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CDA HFD mice analysed for hepatic gene expression after treatment with semaglutide

ABSTRACT: CDA HFD mice analysed for hepatic gene expression after treatment with semaglutide

PROVIDER: PRJNA1250966 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR33137900.fastq.gz	Fastqsanger.gz
	SRR33137901.fastq.gz	Fastqsanger.gz
	SRR33137902.fastq.gz	Fastqsanger.gz
	SRR33137903.fastq.gz	Fastqsanger.gz
	SRR33137904.fastq.gz	Fastqsanger.gz

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CDA HFD mice analysed for hepatic gene expression after treatment with semaglutide

Project description:Metabolic dysfunction-associated steatohepatitis (MASH) is a chronic liver disease strongly associated with cardiometabolic risk factors. Semaglutide, a glucagon-like peptide-1 receptor agonist, improves liver histology in MASH, but the underlying signals and pathways driving semaglutide-induced MASH resolution are not well understood. We show that, in two preclinical MASH models, semaglutide improved histological markers of fibrosis and inflammation, and reduced hepatic expression of fibrosis- and inflammation-related gene pathways. NOTE: dose is 20 µg/kg QD as stated in the publication, not 10 nmol/kg as stated in the fastq file names!

2025-04-25 | GSE294630 | GEO

CDA-HFD induced NASH liver fibrosis

Project description:To understand the fibrotic response in the CDA-HFD induced NASH fibrosis model, we performed RNA-seq on liver samples collected from mice fed with normal chow (week 0) or CDA-HFD chow (weeks 8 and 16).

2022-08-19 | GSE207856 | GEO

DIO-MASH mice analysed for hepatic gene expression after treatment with semaglutide

Project description:Modulation of metabolic, inflammatory, and fibrotic pathways by semaglutide in metabolic dysfunction-associated steatohepatitis Metabolic dysfunction-associated steatohepatitis (MASH) is a chronic liver disease strongly associated with cardiometabolic risk factors. Semaglutide, a glucagon-like peptide-1 receptor agonist, improves liver histology in MASH, but the underlying signals and pathways driving semaglutide-induced MASH resolution are not well understood. We show that, in two preclinical MASH models, semaglutide improved histological markers of fibrosis and inflammation, and reduced hepatic expression of fibrosis- and inflammation-related gene pathways.

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DIO-MASH mice analysed for hepatic gene expression after treatment with semaglutide

Project description:DIO-MASH mice analysed for hepatic gene expression after treatment with semaglutide

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Project description:CDA-HFD induced NASH liver fibrosis

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Genome-wide RNAseq of liver tissue derived from DEN-CDA-HFD mice treated with CLDN1 mAb or vehicle Control

Project description:Seven-week old male C57BL/6J mice received a single i.p. injection of DEN (100 mg/kg) and were subsequently fed with CDA-HFD after 3 weeks. After 6 weeks of diet, the mice were randomized in 2 groups, receiving weekly i.p. injections of 500 µg of either CLDN1 specific mAb or vehicle control for 16 weeks. RNA was extracted from non-tumorous liver tissue of 6 DEN-CDA-HFD mice treated with CLDN1 mAb, 6 DEN-CDA-HFD mice treated with vehicle Control as well as 5 C57BL/6J Control mice fed by regular diet. Libraries were sequenced on the Illumina HiSeq 4000 as Single-Read 50 base reads.

2024-03-12 | GSE174542 | GEO

Semaglutide targets mitochondria to regulate metabolism and inflammation in sarcopenia and osteoarthritis

Project description:Metabolic and inflammatory diseases often coexist, and become important challenges facing global health. As a traditional anti-obesity drug, semaglutide is reported to have therapeutic effects in sarcopenia and osteoarthritis (OA), but its mechanism of action still needs to be explored. Here we employed single-cell sequencing analysis to analyze transcriptome changes cross various tissues of high-fat diet (HFD) and OA model mice, and found that semaglutide significantly improved the metabolic and inflammatory disorders of muscle tissue during HFD and OA. Mechanistically, we found that semaglutide could enhance muscle mitochondrial metabolism and mitophagy, alleviated the activation of inflammatory cytokines caused by hypoxia, and regulated the progression of sarcopenia and OA across tissues. Intramuscular injection of mitochondria, pre-stimulated by semaglutide, could significantly alleviate OA inflammation and pain symptoms. These findings reveal the mitochondrial regulatory mechanism in the muscle-OA axis and provide a new perspective for the application of semaglutide in OA treatment.

