Transcriptome profile of livers from hepatocyte-specific Slc25a34 knockout mice on chow and fast-food diet
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE186314 | GEO | 2022/06/08
REPOSITORIES: GEO
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Project description:Transcriptome profile of livers from hepatocyte-specific Slc25a34 knockout mice on chow and fast-food diet
| PRJNA773383 | ENA
Project description:Background: More than 100 million Americans are living with metabolic syndrome, increasing their propensity to develop heart disease– the leading cause of death worldwide. A major contributing factor to this epidemic is caloric excess, often a result of consuming low cost, high calorie fast food. Several recent seminal studies have demonstrated the pivotal role of gut microbes contributing to cardiovascular disease in a diet-dependent manner. Given the central contributions of diet and gut microbiota to cardiometabolic disease, we hypothesized that novel microbial metabolites originating postprandially after fast food consumption may contribute to cardiometabolic disease progression. Methods: To test this hypothesis, we gave conventionally raised or antibiotic-treated mice a single oral gavage of a fast food slurry or a control rodent chow diet slurry and sacrificed the mice four hours later. Here, we coupled untargeted metabolomics in portal and peripheral blood, 16S rRNA gene sequencing, targeted liver metabolomics, and host liver RNA sequencing to identify novel fast food-derived microbial metabolites. Results: We successfully identified several metabolites that were enriched in portal blood, increased by fast food feeding, and essentially absent in antibiotic-treated mice. Strikingly, just four hours post-gavage, we found that fast food consumption resulted in rapid reorganization of the gut microbial community structure and drastically altered hepatic gene expression. Importantly, diet-driven reshaping of the microbiome and liver transcriptome was dependent on a non-antibiotic ablated gut microbial community. Conclusions: Collectively, these data suggest that single fast food meal is sufficient to reshape the gut microbial community yielding a unique signature of food-derived microbial metabolites. Future studies are warranted to determine if these metabolites are causally linked to cardiometabolic disease.
2021-11-14 | GSE165756 | GEO
Project description:EGFR is a critical regulator of hepatocyte proliferation and liver regeneration. Our recent work indicated EGFR can also regulate lipid metabolism during liver regeneration after partial-hepatectomy. Based on these findings, we investigated role of EGFR in a mouse model of NAFLD utilizing a pharmacological inhibition strategy. C57BL6/J mice were fed chow-diet, or fast-food diet with/without EGFR inhibitor (Canertinib) for 2-months. EGFR inhibition completely prevented development of steatosis and liver injury in this model. In order to study if EGFR inhibition can reverse NAFLD progression, mice were fed fast-food diet for 5-months, with/without Canertinib-treatment for the last 5-weeks of the study. EGFR-inhibition remarkably decreased steatosis, liver injury, fibrosis and improved glucose tolerance. Microarray analysis revealed ~40% of genes altered by fast-food diet were differentially expressed after EGFR-inhibition, and thus, are potentially regulated by EGFR. Several genes and enzymes related to lipid metabolism (particularly fatty-acid synthesis and lipolysis), which were disrupted by fast-food diet, were found to be modulated by EGFR. Several crucial transcription factors that play a central role in regulating these lipid metabolism genes during NAFLD, including PPARγ, SREBF1, ChREBP and HNF4α, were also found to be modulated by EGFR. In fact, ChIP-analysis revealed PPARγ binding to several crucial lipid metabolisms genes (Fasn, Scd1 and Plin2) was drastically reduced by EGFR inhibition. Further upstream, EGFR-inhibition suppressed AKT signaling, which is known to control these transcription factors, including PPARγ and SREBF1, in NAFLD models. Lastly, the effect of EGFR in FFD-induced fatty-liver phenotype was not shared by receptor-tyrosine-kinase MET, as investigated using MET-KO mice. In-conclusion, our study revealed a role of EGFR in NAFLD and the potential of EGFR-inhibition as a treatment strategy for NAFLD. We used microarrays to detail the global programme of gene expression in liver of C57BL6/J mice fed fast-food diet mice treated with EGFR inhibitor (canertinib)
2020-05-02 | GSE130528 | GEO
Project description:Gene expression in livers of male wild-type (WT) and OGG1-deficient (Ogg1-/-) mice fed either a chow diet or a high-fat diet (HFD) were examined. Mice were fed the diet for 10 weeks prior to tissue collection and were 22 weeks of age at the time of tissue collection. 24 Total samples were analyzed. We generated the following pairwise comparisons using GeneSifter: WT Chow vs Ogg1-/- Chow; WT HFD vs. Ogg1-/- HFD using t-test followed by Benjamini and Hochberg correction. An adjusted p-value less than 0.05 was considered to be statistically significant.
