LC-MS_positive_reverse-phase_metabolite_profiling_v2_maf.tsv	Tabular

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Project description:Pancreatic cancer is the 3rd most prevalent cause of cancer related deaths in United states alone, with over 55000 patients being diagnosed in 2019 alone and nearly as many succumbing to it. Late detection, lack of effective therapy and poor understanding of pancreatic cancer systemically contributes to its poor survival statistics. Obesity and high caloric intake linked co-morbidities like type 2 diabetes (T2D) have been attributed as being risk factors for a number of cancers including pancreatic cancer. Studies on gut microbiome has shown that lifestyle factors as well as diet has a huge effect on the microbial flora of the gut. Further, modulation of gut microbiome has been seen to contribute to effects of intensive insulin therapy in mice on high fat diet. In another study, abnormal gut microbiota was reported to contribute to development of diabetes in Db/Db mice. Recent studies indicate that microbiome and microbial dysbiosis plays a role in not only the onset of disease but also in its outcome. In colorectal cancer, Fusobacterium has been reported to promote therapy resistance. Certain intra-tumoral bacteria have also been shown to elicit chemo-resistance by metabolizing anti-cancerous agents. In pancreatic cancer, studies on altered gut microbiome have been relatively recent. Microbial dysbiosis has been observed to be associated with pancreatic tumor progression. Modulation of microbiome has been shown to affect response to anti-PD1 therapy in this disease as well. However, most of the studies in pancreatic cancer and microbiome have remained focused om immune modulation. In the current study, we observed that in a T2D mouse model, the microbiome changed significantly as the hyperglycemia developed in these animals. Our results further showed that, tumors implanted in the T2D mice responded poorly to Gemcitabine/Paclitaxel (Gem/Pac) standard of care compared to those in the control group. A metabolomic reconstruction of the WGS of the gut microbiota further revealed that an enrichment of bacterial population involved in drug metabolism in the T2D group.

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Cesarean section-induced changes in the gut microbiota facilitate metabolic disease in high-fat diet-induced obese mice

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