Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR29348288.fastq.gz | Fastqsanger.gz | |||
| SRR29348289.fastq.gz | Fastqsanger.gz | |||
| SRR29348290.fastq.gz | Fastqsanger.gz | |||
| SRR29348291.fastq.gz | Fastqsanger.gz | |||
| SRR29348292.fastq.gz | Fastqsanger.gz |
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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
Project description:Background: Acute pancreatitis (AP) is a common severe digestive disorder, with severity linked to high-fat diets (HFD). HFD may exacerbate AP by promoting inflammation and altering gut microbiota. Astragalus polysaccharides (APS) possess anti-inflammatory properties, but it is unclear if APS supplementation can mitigate HFD's detrimental effects on AP by modulating gut microbiota. This study investigates the mechanisms by which APS improves HFD-induced AP exacerbation. In this study, C57BL/6 mice were fed HFD or a standard diet, with or without APS, for 12 weeks. AP was induced via intraperitoneal caerulein injection. Analyses included ELISA, Western blotting, histology, immunohistochemistry, immunofluorescence, single-cell RNA sequencing (scRNA-seq), 16S rRNA sequencing of gut microbiota, and short-chain fatty acid (SCFA) analysis to evaluate inflammation and cellular changes. Results: HFD significantly increased AP severity, indicated by elevated serum enzyme and pro-inflammatory cytokine levels, along with extensive pancreatic damage. Single-cell RNA sequencing (scRNA-seq) showed a notable rise in ICAM1+ neutrophils and activation of the NF-κB/necroptosis pathway in HAP mice. APS alleviated these effects by decreasing ICAM1+ neutrophil infiltration, downregulating the NF-κB pathway, and reducing necroptosis. Moreover, APS restored gut microbiota balance, significantly boosting Lactobacillus reuteri (L. reuteri) abundance and propionate (PA) levels. Treatments with L. reuteri and PA independently mitigated HFD-induced AP severity, indicating that APS's protective effects are microbiota-dependent. Conclusion: APS improves HFD-induced gut dysbiosis and intestinal barrier dysfunction by enriching L. reuteri and PA, effectively reducing AP exacerbation. Our findings highlight the gut-pancreas axis as a promising target for addressing AP severity.
2024-10-22 | GSE279876 | GEO
Project description:Liver disease alters the gut microenvironment by liver-gut axis. To investigate the composition and transcriptome changes of various intestinal cell populations in liver cirrhosis, we delineated a single-cell atlas of the colon from mice treated CCl4 for 6 weeks.
2022-11-22 | GSE218371 | GEO
Project description:Recently, gut metabolites have been recognized to play significant roles in liver diseases via the gut-liver axis. In this study, we investigate the regulatory effects of the tryptophan metabolite, indole-3-propionic acid (IPA), on immune cells during liver fibrogenesis using single-cell RNA sequencing (scRNA-seq).
2024-09-20 | GSE277148 | GEO
Project description:Abstract: - Non-alcoholic fatty liver disease (NAFLD) is a complex multifactorial disorder that is associated with gut dysbiosis, enhanced gut permeability, adiposity and insulin resistance. Prebiotics such as human milk oligosaccharide 2’-fucosyllactose are thought to primarily improve gut health and it is uncertain whether they would affect more distant organs. This study investigates whether 2’-fucosyllactose can alleviate NAFLD development in manifest obesity. Obese hyperinsulinemic Ldlr-/-.Leiden mice, after an 8 week run-in on HFD, were treated with 2’-fucosyllactose by oral gavage until week 28 and compared to HFD-vehicle controls. 2’-fucosyllactose did not affect food intake, body weight, total fat mass or plasma lipids. 2’-fucosyllactose altered the fecal microbiota composition which was paralleled by a suppression of HFD-induced gut permeability at t=12 weeks. 2’-fucosyllactose significantly attenuated the development of NAFLD by reducing microvesicular steatosis. These hepatoprotective effects were supported by functional transcriptome analyses showing that 2’-fucosyllactose activated ACOX1 (involved in lipid catabolism), while deactivating SREBF1 (involved in lipogenesis). Furthermore, 2’-fucosyllactose suppressed ATF4, ATF6, ERN1, and NUPR1 all of which participate in ER stress. 2’-fucosyllactose reduced fasting insulin concentrations and HOMA-IR, which was corroborated by decreased intrahepatic diacylglycerols. - In conclusion, long-term prebiotic treatment with 2’-fucosyllactose can counteract the detrimental effects of HFD on gut dysbiosis and gut permeability and attenuates the development of liver steatosis. The observed reduction in intrahepatic diacylglycerols provides a mechanistic rationale for the improvement of hyperinsulinemia and supports the use of 2’-fucosyllactose to correct dysmetabolism and insulin resistance.
2022-05-24 | GSE195862 | GEO
Project description:Non-alcoholic fatty liver disease (NAFLD) influence one of third population around the world. Until now, no effective treatments have been established due to the improper in vitro assays and experimental animal models. By co-culturing human gut and liver cell lines (CaCO2 and HepG2 cells, respectively) interconnected via the microfluidic closed medium circulation loop, we created a gut-liver-on-a-chip (iGLC) platform as an in vitro human model of the gut-liver axis (GLA) in initiation and progression of NAFLD.
2023-03-01 | GSE152091 | GEO
Project description:Non-alcoholic fatty liver disease (NAFLD) influence one of third population around the world. Until now, no effective treatments have been established due to the improper in vitro assays and experimental animal models. By co-culturing human gut and liver cell lines (CaCO2 and HepG2 cells, respectively) interconnected via the microfluidic closed medium circulation loop, we created a gut-liver-on-a-chip (iGLC) platform as an in vitro human model of the gut-liver axis (GLA) in initiation and progression of NAFLD.
2023-03-01 | GSE206417 | GEO
Project description:Title: White adipose tissue inflammation and gut permeability develop prior to NASH development, associated with increased oxidative stress, intrahepatic diacylglycerol and proinflammatory chemokines in the liver of diet-induced obese and hyperinsulinemic Ldlr-/-.Leiden mice Abstract: NAFLD progression from simple steatosis to NASH and fibrosis is driven by an intricate interplay between molecular and cellular mechanisms. These drivers are not limited to the liver itself but also white adipose tissue and gut may contribute. Current knowledge on these drivers is mostly based on studies that investigate these at a single time point (typically end-stage disease). However, such studies provide no insight into the temporal dynamics and chronology, which therefore remain poorly understood. Ldlr-/-.Leiden mice were fed a high-fat diet (HFD) to induce obesity-associated NAFLD and compared to lean controls fed chow. Groups of mice were sacrificed after 8, 16, 28 and 38 weeks to study liver, white adipose tissue, gut and circulating factors to investigate the sequence of pathogenic events in these critical metabolically active organs as well as organ-crosstalk during NAFLD development. Ldlr-/-.Leiden mice on a HFD develop obesity, dyslipidemia and insulin resistance, essentially as observed in obese NASH patients, in this translational context WAT and gut dysfunction precede the development of NASH and liver fibrosis.
2023-03-20 | GSE209762 | GEO