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Semaglutide has beneficial effects on non-alcoholic steatohepatitis in Ldlr-/-.Leiden mice

Project description:Abstract. Background and aims: Semaglutide, a glucagon-like peptide-1 receptor agonist, is an antidiabetic medication that has recently been approved for treatment of obesity as well. Semaglutide is also postulated to be a promising candidate for treatment of non-alcoholic steatohepatitis (NASH). Here, we evaluated the effects of semaglutide in a translational diet-induced model with advanced NASH and fibrosis. Methods: Ldlr-/-.Leiden mice received a fast food diet (FFD) for 25 weeks, followed by another 12 weeks on FFD with daily subcutaneously injections of semaglutide or vehicle (control). Plasma parameters were evaluated, livers and hearts were examined and hepatic transcriptome analysis was performed. Results: In the liver, semaglutide significantly reduced macrovesicular steatosis (-74%, p<0.001), inflammation (-73%, p<0.001) and completely abolished microvesicular steatosis (-100%, p<0.001). Histological and biochemical assessment of hepatic fibrosis showed no significant effects of semaglutide. However, digital pathology revealed significant improvements in the degree of collagen fiber reticulation (-12%, p<0.001). Semaglutide did not affect atherosclerosis relative to controls. Additionally, we compared the transcriptome profile of FFD-fed Ldlr-/-.Leiden mice with a human gene set that differentiates human NASH patients with severe fibrosis from those with mild fibrosis. In FFD-fed Ldlr-/-.Leiden control mice, this gene set was upregulated as well, while semaglutide predominantly reversed this gene expression. Conclusions: Using a translational model with advanced NASH, we demonstrated that semaglutide is a promising candidate with particular potential for treatment of hepatic steatosis and inflammation, while for reversal of advanced fibrosis, combinations with other NASH agents may be necessary.

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Dissecting Semaglutide-dependent transcriptome response in obesity and osteoarthritis across tissues at single-cell resolution

Project description:The clinical observations of semaglutide cannot be fully explained by the classical GLP-1R signaling, indicating that semaglutide may exert its effects through a more complex multi tissue regulatory network. Based on this background, this study utilized high-fat diet (HFD) - induced obesity and surgery induced osteoarthritis (OA) models to simulate metabolic joint complications. By systematically collecting peripheral blood (PB), bone marrow (BM), liver, brain tissue, and skeletal muscle from C57BL/6 mice, and integrating 10x Genomics single-cell transcriptome sequencing, we constructed a cross tissue cell atlas that covers the immune, nervous, and motor metabolic systems under treatment with semaglutide. In addition, we compared the gene expression disturbances in mouse tissues after administration of semaglutide. Through these comparisons, we can more accurately decipher the specific effects of semaglutide treatment on gene expression in mice, thereby gaining a deeper understanding of their mechanisms of action in vivo.

2026-05-06 | GSE310028 | GEO

The hepatoprotective benefits of semaglutide in MASH require the intrahepatic endothelial GLP-1 receptor

Project description:GLP-1 receptor agonists such as semaglutide improve metabolic dysfunction-associated liver disease (MASLD), yet the hepatic cell types mediating these effects remain unclear. GLP-1R expression in the liver is restricted to non-parenchymal cells, but its detection by conventional single-cell RNA sequencing is limited due to low transcript abundance. We performed GEM-X Flex-seq (10x Genomics) single-cell RNA sequencing on liver single-cell suspensions from wild-type C57BL/6J mice fed a standard chow diet, a choline-deficient high-fat diet (CDHFD), or CDHFD with semaglutide treatment. This dataset enables cell type-resolved mapping of Glp1r expression across the hepatic niche and characterization of transcriptomic changes associated with semaglutide treatment, revealing pericentral liver sinusoidal endothelial cells (LSECs) as direct targets mediating weight loss-independent improvements in hepatic inflammation, fibrosis, and immune remodeling.

2026-04-14 | GSE325222 | GEO

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