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Holistic characterization of single hepatocyte transcriptome responses to high fat diet

ABSTRACT: Holistic characterization of single hepatocyte transcriptome responses to high fat diet

PROVIDER: PRJNA660752 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12564645_1.fastq.gz	Fastqsanger.gz
	SRR12564645_2.fastq.gz	Fastqsanger.gz
	SRR12564646_1.fastq.gz	Fastqsanger.gz
	SRR12564646_2.fastq.gz	Fastqsanger.gz
	SRR12564647_1.fastq.gz	Fastqsanger.gz

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Holistic characterization of single hepatocyte transcriptome responses to high fat diet

Project description:Purpose: The goals of this study are to investigate the effects of the long-term high-fat diet to transcriptome of mouse hepatocytes utilizing single cell RNA-seq (scRNA-seq) technology. Methods: Hepatocytes were obtained from three mice that had been fed with the high-fat diet (HFD) and two mice that had been treated with the regular diet (LFD). After isolation and enrichment, hepatocytes were subjected to Drop-seq.

2020-09-21 | GSE157281 | GEO

Holistic characterization of single-hepatocyte transcriptome responses to high-fat diet.

Project description:During nutritional overload and obesity, hepatocyte function is grossly altered, and a subset of hepatocytes begins to accumulate fat droplets, leading to nonalcoholic fatty liver disease (NAFLD). Recent single-cell studies revealed how nonparenchymal cells, such as macrophages, hepatic stellate cells, and endothelial cells, heterogeneously respond to NAFLD. However, it remains to be characterized how hepatocytes, the major constituents of the liver, respond to nutritional overload in NAFLD. Here, using droplet-based, single-cell RNA sequencing (Drop-seq), we characterized how the transcriptomic landscape of individual hepatocytes is altered in response to high-fat diet (HFD) and NAFLD. We showed that the entire hepatocyte population undergoes substantial transcriptome changes upon HFD, although the patterns of alteration were highly heterogeneous, with zonation-dependent and -independent effects. Periportal (zone 1) hepatocytes downregulated many zone 1-specific marker genes, whereas a small number of genes mediating gluconeogenesis were upregulated. Pericentral (zone 3) hepatocytes also downregulated many zone 3-specific genes; however, they upregulated several genes that promote HFD-induced fat droplet formation, consistent with findings that zone 3 hepatocytes accumulate more lipid droplets. Zone 3 hepatocytes also upregulated ketogenic pathways as an adaptive mechanism to HFD. Interestingly, many of the top HFD-induced genes, which encode proteins regulating lipid metabolism, were strongly co-expressed with each other in a subset of hepatocytes, producing a variegated pattern of spatial co-localization that is independent of metabolic zonation. In conclusion, our data set provides a useful resource for understanding hepatocellular alteration during NAFLD at single cell level.

| S-EPMC8260362 | biostudies-literature

Expression data from hepatocyte specific Klf6 knockout mice vs. control on high fat diet

Project description:Dysregulated glucose homeostasis and lipid accumulation characterize non-alcoholic fatty liver disease (NAFLD), but underlying mechanisms are obscure. We report here that KrÃ¼ppel-like factor 6 (KLF6), a ubiquitous transcription factor that promotes adipocyte differentiation, also provokes the metabolic abnormalities of NAFLD. Mice with either hepatocyte-specific knockdown of KLF6 (DeltaHepKlf6) or global KLF6 heterozygosity (Klf6 +/-) have reduced body fat content and improved glucose and insulin tolerance. Mice with KLF6 depletion, compared to wild type mice, are protected from high fat diet-induced steatosis. Three mice with a hepatocyte-specific knockdown of KLF6 (DeltaHepKlf6) on high fat diet and 3 littermate controls on the same diet were sacrificed after 8 weeks of diet. Liver tissue was preserved in RNAlaterÂ® (Ambion, Austin, TX). RNA was isolated from liver tissue and homogenized in TRIzolÂ® reagent (Invitrogen, Carlsbad, CA). In order to identify potential KLF6 targets that contributed to changes in glucose- and lipid-metabolism, we performed an Affymetrix Exon1 S.T. GenearrayÂ® (Affymetrix, Santa Clara, CA).

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Expression data from hepatocyte specific Klf6 knockout mice vs. control on high fat diet

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Hepatocyte RNA-seq analysis in liver-specific XBP1 knockout mice fed a high fat sugar diet

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Project description:We investigated remodeling of the mitochondrial proteome to determine mechanisms of changes to lipid oxidation following high-fat feeding. C57BL/6J mice consumed either a high-fat diet (HFD, 60% fat) or low fat diet (LFD, 10% fat) for 12 weeks. Mice were fasted 4 hours then anaesthetized by sodium pentobarbital for tissue collection. A mitochondrial-enriched fraction was prepared from gastrocnemius muscles and underwent proteomic analysis by high-resolution mass spectrometry.

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Murine Mammary fat pad on high fat diet

Project description:Younger age and obesity increase the incidence and rates of metastasis of triple-negative breast cancer (TNBC), an aggressive subtype of breast cancer. The tissue microenvironment, specifically the extracellular matrix (ECM), is known to promote tumor invasion and metastasis. We sought to characterize the effect of both age and obesity on the ECM of mammary fat pads. We used a diet-induced obesity (DIO) model where 10-week-old female mice were fed a high-fat diet (HFD) for 16 weeks or a control chow diet (CD) where time points were every 4 weeks to monitor age and obesity HFD progression. We isolated the mammary fat pads to characterize the ECM at each time point. Utilizing proteomics, we found that the early stages of obesity were sufficient to induce distinct differences in the ECM composition of mammary fat pads that promote TNBC cell invasion. ECM proteins previously implicated in driving TNBC invasion Collagen IV and Collagen VI, were enriched with weight gain. Together these data implicate ECM changes in the primary tumor microenvironment as mechanisms by which age and obesity contribute to breast cancer progression.

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