Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1180292 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR31178863_1.fastq.gz | Fastqsanger.gz | |||
| SRR31178863_2.fastq.gz | Fastqsanger.gz | |||
| SRR31178864_1.fastq.gz | Fastqsanger.gz | |||
| SRR31178864_2.fastq.gz | Fastqsanger.gz | |||
| SRR31178865_1.fastq.gz | Fastqsanger.gz |
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Similar Datasets
Project description:Scavenger receptor class A member 3 (SR-A3) is implicated in metabolic diseases; however, the relationship between SR-A3 and metabolic dysfunction-associated fatty liver disease (MAFLD) has not been documented. Here, we show that hepatic SR-A3 expression is significantly reduced in human and animal models in the context of MAFLD. Genetic inhibition of SR-A3 in hamsters elicits hyperlipidemia, hyperglycemia, insulin resistance, and hepatic steatosis under chow-diet condition, yet escalates in diet-induced MAFLD. Mechanistically, SR-A3 ablation enhances E3 ligase XIAP-mediated proteasomal ubiquitination of PTEN, leading to AKT hyperactivation. By contrast, hepatic overexpression of human SR-A3 is sufficient to attenuate metabolic disorders in WT hamsters fed a high-fat-high-cholesterol diet and ob/ob mice via suppressing the XIAP/PTEN/AKT axis. In parallel, pharmacological intervention by PTEN agonist oroxin B or lipid lowering agent ezetimibe differentially corrects MAFLD in hamsters.
2025-02-13 | GSE289495 | GEO
Project description:Miniature pigs are useful model animal for gene expression studies on dietary-induced hyperlipidemia, because they have similar digestive physiology to human. Two typical dietary components were used for dietary-induced hyperlipidemia miniature pig models. One is a high-fat and high-cholesterol diet (HFCD) containing 15% lard and 2% cholesterol, the other is a high-fat, high-cholesterol and high-sucrose diet (HFCSD) containing 15% lard, 2% cholesterol and 37% sucrose.
2012-04-25 | GSE32616 | GEO
Project description:Miniature pigs are useful model animal for gene expression studies on dietary-induced hyperlipidemia, because they have similar digestive physiology to human. Two typical dietary components were used for dietary-induced hyperlipidemia miniature pig models. One is a high-fat and high-cholesterol diet (HFCD) containing 15% lard and 2% cholesterol, the other is a high-fat, high-cholesterol and high-sucrose diet (HFCSD) containing 15% lard, 2% cholesterol and 37% sucrose. Whole blood gene expression in HFCD, HFCSD and control male miniature pigs was measured at 10, 19 and 27 weeks of feeding periods.M-cM-^@M-^@White blood cell gene expression in HFCD, HFCSD and control male miniature pigs was measured at 27 weeks of feeding period.
2012-04-24 | E-GEOD-32616 | biostudies-arrayexpress
Project description:We aim to establish NAFLD model of Zebrafish. Zebrafish larvae fed with high cholesterol diet，high fructose diet and overfeed diet to induce liver steatosis. RNA-seq was employed to analyze the effects of different diets on NAFLD development.
2018-12-01 | E-MTAB-6636 | biostudies-arrayexpress
Project description:Okra (Abelmoschus esculentus (L.) Moench) serves as a botanical resource extensively utilized in ethnomedicine. Prior investigations revealed that okra polysaccharide (OP) ameliorated hepatocellular lipotoxicity in vitro context. Nonetheless, the curative efficacy and the precise molecular mechanisms implicated in metabolic-associated fatty liver disease (MAFLD) warrant further elucidation. To address this gap, two murine models of MAFLD, namely obese Ob/Ob mice and high fat/cholesterol/fructose (HFCF) fed mice, were employed. The therapeutic implications of OP supplementation were assessed through quantification of lipid specific biomarkers and hepatic histopathological examination. Complementary transcriptomic, phosphoproteomic, and in vitro analyses were conducted to decipher the molecular underpinnings. In the Ob/Ob mouse model, OP substantively mitigated both circulating and hepatic lipid concentrations, concurrently ameliorating hepatic steatosis. In the context of HFCF-induced MAFLD, OP not only attenuated hepatic lipidic sequestration but also abrogated concomitant inflammation and fibrosis. Subsequent RNA-sequencing analyses on hepatic tissues derived from HFCF-diet mice delineated that OP modulated MAFLD-associated transcriptional signatures. A synergistic assessment of transcriptomics and phosphoproteomics disclosed a salient effect of OP on the Peroxisome Proliferator-Activated Receptor (PPAR) pathway, particularly manifested by the upregulation of PPAR-γ signaling. In murine hepatocytes, OP counteracted steatosis and inflammation via the activation of PPAR-γ signaling. The effects induced by OP were nullified upon administration of the PPAR-γ-specific antagonist GW9662. Collectively, our empirical evidence furnishes the inaugural demonstration that OP mitigates MAFLD pathology through the activation of PPAR-γ signaling, thereby presenting a novel therapeutic avenue for MAFLD intervention.
