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

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

PROVIDER: PRJNA494022 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7944820_1.fastq.gz	Fastqsanger.gz
	SRR7944820_2.fastq.gz	Fastqsanger.gz
	SRR7944821_1.fastq.gz	Fastqsanger.gz
	SRR7944821_2.fastq.gz	Fastqsanger.gz
	SRR7944822_1.fastq.gz	Fastqsanger.gz

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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.

2018-11-27 | GSE120662 | GEO

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

Project description:Nonalcoholic fatty liver disease (NAFLD) is increasing in worldwide prevalence, closely tracking the obesity epidemic, but specific pharmaceutical treatments for NAFLD are lacking. Defining the key molecular pathways underlying the pathogenesis of NAFLD is essential for developing new drugs. Here we demonstrate that inhibition of gut-derived serotonin synthesis ameliorates hepatic steatosis through a reduction in liver serotonin receptor 2A (HTR2A) signaling. Local serotonin concentrations in the portal blood, which can directly travel to and affect the liver, are selectively increased by high-fat diet (HFD) feeding in mice. Both gut-specific Tph1 knockout mice and liver-specific Htr2a knockout mice are resistant to HFD-induced hepatic steatosis, without affecting systemic energy homeostasis. Moreover, selective HTR2A antagonist treatment prevents HFD-induced hepatic steatosis. Thus, the gut TPH1-liver HTR2A axis shows promise as a drug target to ameliorate NAFLD with minimal systemic metabolic effects.

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Intestinal NSD2 aggravates hepatic steatosis during obesity through histone modifications [CUT&Tag]

Project description:The impairment of the intestinal barrier will lead to the accumulation of fat and harmful substances in the liver, inducing hepatic steatosis or steatohepatitis. Zhang et al. identified NSD2 in the intestine as a novel and essential regulator of hepatic steatosis. NSD2 directly regulates transcriptional activation of ERN1 through the modification of H3 dimethylated on lysine 36 (H3K4me36), thereby activating the ERN1-JNK axis to induce inflammatory response, intestinal barrier impairment, and hepatic steatosis. This functional mechanism of NSD2 provides a potential therapeutic target for this disease.

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Intestinal NSD2 aggravates hepatic steatosis during obesity through histone modifications [RNA-seq]

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Critical Roles of the Histone Methyltransferase MLL4/KMT2D in Murine Hepatic Steatosis Directed by ABL1 and PPARγ2

Project description:The pathophysiologic continuum of non-alcoholic fatty liver disease begins with steatosis. Despite great progress in understanding the gene regulatory program directing steatosis, how it is orchestrated epigenetically is unclear. Here we show that the histone H3-lysine-4-methyltransferase, MLL4/KMT2D, plays critical roles in overnutrition-induced murine steatosis via dual mechanisms. First, in response to high fat diet (HFD), MLL4 activates the expression of PPARγ2, an overnutrition-induced steatotic transcription factor. Second, HFD enables the coactivator function of MLL4 for PPARγ2, as overnutrition-activated ABL1 kinase phosphorylates PPARγ2 and enhances its association with MLL4, facilitating recruitment of MLL4 to steatotic target genes of PPARγ2, including the PPARγ2-encoding gene itself, and their transactivation via H3-lysine-4-methylation. Consistently, inhibition of ABL1 improves the fatty liver condition of ob/ob mice by suppressing the pro-steatotic action of MLL4. Our results uncover a critical regulatory axis in overnutrition-directed steatosis, and present this ABL1-PPARγ2-MLL4 axis as a new target for anti-steatosis drug development.

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oyster mushroom against hepatic steatosis in obese Zucker rats

Project description:Hepatic steatosis is a very common response to liver injury and often attributed to metabolic disorders. Prior studies have demonstrated the efficacy of a biotechnologically produced oyster mushroom (Pleurotus sajor-caju, PSC) in alleviating hepatic steatosis in obese Zucker rats. This study aims to elucidate molecular events underlying the anti-steatotic effects of PSC.

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Project description:Hepatic lipid homeostasis is coordinated by various metabolic pathways, such as lipogenesis, lipid uptake, storage, and oxidation. However, the underlying mechanism that orchestrates metabolic crosstalk remains unclarified. Herein, we demonstrated that fumarate hydratase (FH) functioned as an indispensable adaptor governing mitochondria metabolism and lipid droplets (LDs) degradation. Hepatic FH overexpression prevented hepatic steatosis in normal mice and ob/ob mice without interfering mitochondrial lipid oxidation and lipogenesis. Strikingly, we found that FH selectively activated lipophagy-mediated LDs lipidolysis. Mechanistically, FH interacted with ULK1 and stabilized ULK1 through preventing its ubiquitination and degradation, resulting in lipophagy activation and the elimination of hepatic lipid accumulation. Meanwhile, hepatic ULK1 deficiency abrogated the protective effects in FH-overexpressing mice. Also, we clarified that the interaction between FH and ULK1 occurred in cytoplasm, but not in mitochondria. Cytoplasmic FH was sensitive to lipids and downregulated without affecting mitochondrial FH in vivo. Moreover, the FH-ULK1 axis was identified closely associated with hepatic steatosis in human patients. Taken together, our research demonstrates a “two-side” insight of FH on hepatic lipid metabolism and provides a promising strategy for fatty liver treatment.

2024-02-26 | GSE256510 | GEO

Specific macronutrients exert unique influences on the adipose-liver axis to promote hepatic steatosis in mice

Project description:Testing the effect of specific macronutrient combinations on mouse metabolism in vivo, we determined that diets pairing starch as carbohydrate with oleate as fat (42%:42% kcal) induced significant white adipose tissue pathology and hepatic steatosis compared to other isocaloric combinations.

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Hepatic DKK1 driven steatosis is CD36-dependent

Project description:Hepatic DKK1 driven steatosis is CD36-dependent

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