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The gut microbiota modulates host energy and lipid metabolism in mice.

ABSTRACT: The gut microbiota has recently been identified as an environmental factor that may promote metabolic diseases. To investigate the effect of gut microbiota on host energy and lipid metabolism, we compared the serum metabolome and the lipidomes of serum, adipose tissue, and liver of conventionally raised (CONV-R) and germ-free mice. The serum metabolome of CONV-R mice was characterized by increased levels of energy metabolites, e.g., pyruvic acid, citric acid, fumaric acid, and malic acid, while levels of cholesterol and fatty acids were reduced. We also showed that the microbiota modified a number of lipid species in the serum, adipose tissue, and liver, with its greatest effect on triglyceride and phosphatidylcholine species. Triglyceride levels were lower in serum but higher in adipose tissue and liver of CONV-R mice, consistent with increased lipid clearance. Our findings show that the gut microbiota affects both host energy and lipid metabolism and highlights its role in the development of metabolic diseases.

SUBMITTER: Velagapudi VR

PROVIDER: S-EPMC2853437 | biostudies-literature | 2010 May

REPOSITORIES: biostudies-literature

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The gut microbiota modulates host energy and lipid metabolism in mice.

Velagapudi Vidya R VR Hezaveh Rahil R Reigstad Christopher S CS Gopalacharyulu Peddinti P Yetukuri Laxman L Islam Sama S Felin Jenny J Perkins Rosie R Borén Jan J Oresic Matej M Bäckhed Fredrik F

Journal of lipid research 20091229 5

The gut microbiota has recently been identified as an environmental factor that may promote metabolic diseases. To investigate the effect of gut microbiota on host energy and lipid metabolism, we compared the serum metabolome and the lipidomes of serum, adipose tissue, and liver of conventionally raised (CONV-R) and germ-free mice. The serum metabolome of CONV-R mice was characterized by increased levels of energy metabolites, e.g., pyruvic acid, citric acid, fumaric acid, and malic acid, while ...[more]

PMID: 20040631

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Project description:Background: Gut microbiota, which plays a crucial role in inflammatory bowel diseases (IBD), might have therapeutic benefits for ulcerative colitis or Crohn's disease. Targeting gut microbiota represents a new treatment strategy for IBD patients. Rhein is one of the main components of rhubarb and exhibits poor oral bioavailability but still exerts anti-inflammatory effects in some diseases. Therefore, we investigated the effect of rhein on colitis and studied its possible mechanisms. Methods: The chronic mouse colitis model was induced by four rounds of 2% dextran sulfate sodium (DSS) treatment. The mice were treated with 50 mg/kg and 100 mg/kg rhein daily, body weight, colon length, histological score, inflammatory cytokines in serum or intestine, and fecal lipocalin 2 concentration were determined. Th17 cell, Th1 cell and Th2 cell infiltration in the mesenteric lymph node were analyzed by flow cytometry. Metabolic profiles were collected by non-targeted metabolomics and key metabolic pathways were identified using MetaboAnalyst 4.0. We also assessed intestinal barrier permeability and performed 16s rDNA sequencing. Lactobacillus sp. was cultured, and fecal microbiota transplantation (FMT) was employed to evaluate the contribution of gut microbiota. Results: Rhein could significantly alleviate DSS-induced chronic colitis. Uric acid was identified as a crucial modulator of colitis and rhein treatment led to decreased uric acid levels. We determined that rhein changed purine metabolism indirectly, while the probiotic Lactobacillus was involved in the regulation of host metabolism. Uric acid resulted in a worsened intestinal barrier, which could be rescued by rhein. We further confirmed that rhein-treated gut microbiota was sufficient to relieve DSS-induced colitis by FMT. Conclusion: We showed that rhein could modulate gut microbiota, which indirectly changed purine metabolism in the intestine and subsequently alleviated colitis. Our study has identified a new approach to the clinical treatment of colitis.

Project description:We aimed to determine the prebiotic impact of Mushroom Bulgaria inquinans (BI) on the host immune response and gut microbiota. Male C57BL/6 mice were fed a diet supplemented with 0, 1, or 2% BI for 4 wks. Compared to mice fed with a control diet (0% BI), mice fed with 1 or 2% BI had an increase of T cell proliferation from the spleen, but such change was not found between 1 and 2% BI treated mice. Also, BI at 2% increased the production of IL-2 of splenocytes stimulated with T-cell mitogens, but BI at 1 and 2% did not affect productions of other splenic-T cell cytokines including IL-4, IL-10, and IFN-γ. Interestingly, BI at 1 or 2% inhibited T cell proliferation of mesenteric lymph node (mLN) but this effect was not found between 1 and 2% BI treated mice. Furthermore, BI inhibited the production of IL-2 in anti-CD3/CD28-stimulated T cells from mLN in a dose-dependent manner. Meanwhile, BI at 2%, not 1% inhibited the production of IL-4, IL-10, and IFN-γ of mLN. Since BI at 2% produced a more significant effect on the immune response, we further used BI at 2% to evaluate the effect of BI on gut microbiota. Of note, BI reduced the diversity of gut microbiota and resulted in an increase of Faecalibaculum and Parabacteroides abundance and the decrease of Allobaculum, Candidatus_Saccharimonas, and Rikenella abundance at the genus level. Finally, the correlation was observed between specific bacteria genera and the productions of T-cell cytokines from mesenteric lymphocytes: Rikenella and Candidatus_Saccharimonas correlated positively with IL-2, IL-4, IL-10, and IFN-γ; Bacteroides and Parabacteroides correlated negatively with IL-2 and IL-4; Faecalibaculum correlated negatively with IFN-γ and IL-4 and Bacteroides and Bifidobacterium correlated negatively with IFN-γ. The specific role of each intestinal microbiota observed is still unclear, but BI might exert a prebiotic effect on gut microbiota by increasing the abundance of potentially beneficial bacteria (Faecalibaculum). This is helpful for further demonstrating the healthy-promotion mechanism of B. inquinans.

Dataset Information

The gut microbiota modulates host energy and lipid metabolism in mice.

Publications

The gut microbiota modulates host energy and lipid metabolism in mice.

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