Comprehensive Analysis of the Translatome in High Fat Diet-Induced Liver Steatosis
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA611552 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR11268500_1.fastq.gz | Fastqsanger.gz | |||
| SRR11268500_2.fastq.gz | Fastqsanger.gz | |||
| SRR11268501_1.fastq.gz | Fastqsanger.gz | |||
| SRR11268501_2.fastq.gz | Fastqsanger.gz | |||
| SRR11268502_1.fastq.gz | Fastqsanger.gz |
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Project description:We performed translatome and transcriptome sequencing (RNC-seq and RNA-seq) on the livers of normal chow diet-, high-fat diet- and High-fat diet plus lycopene-fed mice.
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2021-06-17 | GSE178322 | 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:Non-alcoholic fatty liver disease (NAFLD) is most prevalent form of liver disease, affecting over 30% of Americans. Perfluoroalkyl substances (PFAS) represent a family of environmental toxicants that have infiltrated the living world. This study explores diet-PFAS interactions and their potential role in the increasing global incidence of NAFLD. Male C57BL/6 mice were fed with either a low-fat diet (11% kcal from fat) or a high fat (58% kcal from fat) high carbohydrate (42g/L) diet with or without PFOS or PFHxS in feed (0.0003% w/w) for 29 weeks. Proteomic, lipidomic, and gene expression measurement techniques were utilized to explore mechanistic pathways. With administration of a high fat high carbohydrate (HFHC) diet, PFOS and PFHxS augmented macrovesicular steatosis, indicative of fatty liver. There was a clear shift in the lipidome of the serum phosphatidylcholines, phosphatidylethanolamines, and triglycerides with PFAS exposure. Finally, chain length exerted significant influence on tissue partitioning and the resulting hepatic gene and protein signatures of PFHxS and PFOS in vivo.
2020-09-15 | PXD015976 | Pride
Project description:Using a C57BL6/J mouse model of diet-induced obesit,we observed that mannose supplementation of high fat diet (HFD)-fed mice prevents weight gain,lowers adiposity, reduces liver steatosis, and improves glucose tolerance and insulin sensitivity. We used microarrays to determine the gene expression pattern in epididymal fat frommice weaned on Normal diet (ND), HFD and HFD with mannose (HFDM)
2018-11-06 | GSE110333 | GEO
Project description:ApoE-knockout mice liver on high fat diet developing liver steatosis were treated with trehalose or agmatine for 16 weeks.
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Project description:To assess the effect of steatosis and oxidative stress on progression of liver fibrosis, we have employed whole genome microarray expression profiling as a discovery platform to identify genes that are related with oxidative stress- and steatosis-induced hepatic fibrogenesis. When wild type mice were fed high-fat/high-sucrose diet for 24 weeks, expression of 69 genes was changed more than 10-fold compared with wild type animals fed normal diet, 11 of which were categorized to lipid metabolic process. Moreover, expression of 208 genes showed more than 5-fold changes in Tet-mev-1 mice fed high-fat/high-sucrose diet compared with the same transgenic animals fed normal diet, and gene ontology analyses indicated significant changes in chemokine activity and chemokine receptor binding as well as defense and immune responses. oxidative stress and high fat high calorie induced gene expression in wild type or Tet-mev-1 mouse liver tissue. wild type and Tet-mev-1 mice were fed either normal diet or high fat high sucrose diet for 4 months, and have been given doxycycline-containing water from embryo. Each group were perfomed by duplicate.
2015-05-07 | E-GEOD-68632 | biostudies-arrayexpress
Project description:Adipose tissue dysfunction is closely associated with the development and progression of nonalcoholic fatty liver disease (NAFLD). Recent studies have implied an important role of prohibitin-1 (PHB1) in adipose tissue function. In the current study, we aimed to explore the function of adipocyte PHB1 in the development and progression of NAFLD. The PHB1 protein levels in adipose tissues were markedly decreased in mice fed a high-fat diet (HFD) compared to those fed a chow diet. To explore the function of adipocyte PHB1 in the progression of NAFLD, mice with adipocyte-specific (adipo) deletion of Phb1 (Phb1adipo-/- mice) were generated. Notably, Phb1adipo-/- mice did not develop obesity but displayed severe liver steatosis under HFD feeding. Compared to HFD-fed wild-type (WT) mice, HFD-fed Phb1adipo-/- mice displayed dramatically lower fat mass with significantly decreased levels of total adipose tissue inflammation, including macrophage and neutrophil number as well as the expression of inflammatory mediators. To our surprise, although liver steatosis in Phb1adipo-/- mice was much more severe, liver inflammation and fibrosis were similar to WT mice after HFD feeding. RNA sequencing analyses revealed that the interferon pathway was markedly suppressed while the bone morphogenetic protein 2 pathway was significantly up-regulated in the liver of HFD-fed Phb1adipo-/- mice compared with HFD-fed WT mice. Conclusion: HFD-fed Phb1adipo-/- mice display a subtype of the lean NAFLD phenotype with severe hepatic steatosis despite low adipose mass. This subtype of the lean NAFLD phenotype has similar inflammation and fibrosis as obese NAFLD in HFD-fed WT mice; this is partially due to reduced total adipose tissue inflammation and the hepatic interferon pathway.
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Project description:The metabolic syndrome represents a cluster of well-documented risk factors for the development of type 2 diabetes and cardiovascular disease. Next to visceral obesity, dyslipidemia and insulin resistance, excessive triglyceride accumulation in the liver has been implicated to play a role in the development of the metabolic syndrome. To investigate the underlying molecular changes leading to hepatic steatosis we performed microarray analysis on livers of mice either fasted over night or fed a high fat diet for 2 Weeks. We analysed 7 500 genes and subsequently performed a pathway analysis to identify changes in hepatic genes in both models. Fasting induced a high number of differentially expressed hepatic genes, resulting in an change towards an energy saving phenotype. In contrast only a small number of genes were differentially expressed after high fat diet. Fasting promoted gluconeogenesis and b-oxidation, strongly suppressed cholesterol synthesis and activated pathways to preserve hepatic function. High fat diet induced steatosis was accompanied by the activation of the stearoyl-CoA desaturase and the lipogenic transcription factor Srebp-1c, both implicated in the development of hepatic insulin resistance. These changes reflect the activation of different gene expression programs in response to plasma lipid overload. Keywords: Diet intervention Two conditions, fasting and high fat diet. 5 biological replicates for comparison of high fat diet versus fasting and controls versus high fat diet, 4 biological replicates for the comparison of controls versus fasting. All biological replicates are performed as technical replicates in the form of a dye-swap. Total number of arrays hybridises is therefore 28.
2011-04-02 | E-GEOD-8576 | biostudies-arrayexpress
Project description:Diet steatosis in commercial crossbreed swine
| PRJNA541949 | ENA