2012-12-16 | E-GEOD-35497 | biostudies-arrayexpress
Project description:Gene expression in livers of male wild-type (WT) and OGG1-deficient (Ogg1-/-) mice fed either a chow diet or a high-fat diet (HFD) were examined. Mice were fed the diet for 10 weeks prior to tissue collection and were 22 weeks of age at the time of tissue collection.
2012-12-16 | GSE35497 | GEO
Project description:Fast food diet consumption and sedentary life style leads to energy excess, which elevates risks for obesity, metabolic syndrome, non-alcoholic fatty liver disease (NAFLD), and cancer. Exercise training conveys many health benefits in populations with or without these chronic conditions. Diet and exercise regulate gene expression by mediating epigenetic mechanisms globally and at select loci in an array of human tissues, however, such effects are less well documented in liver tissue. To dissect the epigenetic consequences of diet and exercise in liver, we measured DNA methylation using reduced representation bisulfite sequencing (RRBS) and transcriptome using RNA-seq in mice maintained on a fast food diet with sedentary lifestyle (FFC) or exercise (FFE) compared to control diet with (NCE) and without exercise (NCC). Our analyses demonstrate genome-wide differential DNA methylation at key regulatory regions, including different classes of promoters and enhancers, and differential regulation of gene clusters in each condition group. FFE gene expression is most differentially regulated, with enrichment of carbohydrate/lipid metabolic pathways and skeletal muscle development in altered gene sets. Through evaluation of putative protective effects of exercise on diet-induced DNA methylation and gene expression, we show that hypermethylation is effectively prevented, especially at promoters and enhancers, and hypomethylation is partially attenuated. We assessed diet-induced DNA methylation changes associated with cancer-related epigenetic modifications and identified significant increases at liver-specific enhancers in FFC and FFE, suggesting a repressive effect on the epigenomic signature specifying liver identity. Gaining methylation at a subset of gene promoters was associated with inhibition of tissue development and promotion of carcinogenic process. Taken together, our study demonstrates large-scale diet- and exercise-induced effects on the epigenetic landscape, emphasizing the functional relevance of epigenetic mechanisms as an interface between life-style modifications and phenotypic alterations.
2017-08-25 | GSE85772 | GEO
Project description:We performed RNA sequencing of the aortic valves of C57BL/6J (the wild type with chow diet), Ldlr-/- (1. with chow diet, 2. with WD), and Apoe-/- mice (1. with chow diet, 2. with WD) to compare the overall transcriptomic characteristics within genetic differences (wild type, Ldlr-/-, Apoe-/-) or in dietary differences (chow diet versus WD).
2022-08-22 | GSE205587 | GEO
Project description:Both PIK3R1(Y657X) mutant and wild-type C57Bl/6J mice were maintained on chow until 16 weeks old, at which time they were fasted for 16 hours and then refed chow for 6 hours. The tissues were harvested and snap-frozen at three time points: chow diet before overnight fast (ad libitum chow, ALC), after 16 hour fast (overnight fast, ONF), and after 6 hour refeeding (refed 6 hours, RF6).
2020-06-30 | GSE153431 | GEO
Project description:Proteomics of liver tissue from mice fed a high fat diet (HFD) or regular chow diet. Data accompany our paper entitled “Dynamic Regulation of N6,2′-O-dimethyladenosine (m6Am) in Obesity” scheduled for publication in Nature Communications, 2021
2021-10-27 | PXD029280 | Pride
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.
2015-08-28 | GSE68360 | GEO