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The intestinal microbiota reprograms intestinal lipid metabolism through long non-coding RNA Snhg9

ABSTRACT: The intestinal microbiota reprograms intestinal lipid metabolism through long non-coding RNA Snhg9

PROVIDER: PRJNA858024 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR20097156_1.fastq.gz	Fastqsanger.gz
	SRR20097156_2.fastq.gz	Fastqsanger.gz
	SRR20097157_1.fastq.gz	Fastqsanger.gz
	SRR20097157_2.fastq.gz	Fastqsanger.gz
	SRR20097158_1.fastq.gz	Fastqsanger.gz

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The intestinal microbiota reprograms intestinal lipid metabolism through long non-coding RNA Snhg9

Project description:The intestinal microbiota is a key regulator of mammalian lipid absorption, metabolism, and storage. Here we show that the microbiota reprograms intestinal lipid metabolism in mice by repressing the expression of long non-coding RNA (lncRNA) Snhg9 in small intestinal epithelial cells. Snhg9 suppressed the activity of the transcription factor peroxisome proliferator–activated receptor γ (PPARγ) – a central regulator of lipid metabolism – by dissociating the PPARγ inhibitor Sirtuin 1 from cell cycle and apoptosis protein 2 (CCAR2). Forced expression of Snhg9 in the intestinal epithelium of conventional mice lowered dietary lipid absorption, reduced body fat, and protected against diet-induced obesity. The microbiota repressed Snhg9 expression through an immune cell signaling relay encompassing myeloid cells and innate lymphoid cells. Our findings thus identify an unanticipated role for a lncRNA in microbial control of host metabolism.

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The gut microbiota reprograms intestinal lipid metabolism through long noncoding RNA <i>Snhg9</i>.

Project description:The intestinal microbiota regulates mammalian lipid absorption, metabolism, and storage. We report that the microbiota reprograms intestinal lipid metabolism in mice by repressing the expression of long noncoding RNA (lncRNA) Snhg9 (small nucleolar RNA host gene 9) in small intestinal epithelial cells. Snhg9 suppressed the activity of peroxisome proliferator-activated receptor γ (PPARγ)-a central regulator of lipid metabolism-by dissociating the PPARγ inhibitor sirtuin 1 from cell cycle and apoptosis protein 2 (CCAR2). Forced expression of Snhg9 in the intestinal epithelium of conventional mice impaired lipid absorption, reduced body fat, and protected against diet-induced obesity. The microbiota repressed Snhg9 expression through an immune relay encompassing myeloid cells and group 3 innate lymphoid cells. Our findings thus identify an unanticipated role for a lncRNA in microbial control of host metabolism.

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Project description:Intestinal lipid metabolism regulates absorption and surface of gut epithelium

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Feedback regulation of cholesterol metabolism by LeXis, a lipid-responsive non-coding RNA

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