Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA384174 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Fatty Acid Oxidation and Glycolysis Regulate Skin ECM Homeostasis by Shifting Fibroblasts between Catabolism and Anabolism
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Project description:Fatty Acid Oxidation and Glycolysis Regulate Skin ECM Homeostasis by Shifting Fibroblasts between Catabolism and Anabolism (RNA-Seq)
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Project description:The alphaproteobacterium Paracoccus denitrificans Pd1222 has two different, yet functionally redundant acetyl-CoA assimilation routes: the Ethylmalonyl-CoA pathway (EMCP) and the glyoxylate cycle (GC). The EMPC and the GC each tightly control the balance between catabolism and anabolism by shifting flux away from the oxidation of acetyl-CoA in the tricarboxylic acid (TCA) cycle towards biomass formation. RamB (encoded by Pden_1365), a member of the ScfR family, is a transcriptional regulator in P. denitrificans Pd1222 that controls expression of GC. To analyze the role of RamB in the coordinated regulation of metabolic plasticity, we analyzed the global transcriptome of P. denitrificans Pd1222, as well as the ramB-deletion strain during mid-exponential growth phase on defined minimal medium with acetate or succinate as carbon sources.
2023-06-06 | E-MTAB-12482 | biostudies-arrayexpress
Project description:Sirtuins are a family of protein deacetylases, deacylases, and ADP-ribosyltransferases that regulate life span, control the onset of numerous age-associated diseases, and mediate metabolic homeostasis. We have uncovered a novel role for the mitochondrial sirtuin SIRT4 in the regulation of hepatic lipid metabolism during changes in nutrient availability. We show that SIRT4 levels decrease in the liver during fasting and that SIRT4 null mice display increased expression of hepatic peroxisome proliferator activated receptor (PPAR ) target genes associated with fatty acid catabolism. Accordingly, primary hepatocytes from SIRT4 knockout (KO) mice exhibit higher rates of fatty acid oxidation than wild-type hepatocytes, and SIRT4 overexpression decreases fatty acid oxidation rates. The enhanced fatty acid oxidation observed in SIRT4 KO hepatocytes requires functional SIRT1, demonstrating a clear cross talk between mitochondrial and nuclear sirtuins. Thus, SIRT4 is a new component of mitochondrial signaling in the liver and functions as an important regulator of lipid metabolism. SIRT4 knockout (KO) and wild-type (WT) littermates (male; n 6 per genotype; 7- to 8-month-old littermates) were sacrificed after a 16-h overnight fast. Samples were individually hybridized on Affymetrix Mouse Genome 430 2.0 GeneChips by the Biopolymers Facility (Harvard Medical School).
2014-03-28 | E-GEOD-56321 | biostudies-arrayexpress
Project description:Better understanding of the early molecular events and underlying mechanism will benefit the early-stage diagnose and clinical therapy of OA. In this study, we demonstrated the functions of ZBTB20 in OA pathogenesis via regulating ECM homeostasis. Chondrocytes-specific depletion of Zbtb20 in adult mice attenuated DMM-induced OA progress, restored the balance of ECM anabolism and catabolism. To investigate the underlying mechanism of ZBTB20 in OA progress, RNA-seq was carried out using cultured primary chondrocytes from control and Zbtb20-cKO mice, treated by IL-1β.
2025-03-19 | GSE269579 | GEO
Project description:Quiescent endothelial cells upregulate fatty acid -oxidation for vasculoprotection via redox homeostasis
2018-06-04 | E-MTAB-6595 | ExpressionAtlas
Project description:Sirtuins are a family of protein deacetylases, deacylases, and ADP-ribosyltransferases that regulate life span, control the onset of numerous age-associated diseases, and mediate metabolic homeostasis. We have uncovered a novel role for the mitochondrial sirtuin SIRT4 in the regulation of hepatic lipid metabolism during changes in nutrient availability. We show that SIRT4 levels decrease in the liver during fasting and that SIRT4 null mice display increased expression of hepatic peroxisome proliferator activated receptor (PPAR ) target genes associated with fatty acid catabolism. Accordingly, primary hepatocytes from SIRT4 knockout (KO) mice exhibit higher rates of fatty acid oxidation than wild-type hepatocytes, and SIRT4 overexpression decreases fatty acid oxidation rates. The enhanced fatty acid oxidation observed in SIRT4 KO hepatocytes requires functional SIRT1, demonstrating a clear cross talk between mitochondrial and nuclear sirtuins. Thus, SIRT4 is a new component of mitochondrial signaling in the liver and functions as an important regulator of lipid metabolism.
