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The transcription factor Hepatocyte Nuclear Factor 4A acts in the intestine to promote white adipose tissue energy storage

ABSTRACT: The transcription factor Hepatocyte Nuclear Factor 4A acts in the intestine to promote white adipose tissue energy storage

PROVIDER: PRJNA783018 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17020831_1.fastq.gz	Fastqsanger.gz
	SRR17020831_2.fastq.gz	Fastqsanger.gz
	SRR17020832_1.fastq.gz	Fastqsanger.gz
	SRR17020832_2.fastq.gz	Fastqsanger.gz
	SRR17020833_1.fastq.gz	Fastqsanger.gz

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2015-05-14 | ST000167 | MetabolomicsWorkbench

The transcription factor Hepatocyte Nuclear Factor 4A acts in the intestine to promote white adipose tissue energy storage

Project description:HNF4A is a transcription factor that controls metabolic features of several endodermal epithelia. Using an intestinal conditional mouse model, here we demonstrate that HNF4A is not required for intestinal lipid metabolism per se, but unexpectedly influences whole body energy expenditure under diet-induced obesity (DIO). Deletion of intestinal HNF4A causes mice to become DIO-resistant with preference for fat as an energy substrate and energetic changes in association with white adipose tissue (WAT) beiging. Intestinal HNF4A is crucial for fat-induced release of glucose-dependent insulinotropic polypeptide (GIP), while reintroduction of a stabilized GIP analog rescues the DIO-resistance phenotype of the mutant mice. Our study provides evidence that intestinal HNF4A plays a non-redundant role in whole body lipid homeostasis and points to a novel non-cell-autonomous regulatory circuit for body fat management.

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The transcription factor hepatocyte nuclear factor 4A acts in the intestine to promote white adipose tissue energy storage.

Project description:The transcription factor hepatocyte nuclear factor 4 A (HNF4A) controls the metabolic features of several endodermal epithelia. Both HNF4A and HNF4G are redundant in the intestine and it remains unclear whether HNF4A alone controls intestinal lipid metabolism. Here we show that intestinal HNF4A is not required for intestinal lipid metabolism per se, but unexpectedly influences whole-body energy expenditure in diet-induced obesity (DIO). Deletion of intestinal HNF4A caused mice to become DIO-resistant with a preference for fat as an energy substrate and energetic changes in association with white adipose tissue (WAT) beiging. Intestinal HNF4A is crucial for the fat-induced release of glucose-dependent insulinotropic polypeptide (GIP), while the reintroduction of a stabilized GIP analog rescues the DIO resistance phenotype of the mutant mice. Our study provides evidence that intestinal HNF4A plays a non-redundant role in whole-body lipid homeostasis and points to a non-cell-autonomous regulatory circuit for body-fat management.

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Hepatocyte growth factor time course

Project description:Cultured Madin-Darby canine kidney (MDCK) cells treated with hepatocyte growth factor (HGF) for 0, 3 and 24 hours. Each time point in triplicate. Keywords: time-course

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Hepatocyte Nuclear Factor 1 coordinates multiple functions of intestinal epithelial cells

Project description:Background and Aims: Hepatocyte nuclear factor 1 (HNF1) transcription factors direct tissue specific gene regulation in liver, pancreas and kidney and are associated with diabetes. Here we investigate the transcriptional network governed by HNF1 in an intestinal epithelial cell line. Methods: Chromatin immunoprecipitation followed by direct sequencing (ChIP-seq) was used to identify HNF1 binding sites genome-wide. Direct targets of HNF1 were validated using conventional ChIP assays. siRNA-mediated depletion of HNF1 followed by RT-qPCR further confirmed target genes. The effect of HNF1 reduction on glucose uptake was measured by fluorescence activated cell sorting (FACS) following treatment of intestinal epithelial cells with 2-[N-(7-nitrobenz-2-oxa-1,3-diazol-4-yl) amino]-2-deoxy-d-glucose (2-NBDG, a fluorescent glucose mimic). Results: HNF1 controls multiple pathways that are critical for intestinal epithelial cell function, including properties of the cell membrane, cellular response to hormones, and regulation of biosynthetic processes. Approximately 50% of HNF1 binding sites are also occupied by hepatocyte nuclear factor 4A (HNF4A), caudal type homeobox 2 (CDX2), and forkhead box A2 (FOXA2). Depletion of HNF1 increases FOXA2 abundance and decreases levels of CDX2. Moreover, loss of HNF1 inhibits glucose uptake by the intestinal epithelial cell line. Conclusions: These data show that HNF1 plays a critical role in regulating intestinal epithelial cell functions including glucose absorption. HNF1 interacts with other tissue-specific transcription factors to regulate differentiated properties of these cells.

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Project description:Hepatocyte nuclear factor 4 (HNF4) is a transcription factor that acts as a master regulator of genes in several endodermal-derived tissues, including the intestine in which it plays a central role during development and tumorigenesis. To better delineate the mechanisms by which HNF4 can interfere during these processes, we combined stable isotope labelling with amino acids in cell culture (SILAC)-based quantitative proteomics with immunoprecipitation of green fluorescent protein (GFP) as well as with proximity-dependent purification by the biotin ligase BirA, both fused to HNF4. Surprisingly, these analyses identified a significant enrichment of proteins falling into the DNA repair gene ontology term, a so far unidentified biological feature of this transcription factor. Several of these proteins including PARP1, RAD50 and DNA-PKcs were confirmed to interact with HNF4in colorectal cancer cell lines. During DNA damage response, HNF4 localized to double strand DNA breaks in these cells. HNF4was able to interfere functionally during non-homologous end-joining (NHEJ). Overall, these observations identify an unsuspected role for this transcription factor during the DNA damage response.

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Effect of depletion of Drosophila Hepatocyte Nuclear Factor 4 (dHNF4) in enterocytes on gene expression in the adult midgut

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