DNA methylation during human adipogenesis and impact of fructose
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE119539 | GEO | 2020/12/08
REPOSITORIES: GEO
Similar Datasets
Project description:This data set consists of a time series of transcriptional profiles of differentiating human adipocytes in vitro a for different fructose concentration
2020-12-08 | GSE119593 | GEO
Project description:DNA methylation during human adipogenesis and impact of fructose
| PRJNA489481 | ENA
Project description:This data set consists of a time series of transcriptional profiles of differentiating human adipocytes in vitro.
2016-07-08 | GSE76131 | GEO
Project description:BackgroundIncreased adipogenesis and altered adipocyte function contribute to the development of obesity and associated comorbidities. Fructose modified adipocyte metabolism compared to glucose, but the regulatory mechanisms and consequences for obesity are unknown. Genome-wide methylation and global transcriptomics in SGBS pre-adipocytes exposed to 0, 2.5, 5, and 10 mM fructose, added to a 5-mM glucose-containing medium, were analyzed at 0, 24, 48, 96, 192, and 384 h following the induction of adipogenesis.ResultsTime-dependent changes in DNA methylation compared to baseline (0 h) occurred during the final maturation of adipocytes, between 192 and 384 h. Larger percentages (0.1% at 192 h, 3.2% at 384 h) of differentially methylated regions (DMRs) were found in adipocytes differentiated in the glucose-containing control media compared to adipocytes differentiated in fructose-supplemented media (0.0006% for 10 mM, 0.001% for 5 mM, and 0.005% for 2.5 mM at 384 h). A total of 1437 DMRs were identified in 5237 differentially expressed genes at 384 h post-induction in glucose-containing (5 mM) control media. The majority of them inversely correlated with the gene expression, but 666 regions were positively correlated to the gene expression.ConclusionsOur studies demonstrate that DNA methylation regulates or marks the transformation of morphologically differentiating adipocytes (seen at 192 h), to the more mature and metabolically robust adipocytes (as seen at 384 h) in a genome-wide manner. Lower (2.5 mM) concentrations of fructose have the most robust effects on methylation compared to higher concentrations (5 and 10 mM), suggesting that fructose may be playing a signaling/regulatory role at lower concentrations of fructose and as a substrate at higher concentrations.
| S-EPMC7691080 | biostudies-literature
Project description:Active thermogenic adipocytes voraciously consume energy substrates like fatty acids and glucose to maintain body temperature upon cold exposure. Despite strong evidence for the involvement of brown adipose tissue (BAT) in controlling systemic energy homeostasis upon nutrient excess, it is unclear how the activity of brown adipocytes is regulated in times of nutrient scarcity. Therefore, this study aimed to scrutinize factors that modulate BAT activity to balance thermogenic and energetic needs upon simultaneous fasting and cold-exposure. For an unbiased view we performed transcriptomic and miRNA sequencing analysis of BAT from acutely fasted (24 hours) mice under mild cold exposure. Combining these data with in-depth bioinformatic analyses and in vitro experiments, we defined a previously undescribed axis of p53 and miR-92a-1-5p that is highly upregulated by fasting in thermogenic adipocytes. p53, a fasting-responsive transcription factor, was previously shown to control genes involved in the thermogenic program and miR-92a-1-5p was found to negatively correlate with human BAT activity. Here, we elucidated fructose transporter Slc2a5 as one direct downstream target of this axis and show that fructose can be taken up by and metabolized in brown adipocytes. In sum, this study delineates a fasting-induced pathway involving p53 and miR-92a-1-5p impinging on Slc2a5 and suggests a contribution of fructose as an energy substrate in thermogenic adipocytes.