2014-03-28 | GSE56321 | GEO
Project description:We identified rv0158 gene as a major determinant of redox homeostasis in Mtb. Disruption of rv0158 perturbed redox balance in a carbon source-specific manner, promoted killing in response to anti-TB drugs, reduced survival in macrophages, and persistence in mice. RNA sequencing analysis was performed to identify its regulon. The data indicated that rv0158 is required to balance the deployment of fatty acid substrates between lipid anabolism and oxidation.
2023-09-04 | GSE196844 | GEO
Project description:The liver is critical for maintaining systemic energy balance during starvation. To understand the role of hepatic fatty acid β-oxidation on this process, we generated mice with a liver-specific knockout of carnitine palmitoyltransferase 2 (Cpt2L-/-), an obligate step in mitochondrial long-chain fatty acid β-oxidation. Surprisingly, Cpt2L-/- mice survived the perinatal period and a 24hr fast with sufficient blood glucose. The loss of hepatic fatty acid oxidation resulted in a significant loss in circulating ketones that remained unaltered by fasting. Fasting induced serum dyslipidemia, hepatic steatosis and adaptations in hepatic and systemic oxidative gene expression in Cpt2L-/- mice to maintain systemic energy homeostasis. Alternatively, feeding a ketogenic diet resulted in severe hepatomegaly, liver damage and death within one week with a complete absence of adipose triglyceride stores. These data show that hepatic fatty acid oxidation is not required for survival during acute food deprivation but essential for constraining adipocyte lipolysis and regulating systemic catabolism when glucose is limiting. In this dataset, we include the expression data obtained from dissected mouse liver from mice fasted for 24 hours with and without the deletion of carnitine palmitoyltransferase 2 (i.e. hepatocytes unable to beta-oxidize long chain fatty acids in mitochondria). WildType and KnockOut mice were fasted for 24 hours. Three biologic replicates were compared per class, thus six mice.
2016-06-16 | E-GEOD-76079 | biostudies-arrayexpress
Project description:The liver is critical for maintaining systemic energy balance during starvation. To understand the role of hepatic fatty acid β-oxidation on this process, we generated mice with a liver-specific knockout of carnitine palmitoyltransferase 2 (Cpt2L-/-), an obligate step in mitochondrial long-chain fatty acid β-oxidation. Surprisingly, Cpt2L-/- mice survived the perinatal period and a 24hr fast with sufficient blood glucose. The loss of hepatic fatty acid oxidation resulted in a significant loss in circulating ketones that remained unaltered by fasting. Fasting induced serum dyslipidemia, hepatic steatosis and adaptations in hepatic and systemic oxidative gene expression in Cpt2L-/- mice to maintain systemic energy homeostasis. Alternatively, feeding a ketogenic diet resulted in severe hepatomegaly, liver damage and death within one week with a complete absence of adipose triglyceride stores. These data show that hepatic fatty acid oxidation is not required for survival during acute food deprivation but essential for constraining adipocyte lipolysis and regulating systemic catabolism when glucose is limiting. In this dataset, we include the expression data obtained from dissected mouse liver from mice fasted for 24 hours with and without the deletion of carnitine palmitoyltransferase 2 (i.e. hepatocytes unable to beta-oxidize long chain fatty acids in mitochondria).
2016-06-16 | GSE76079 | GEO