2024-08-21 | GSE273255 | GEO
Project description:Understanding mechanisms causing MAFLD (Metabolic Associated Fatty Liver Disease) and its progression to MASH (metabolic dysfunction-associated steatohepatitis) is clinically important and scientifically challenging. Hepatic insulin resistance is a common component in the progression of MAFLD in patients and experimental animals; however, hepatic steatosis caused by the HFD45% (high-fat diet) decreases during chronic hepatic IR generated by inactivation of Irs1/2 (LDKO), AKT1/2, or InsR 1-3—which is inconsistent with the expected relationship between IR and MAFLD in humans4. Here we found that complete hepatic insulin resistance promotes the fructose-enriched GAN diet-induced MAFLD, including acute inflammation and MASH in LDKO mice. Unexpectedly, fructose phosphorylation catalyzed by hepatic Khk (ketohexokinase) was not required as acute MAFLD progressed strongly in LDKOKhkL/L mice fed the GAN diet. FoxO1 activated during hepatic IR induces Fst (Follistatin) expression and secretion from the liver of LDKO mice. Inactivation of hepatic FoxO1 in LTKO mice (LDKO•FoxO1L/L) or Fst in LDKOFstKO mice prevented acute MAFLD during the GAN diet. Consistently, overexpression of hepatic Fst promoted GAN diet-induced MAFLD/MASH and hepatic carcinoma. Mechanistically, circulating Fst promoted adipose tissue IR and lipolysis, which can deliver FFA (free fatty acid) to the liver for esterification with excess Gro3P (glycerol 3-phosphate) generated by fructose metabolism, although hepatic DNL (de novo lipogenesis) decreased strongly in LDKO mice while. Since circulating FST correlates positively with both T2D and MAFLD in humans, our results suggests that hepatic FST induced by progressive hepatic IR might promote MAFLD/MASH during the consumption of sugar-sweetened food and beverages consumed frequently by people and animals with T2D.
2024-06-23 | GSE270246 | GEO
Project description:Long-term high fat feeding leads to hepatic steatosis, dyslipidemia, and a pro-inflammatory state. In a previous study, we observed this dysregulated metabolic phenotype when C57BL/6 mice were fed a high fat diet (HFD) for sixteen weeks. Additionally, a five-fold increase in liver gene expression of serum amyloid A-1 (SAA-1), an acute phase response protein that associates with high density lipoprotein (HDL), was observed. Inflammation induced changes composition may alter HDL functions, including anti-oxidant, anti-inflammatory and reverse cholesterol transport properties. Diet-induced onset and progression of HDL dysfunction is poorly understood. To examine the relationship between high fat diet and HDL dysfunction, we performed a short-term diet study. Four-week high fat feeding caused an increase in total plasma cholesterol compared with mice fed normal control diet (ND). No change in plasma triglycerides or development of hepatic steatosis was observed. These mice did however show evidence for increase in acute phase reactants, with a 3.25-fold increase in SAA-1 expression in liver. Heavy water labelling was used to determine the turnover rates of proteins associated with HDL. High fat diet resulted in increased fractional catabolic rate (HFD vs ND) of several acute phase response proteins involved ininnate immunity , including – Complement C3 (7.06 ± 0.99 vs 5.20 ± 0.56 %/h, p < 0.005), complement factor B (6.17 ± 0.59 vs 5.09 ± 0.87 %/h, p < 0.05), complement Factor H (4.16 ± 0.41 vs 3.56 ± 0.36 %/h, p < 0.05), and Complement factor I (3.50 ± 0.26 vs 2.75 ± 0.14 %/h, p < 0.005). Our findings suggest that early immune response-induced inflammatory remodeling of HDL precedes the diet-induced steatosis and dyslipidemia. Early HDL dysfunction reflected on impaired reverse cholesterol transport likely results in increase in plasma cholesterol in the absence of other lipid abnormalities.