2022-05-11 | GSE199963 | GEO
Project description:To decipher the beneficial effects of Polyphenols on health, healthy volunteers were randomized into two groups and were submitted to either a red grape polyphenol rich extract supplemented diet (PP) or a placebo diet (PCB) during 8 weeks. Then they were submitted to a fructose load (3g/kg Fat Free Mass/day) during 7 days. Muscle biopsies were taken before the protocol, 8 weeks after PP or PCB diet and after the 7 days fructose load. We have employed whole genome microarray expression profiling as a discovery platform to identify genes regulated by fructose and to identify the mechanism of action of Polyphenols. Healthy volunteers were randomized into two groups and were submitted to either a red grape polyphenol rich extract supplemented diet (PP) or a placebo diet (PCB) during 8 weeks. Then they were submitted to a fructose load (3g/kg Fat Free Mass/day) during 7 days. Muscle biopsies were taken before the protocol, 8 weeks after PP or PCB diet and after the 7 days fructose load. We have employed whole genome microarray expression profiling as a discovery platform to identify genes regulated by fructose and to identify the mechanism of action of Polyphenols. Ten biological replicates were processed for PP diet, nine for PCB diet.
2013-02-04 | E-GEOD-35764 | biostudies-arrayexpress
Project description:Background: An increasing body of evidence has linked fructose intake to colorectal cancer (CRC). African Americans (AAs) consume greater quantities of fructose and are more likely to develop right-side colon cancer than European Americans. Objective: We examined the hypothesis that fructose consumption leads to genomic differences associated with CRC tumor biology. Methods: DNA methylation data from this study was obtained using the Illumina Infinium MethylationEPIC kit (GSE151732). Right and left colon differentially methylated regions (DMRs) were identified using DMRcate through analysis of fructose consumption in normal AA colon biopsies (n=79) undergoing screening colonoscopy. Secondary analysis of CRC tumors was carried out using data derived from TCGA-COAD, GSE101764 and GSE193535. Right colon organoids derived from AA normal colon tissues were exposed to 4.4mM of fructose for 72 hours. Fructose-associated differentially expressed genes (DEGs) were identified using DESeq2. This package was also used to identify DEGs in CRC tumors from TCGA-COAD. Results: We identified 4,263 right colon fructose-associated DMRs (FDR<0.05). In contrast, only 24 DMRs survived multiple testing corrections (FDR<0.05) in matched, left colon. Almost 50% of right colon fructose-associated DMRs overlapped regions implicated in CRC in at least one of three datasets. A highly significant enrichment was also observed between genes corresponding to right colon fructose-associated DMRs and DEGs associated with fructose exposure in AA right colon organoids (P=3.28E-30). Further, overlapping and significant enrichments for a number of fatty acid metabolism, glycolysis and cell proliferation pathways were also found. By further examining the overlap of genes within these pathways that were also differentially expressed in TCGA-COAD, our analysis reveals potential role for PFKP and ANKRD23 in fructose-mediated CRC risk. Conclusions: Our data support that dietary fructose exerts a greater CRC risk-related effect in right than left colon among AAs, alluding to its potential role in contributing to racial disparities in CRC.
2025-03-15 | GSE261717 | GEO
Project description:DNA methylation profile for male SD Rats upon fructose treatment by RRBS
2016-10-19 | GSE59893 | GEO
Project description:This SuperSeries is composed of the following subset Series: GSE18598: Differentiating 3T3-L1 adipocytes, introduced with siRNA against aof2 and rfk genes, or treated with tranylcypromine GSE18599: Differentiating 3T3-L1 adipocytes, introduced with siRNA against phf21a gene Refer to individual Series
2012-04-04 | E-GEOD-18600 | biostudies-arrayexpress
Project description:This proposed study is designed to investigate the specific uptake of fructose by human colorectal tumors. In this study, subjects with colorectal cancer undergoing surgery will receive an oral sugar solution containing fructose or xylose prior to surgery. The tumor will then be resected, and a portion of the tissue will be used to measure the abundance of fructose and xylose. The study hypothesis is that the tumors will take up fructose sugar but not xylose sugar. A comparison of the sugar uptake between the tumor and normal tissues from the adjacent intestinal epithelium and smooth muscle and the liver will be conducted. This proposal will confirm that human colorectal cancer tumors can directly absorb dietary sugars, which has never been demonstrated.
| 2396702 | ecrin-mdr-crc