Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Comparision of hepatic gene expression between HFHS diet-fed WT and CREBH-Tg mice

ABSTRACT: Comparision of hepatic gene expression between HFHS diet-fed WT and CREBH-Tg mice

PROVIDER: PRJNA600434 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

Comparision of hepatic gene expression between HFHS diet-fed WT and CREBH-Tg mice

Project description:To determine CREBH-mediated hepatic gene expression changes in hifh-fat high-sucrose (HFHS) dit feeding, we employed the microarray analysis. We collected the livers from male WT and CREBH-Tg mice fed with HFHS diet for 12 weeks from 6 weeks old.

2020-01-11 | GSE143421 | GEO

Inducible hepatic expression of CREBH mitigates diet-induced obesity, insulin resistance and hepatice steatosis in mice.

Project description:Cyclic AMP-responsive element-binding protein H (CREBH, encoded by Creb3l3) is a transcription factor that regulates the expression of genes that control lipid and glucose metabolism, as well as inflammation. CREBH is upregulated in the liver under conditions of overnutrition, and mice globally lacking the gene (CREBH-/-) are highly susceptible to diet-induced obesity, insulin resistance (IR) and hepatic steatosis. The net protective effects of CREBH have been attributed in large part to the activities of Fibroblast growth factor (Fgf)-21 (Fgf21), a target gene that promotes weight loss, improves glucose homeostasis and reduces hepatic lipid accumulation. To explore the possibility that activation of the CREBH-Fgf21 axis could ameliorate established effects of high fat feeding, we generated an inducible transgenic hepatocyte-specific CREBH overexpression mouse model (Tg-rtTA). Acute overexpression of CREBH in livers of Tg-rtTA mice effectively reversed diet-induced obesity, IR and hepatic steatosis. These changes were associated with increased activities of thermogenic brown and beige adipose tissues in Tg-rtTA mice, leading to reductions in fat mass, along with enhanced insulin sensitivity and glucose tolerance. Genetically silencing of Fgf21 in Tg-rtTA mice abrogated the CREBH-mediated reductions in body weight loss, but only partially reversed the observed improvements in glucose metabolism. These findings reveal that the protective effects of CREBH activation may be leveraged to mitigate diet-induced obesity and associated metabolic abnormalities in both Fgf21-dependent and -independent pathways.

2021-04-30 | GSE173548 | GEO

Comparision of hepatic gene expression between fasted and fed ad lib states in C57B6J (WT) and CREBH KO mice

Project description:To determine hepatic gene expression changes in fasted state, we employed the microarray analysis. We collected the livers from 8-weeks-old male WT and CREBH KO mice in both fasted and fed ad lib states.

2020-01-11 | GSE143420 | GEO

Comparision of hepatic gene expression between fasted and fed ad lib states in C57B6J (WT) and CREBH KO mice

Project description:Comparision of hepatic gene expression between fasted and fed ad lib states in C57B6J (WT) and CREBH KO mice

| PRJNA600435 | ENA

CREBH Regulates Mitochondrial Unfolded Protein Response to Maintain Energy Homeostasis

Project description:The Mitochondrial Unfolded Protein Response (UPRmt), a mitochondria-originated stress response to altered mitochondrial proteostasis, plays important roles in various pathophysiological processes. In this study, we revealed that the endoplasmic reticulum (ER)-tethered stress sensor CREBH regulates UPRmt to maintain mitochondrial homeostasis and function in the liver. CREBH is enriched in and required for hepatic Mitochondria-Associated Membrane (MAM) expansion induced by energy demands. Under a fasting challenge or during the circadian cycle, CREBH is activated to promote expression of the genes encoding the key enzymes, chaperones, and regulators of UPRmt in the liver. Activated CREBH, cooperating with peroxisome proliferator-activated receptor α (PPARα), activates expression of Activating Transcription Factor (ATF) 5 and ATF4, two major UPRmt transcriptional regulators, independent of the ER-originated UPR (UPRER) pathways. Hepatic CREBH deficiency leads to accumulation of mitochondrial unfolded proteins, decreased mitochondrial membrane potential, and elevated cellular redox state. Dysregulation of mitochondrial function caused by CREBH deficiency coincides with increased hepatic mitochondrial oxidative phosphorylation (OXPHOS) but decreased glycolysis. CREBH knockout mice display defects in fatty acid oxidation and increased reliance on carbohydrate oxidation for energy production. In summary, our studies uncover that hepatic UPRmt is activated through CREBH under physiological challenges, highlighting a molecular link between ER and mitochondria in maintaining mitochondrial proteostasis and energy homeostasis under stress conditions.

