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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.

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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

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CDA-HFD induced NASH liver fibrosis

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 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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Genome-wide RNAseq of liver tissue derived from humanized mice fed by CDA-HFD and treated with CLDN1 mAb or vehicle Control

Project description:Six-week old Fah−/−/Rag2−/−/Il2rg −/− (FRG) –NOD breeding mice were intravenously injected with 1.5 x 10^9 plaque forming units (pfu) of an adenoviral vector encoding the secreted form of the human urokinase-like plasminogen activator (Ad-uPA). Forty-eight hours later, 10^6 PHH were injected intrasplenically. Successfully transplanted mice were fed with CDA-HFD for 16 weeks and then treated with humanized CLDN1 specific mAb 500 µg or vehicle for additional 8 weeks. RNA was extracted from non-tumorous liver tissue of 4 NASH fibrosis mice treated with CLDN1 mAb, 3 vehicle Control treated NASH fibrosis mice as well as 3 humanized mice fed by regular diet. Libraries were sequenced on the Illumina HiSeq 4000 as Single-Read 50 base reads.

2024-03-12 | GSE174543 | GEO

Genome-wide expression profile of livers from mice fed HFD,SO-HFD or Viv chow [RNAseq]

Project description:Purpose: Aim of the study is to identify changes in hepatic gene expression induced by either a 40kcal% coconut oil rich high fat diet (HFD), a 40kcal% soybean oil plus coconut oil high fat diet (SO-HFD) or a low fat vivarium chow diet (Viv). Methods: Livers from mice that had been fed one of the above mentioned diets for 35 weeks, were used to make cDNA libraries that were then sent for deep sequencing, using the Illumina TruSeq RNA. Result: Many genes involved in metabolism, lipid binding, transport and storage and many Cyp genes are dysregulated in the two high fat diets as compared to Viv HFDs in SO-HFD mice. Comparing the two HFDs shows more metabolism and disease related genes dysregulated in SO-HFD vs HFD. Conclusion: A diet high in soybean oil may be more detrimental to metabolic health than a diet high in saturated fats. cDNA isolated from livers from mice fed HFD, SO-HFD or Viv for 35 weeks, were 50bp pair-ended sequenced in triplicate using Illumina TruSeq RNA Sample Prep v2 Kit.

2015-08-28 | E-GEOD-68360 | biostudies-arrayexpress

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