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Mouse gut metagenome

ABSTRACT: Farnesoid X Receptor Signaling Shapes the Gut Microbiota and Controls Hepatic Lipid Metabolism

PROVIDER: PRJNA342660 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR4239541_1.fastq.gz	Fastqsanger.gz
	SRR4239541_2.fastq.gz	Fastqsanger.gz
	SRR4239771_1.fastq.gz	Fastqsanger.gz
	SRR4239771_2.fastq.gz	Fastqsanger.gz
	SRR4239542_1.fastq.gz	Fastqsanger.gz

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Bioenergetic cues shift FXR splicing towards FXRα2 to modulate hepatic lipolysis and fatty acid metabolism

Project description:Farnesoid X receptor (FXR) plays a prominent role in hepatic lipid metabolism. The FXR gene encodes four proteins with structural differences suggestive of discrete biological functions about which little is known. We show that FXR isoforms have specific effects on hepatic metabolism and uncover novel pathways under their control. Gene expression profiling of hepatocytes expressing each FXR variant revealed large differences in their target gene sets. Notably, FXRα2 (but not α1) activates a broad transcriptional program in hepatocytes conducive to lipolysis, fatty acid oxidation, and ketogenesis. Consequently, FXRα2 decreases cellular lipid accumulation and improves insulin sensitivity. FXRα2 expression in Fxr-/- mouse liver activates a similar gene program and robustly decreases hepatic triglyceride levels. On the other hand, FXRα1 reduces hepatic triglyceride content to a lesser extent and does so through regulation of lipogenic gene expression. Bioenergetic cues, such as fasting and exercise, dynamically regulate Fxr splicing in mouse liver to increase Fxrα2 expression. Our results show that the main FXR variants in human liver (α1 and α2) reduce hepatic lipid accumulation through distinct mechanisms and to different degrees. Thus, pharmacological or lifestyle interventions, such as exercise, aimed at modulating hepatic FXR splicing may improve the therapeutic efficacy of FXR agonists.

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Serotonin signals through a gut-liver axis to regulate hepatic steatosis

Project description:Purpose: While various functions of peripheral serotonin are known, the direct role of serotonin in regulating hepatic lipid metabolism in vivo is not well understood. We studied whether serotonin directly acts on liver to regulate lipid metabolism. Methods: Methods: 12 weeks aged liver-specific Htr2a KO (Albumin-Cre+/-; Htr2aflox/flox, herein named Htr2a LKO) mice and wildtype (WT) littermates were fed a high-fat diet (HFD, 60% fat calories) for 8 weeks. Results: Hepatic lipid droplet accumulation, NAFLD activity score, and hepatic triglyceride levels were dramatically reduced in HFD-fed Htr2a LKO mice compared to WT littermates. Conclusions: Gut-derived serotonin is a direct regulator of hepatic lipid metabolism via a gut TPH1-liver HTR2A endocrine axis. And shows promise as a novel drug target to ameliorate NAFLD with minimal systemic metabolic effects.

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Project description:Farnesoid x receptor signaling in fetal liver

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Iron capture through CD71 dictates perinatal and tumoral Treg expansion modulating iron homeostasis and gut microbiota colonization

Project description:Beside suppressing immune responses, regulatory T cells (Tregs) maintain tissue homeostasis and control systemic metabolism. Whether iron, a fundamental element for all living cells, is required for Treg expansion, is completely unknown. Here, we showed that the transferrin receptor CD71 was upregulated on activated proliferating Tregs infiltrating human liver cancer. Mice with a Treg-restricted CD71 deficiency spontaneously developed a scurfy-like disease, caused by a severe impairment in perinatal Treg expansion. CD71-null Tregs display decreased proliferation and mitochondrial functions, and a tissue-Treg signature loss. In the perinatal life, CD71 deficiency in Tregs triggered a hepatic response to iron overload, characterized by increased hepcidin transcription and iron accumulation in macrophages. A lower bacterial diversity, and a reduction of beneficial species, were detected in the faecal microbiota of CD71 conditional knock-out neonates. Our findings indicate that the CD71-mediated iron absorption is required for Treg perinatal expansion and controls the systemic iron homeostasis, which in turn shapes the bacterial gut colonization.

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