2024-11-15 | GSE281608 | GEO

Hepatic Sel1L-Hrd1 ER-Associated Degradation (ERAD) manages FGF21 levels and systemic metabolism via CREBH

Project description:Fibroblast growth factor 21 (Fgf21) is a liver-derived, fasting-induced hormone with broad effects on growth, nutrient metabolism and insulin sensitivity. Here, we report the discovery of a novel mechanism regulating Fgf21 expression under growth and fasting-feeding. The Sel1LHrd1 complex is the most conserved branch of mammalian endoplasmic reticulum (ER)- associated degradation (ERAD) machinery. Mice with liver-specific deletion of Sel1L exhibit growth retardation with markedly elevated circulating Fgf21, reaching levels close to those in Fgf21 transgenic mice or pharmacological models. Mechanistically, we show that the Sel1LHrd1 ERAD complex controls Fgf21 transcription by regulating the ubiquitination and turnover (and thus nuclear abundance) of ER-resident transcription factor Crebh, while having no effect on the other well-known Fgf21 transcription factor Pparα. Our data reveal a physiologically regulated, inverse correlation between Sel1L-Hrd1 ERAD and Crebh-Fgf21 levels under fasting-feeding and growth. This study not only establishes the importance of Sel1L-Hrd1 ERAD in the liver in the regulation of systemic energy metabolism, but also reveals a novel hepatic “ERADCrebh- Fgf21” axis directly linking ER protein turnover to gene transcription and systemic metabolic regulation.

2018-08-17 | GSE118658 | GEO

Epigenome analysis of liver tissues from Pemt-/- and Pemt+/+ under high fat-high sucrose (HFHS) diet

Project description:Genome wide DNA methylation profiling of liver tissues from Pemt-/- and Pemt+/+ under HFHS diets. Pemt-/- and Pemt+/+ mice were fed HFHS from 5 to 25 weeks of age and liver tissues were obtained at 25 weeks. Bisulphite converted DNAs were enriched with EpiXplore Methylation DNA Enrichment Kit (Clontech). Genomic DNA libraries was prepared by TruSeq ChIP Sample Preparation Kit.

2015-04-14 | E-GEOD-67791 | biostudies-arrayexpress

Expression data from liver samples of Pemt-/- and Pemt+/+ mice under high fat-high-sucrose (HFHS) diet

Project description:We used microarrays to detail the global programme of gene expression in the liver of Pemt-/- and Pemt+/+ under HFHS diets. Liver sample of Pemt-/- and Pemt+/+ mice under HFHS for 1, 2, 3, 4 weeks were used for RNA extraction and hybridization on Affymetrix microarrays. Genes in liver of Pemt-/- mice, successively suppressed compared with Pemt+/+ mice, were obtained.

2015-04-14 | E-GEOD-67792 | biostudies-arrayexpress

Gene expression profile at single cell level of cells derived from the arcuate nucleus of the hypothalamus (ARC) of mice fed with standard chow (SC) or high-fat high-sugar (HFHS) diet

Project description:Hypercaloric diet affects hypothalamic cells at different levels. However, the time-dependent transcriptional changes of hypothalamic cells, and more particularly ARC cells, following the exposure to a HFHS diet are largely unknown. We used single cell RNA sequencing (scRNA-Seq) to analyze the impact of HFHS diet feeding on the transcriptional profile of ARC cells at different timepoints, with a special focus on astrocytes. The timepoints analyzed consist in 5 and 15 days of HFHS diet exposure, at which mice gain a not significant or a significant body weight respectively.

2022-06-10 | GSE205667 | GEO