2021-09-08 | PXD010272 | Pride
Project description:Two-month-old C57BL/6J male mice were placed on chow diet or a diet enriched in high fat, cholesterol, and fructose (Research diet D09100301: 40 kcal% fat, 2% cholesterol, 20 kcal% fructose, HFCF diet) for 1 or 3 months. Liver RNA was isolated and submitted for small RNA sequencing.
2020-03-30 | GSE135106 | GEO
Project description:Germfree (GF) mice have been used as a model to study the contribution of the intestinal microbiota to metabolic energy balance of the host. Despite a wealth of knowledge accumulated since the 1940’s, the response of GF mice to a high fat diet is largely unknown. In the present study, we compared the metabolic consequences of a high fat (HF) diet on GF and conventional (Conv) C57BL/6J mice. As expected, Conv mice developed obesity and glucose intolerance with a HF diet. In contrast, GF mice remained lean and resisted the HF diet-induced insulin resistance. The anti-obesity phenotype of GF/HF mice was accompanied by reduced caloric intake, diminished food efficiency, and excessive fecal lipid excretion contributed to the reduced food efficiency. In addition, HF diet-induced hypercholesterolemia was ameliorated, which was partially due to an increase in fecal cholesterol excretion. However, hepatic cholesterols were increased in GF/HF mice. Elevated nuclear SREBP2 proteins and the up-regulation of cholesterol biosynthesis genes support the increased liver cholesterol biosynthesis in GF/HF mice. The resistance to HF diet-induced metabolic abnormalities in GF mice was also associated with a reduced immune response, indicated by low plasma pro-inflammatory and anti-inflammatory markers. These data suggest that the gut microbiota of Conv mice contributes to HF diet-induced obesity, insulin resistance, dyslipidemia and hepatic steatosis in mice. Thus, results of the present study describe the metabolic responses of GF mice to a HF diet and further our understandings of the relationship between the gut microbiota and the host. Germfree and conventional C57BL/6J mice were fed with a high fat diet for 11 weeks. Then, all mice were sacrified under 10-h food deprevation, and liver samples of germfree (n=14) and conventional (n=16) were examined.
2010-08-20 | E-GEOD-19038 | biostudies-arrayexpress
Project description:Background Small intestine and liver greatly contribute to whole body lipid, cholesterol and phospholipid metabolism but to which extent cholesterol and phospholipid handling in these tissues is affected by high fat Western-style obesogenic diets remains to be defined. We therefore quantified cholesterol and phospholipid concentrations in intestine and liver and determined fecal neutral sterol and bile acid excretion in C57Bl/6N mice fed for 12 weeks either a cholesterol-free high carbohydrate control diet or a high fat diet containing 0.03 % (w/w) cholesterol. To identify underlying mechanisms of dietary adaptation in intestine and liver, changes in gene expression were assessed by microarray and qPCR profiling, respectively. Results Animals on high fat diet showed increased plasma cholesterol levels, associated with the higher dietary cholesterol supply, yet, significantly reduced cholesterol levels were found in intestine and liver. Transcript profiling revealed evidence that expression of numerous genes involved in cholesterol synthesis and uptake via LDL, but also in phospholipid metabolism, underwent compensatory regulations in both tissues. Alterations in glycerophospholipid metabolism were confirmed at the metabolite level by phospolipid profiling via mass spectrometry. Conclusions Our findings suggest that intestine and liver react to a high dietary fat intake by an activation of de novo cholesterol synthesis and other cholesterol-saving mechanisms, as well as with major changes in phospholipid metabolism, to accommodate to the fat load. The proximal part of the intestine of mice fed either a control or a high fat diet were analyzed. 5 replicates each.
2011-08-31 | E-GEOD-29748 | biostudies-arrayexpress