GNPS_Bile_acids_gavage_experiment
Ontology highlight
ABSTRACT:
INSTRUMENT(S): maXis 4G
ORGANISM(S): Mus Musculus (ncbitaxon:10090)
SUBMITTER: 
Pieter Dorrestein
PROVIDER: MSV000083004 | GNPS | Fri Oct 05 18:26:00 BST 2018
REPOSITORIES: GNPS
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Project description:In addition to their role as a digestive detergent, bile acids have the ability to modulate the expression of genes. The intestinal content of cholic acids (CA) fluctuated in response to the daily feeding-fasting cycle; therefore, we hypothesized that the temporal accumulation of CA may affect the expression of genes in intestinal epithelial cells. To screen bile acid-regulated genes, we performed oligonucleotide microarray analyses using RNA isolated from the CA-treated intestinal cells of mice. Several types of genes were screened as candidates for bile acid-regulated genes. They included genes that encoded lipid metabolism-related proteins, receptors, transcriptional factors, and plasma-membrane transporters.
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Project description:Dietary intervention constitutes a feasible approach for modulating metabolism and improving healthspan and lifespan. Methionine restriction (MR) delays the appearance of age-related diseases and increases longevity in normal mice. However, the effect of MR on premature aging remains to be elucidated. Here, we describe that MR extends lifespan in two different mouse models of Hutchinson-Gilford progeria syndrome (HGPS) by reversing the transcriptome alterations in inflammation and DNA-damage response genes present in this condition. Further, MR improves the lipid profile and alters the levels of bile acids, both in wild-type and in progeroid mice. Notably, treatment with the bile acid cholic acid improves healthspan and lifespan in vivo. These results suggest the existence of a metabolic pathway involved in the longevity extension achieved by MR and support the possibility of dietary interventions for treating progeria.
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Project description:Deoxycholic acid (DCA) is a secondary bile acid produced by a small number of commensal species of bacteria present in the mammalian gut. Elevated DCA concentration correlates with disease states including colon cancer and cholesterol gallstones, but the associated mechanisms are not fully understood. Both primary and secondary bile acids are also capable of affecting gene expression through nuclear receptors such as FXR. To better understand the impact of a commensal-derived secondary bile acid on host metabolism we fed DCA to germ-free (GF) mice, which normally lack DCA, and compared the hepatic transcriptomes of bile acid fed GF mice to GF mice receiving a control diet, as well as to those of conventionally housed control animals. Interestingly, the feeding of DCA to GF mice, but not the feeding of cholic acid (CA) from which DCA is derived, results in an up-regulation of genes of cholesterol biosynthetic pathways. GF mice normally have elevated hepatic cholesterol compared to conventionally housed mice. Despite increase in the expression of cholesterol biosynthetic genes, the DCA fed GF mice showed a markedly decreased level of hepatic cholesterol equivalent to the hepatic cholesterol concentration of conventionally colonized animals. Total cholesterol in the serum was unaffected by DCA, but there was a decrease in the HDL lipoprotein fraction as well as an increase in the non-HDL lipoprotein fraction of the serum cholesterol. DCA, but not CA, is sufficient to modulate host lipoprotein metabolism. Taken together, these results suggests that a minor component of the gut microbiome has a significant impact on cholesterol homeostasis through secondary metabolism of bile acids and suggests a possible therapeutic intervention route through the microbial metabolic pathways.
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