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Bilophila wadsworthia worsens high-fat diet-induced metabolic impairments in inflammation dependent and independent manners [mouse gene expression]

ABSTRACT: Dietary lipids favor the growth of the pathobiont Bilophila wadsworthia, but the relevance of this expansion in metabolic syndrome pathogenesis remains unknown. Here, we showed that B. wadsworthia synergize with HFD to promote higher inflammation, intestinal barrier dysfunction and bile acid dysmetabolism, leading to higher glucose dysmetabolism and hepatic steatosis. Host-microbiota transcriptomics analysis unraveled pathways, particularly butanoate metabolism, which may underlie the metabolic effects mediated by B. wadsworthia. Pharmacological suppression of B. wadsworthia-associated inflammation unmasked the bacterium’s intrinsic capacity to induce a negative impact on glycemic control and hepatic function. Finally, the probiotic Lactobacillus rhamnosus CNCM I-3690 was able to limit B. wadsworthia-induced immune and metabolic impairment by limiting its expansion, reducing inflammation and reinforcing intestinal barrier. Our results support a new avenue for interventions against western diet-driven inflammatory and metabolic diseases.

ORGANISM(S): Mus musculus

PROVIDER: GSE111451 | GEO | 2018/05/26

REPOSITORIES: GEO

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Bilophila wadsworthia worsens high-fat diet-induced metabolic impairments in inflammation dependent and independent manners [bacterial gene expression]

Project description:Dietary lipids favor the growth of the pathobiont Bilophila wadsworthia, but the relevance of this expansion in metabolic syndrome pathogenesis remains unknown. Here, we showed that B. wadsworthia synergize with HFD to promote higher inflammation, intestinal barrier dysfunction and bile acid dysmetabolism, leading to higher glucose dysmetabolism and hepatic steatosis. Host-microbiota transcriptomics analysis unraveled pathways, particularly butanoate metabolism, which may underlie the metabolic effects mediated by B. wadsworthia. Pharmacological suppression of B. wadsworthia-associated inflammation unmasked the bacterium’s intrinsic capacity to induce a negative impact on glycemic control and hepatic function. Finally, the probiotic Lactobacillus rhamnosus CNCM I-3690 was able to limit B. wadsworthia-induced immune and metabolic impairment by limiting its expansion, reducing inflammation and reinforcing intestinal barrier. Our results support a new avenue for interventions against western diet-driven inflammatory and metabolic diseases.

2018-05-26 | GSE112387 | GEO

Bilophila wadsworthia worsens high-fat diet-induced metabolic impairments in inflammation dependent and independent manners

Project description:Bilophila wadsworthia worsens high-fat diet-induced metabolic impairments in inflammation dependent and independent manners

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Transcriptomic analysis of mice treated with Lactobacillus rhamnosus CNCM i-3690 and different mutants and variants generated from this strain

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Bilophila wadsworthia worsens high-fat diet-induced metabolic impairments in inflammation dependent and independent manners [bacterial gene expression]

Project description:Bilophila wadsworthia worsens high-fat diet-induced metabolic impairments in inflammation dependent and independent manners [bacterial gene expression]

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Bilophila wadsworthia worsens high-fat diet-induced metabolic impairments in inflammation dependent and independent manners [mouse gene expression]

Project description:Bilophila wadsworthia worsens high-fat diet-induced metabolic impairments in inflammation dependent and independent manners [mouse gene expression]

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Hepatic Lysosomal Acid Lipase Overexpression Worsens Hepatic Inflammation in Mice Fed a Western Diet

Project description:Hepatic Lysosomal Acid Lipase Overexpression Worsens Hepatic Inflammation in Mice Fed a Western Diet

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Bilophila wadsworthia worsens high-fat diet-induced metabolic impairments in inflammation dependent and independent manners

Project description:This SuperSeries is composed of the SubSeries listed below.

2018-05-26 | GSE112388 | GEO

Hepatic Lysosomal Acid Lipase Overexpression Worsens Hepatic Inflammation in Mice Fed a Western Diet

Project description:Non-alcoholic fatty liver disease (NAFLD) is characterized by the accumulation of lipid droplets (LD) in hepatocytes. NAFLD development and progression is associated with an increase in hepatic cholesterol and decreased autophagy and lipophagy flux. Previous studies have shown that the expression of lysosomal acid lipase (gene=LIPA, protein=LAL), which can hydrolyze both triglyceride and cholesteryl esters, is inversely correlated with the severity of NAFLD. In addition, ablation of LAL activity results in profound NAFLD. Based on this, we predicted that overexpressing LIPA in the livers of mice fed a Western diet (FPC) would prevent the development of NAFLD. As expected, mice fed the FPC diet exhibited numerous markers of NAFLD including hepatomegaly, lipid accumulation, and inflammation. Unexpectedly, LAL overexpression did not attenuate steatosis and had only minor effects on neutral lipid composition. However, LAL overexpression exacerbated inflammatory gene expression and infiltration of immune cells in mice fed the FPC diet. LAL overexpression also resulted in abnormal phagosome accumulation and lysosomal lipid accumulation depending upon the dietary treatment. Hepatic overexpression of LAL drove immune cell infiltration and inflammation and did not attenuate the development of NAFLD suggesting that targeting LAL expression is not a viable route to treat NAFLD.

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2023-07-11 | GSE169501 | GEO

Sacha inchi oil alleviates gut microbiota dysbiosis and improves hepatic lipid dysmetabolism in high-fat diet-fed rats

Project description:Dietary ω-3 polyunsaturated fatty acids (PUFAs) are beneficial for humans against the development of hyperlipidaemia, but the underlying mechanisms are still poorly understood. Here, we demonstrated that oral consumption of sacha inchi oil, which is rich in α-linolenic acid, alleviated dyslipidemia, hepatic steatosis and inflammatory infiltration in high-fat diet (HFD)-fed rats. Sacha inchi oil administration reversed gut microbiota dysbiosis and altered the gut microbiota metabolome and in particular prevented bile acid dysmetabolism caused by a HFD. Sacha inchi oil intake ameliorated hepatic lipid dysmetabolism in HFD-fed rats, via potentiating the biosynthesis and reuptake of bile acids, reducing the de novo lipogenesis, promoting fatty acid beta-oxidation, and alleviating the dysregulation of glycerolipid, glycerophospholipid, and sphingolipid metabolisms. The results showed that dietary sacha inchi oil can alleviate gut microbiota dysbiosis and reduce lipid dysmetabolism in HFD rats, and provide novel insights into the molecular mechanisms by which plant-derived ω-3 PUFAs prevent the development of hyperlipidaemia.

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