Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA384171 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR5479730_1.fastq.gz | Fastqsanger.gz | |||
| SRR5479730_2.fastq.gz | Fastqsanger.gz | |||
| SRR5479731_1.fastq.gz | Fastqsanger.gz | |||
| SRR5479731_2.fastq.gz | Fastqsanger.gz | |||
| SRR5479732_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 24 |
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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: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.
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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
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2021-12-31 | GSE113199 | GEO
Project description:Background: Inner Mongolia is a major raw-cashmere-producing province in China, Inner Mongolia cashmere goat harbors three types —Erlangshan, Aerbasi and Alashan. Nearly 700,000 Aerbasi cashmere goats are fed per year, and meat production is nearly 10,000 tons. However, there are no reports on the meat of this goat. To better understand the molecular variations underlying intramuscular fat (IMF) anabolism and catabolism in Inner Mongolian cashmere goat, the proteomic differences between the biceps femoris (BF) and longissimus dorsi (LD) were investigated by label-free strategy. Then, the proteins were verified by western blot analysis as being involved in IMF anabolism and catabolism. Results: The IMF content was significantly higher in the BF than in the LD, suggesting that IMF is accumulated more in the BF or metabolized more in the LD. We performed proteomic analysis of IMF anabolism and catabolism at the proteomic level, and 1209 proteins were identified in the BF (high-IMF) and LD (low-IMF) groups, with 993 and 896 proteins in each group. Among them, 110 were differentially expressed proteins (DEPs). Gene ontology (GO) classification statistics showed that the 110 DEPs were functionally classified into 100 annotation clusters. Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis showed that three pathways were related to IMF metabolism and deposition—fatty acid metabolism, fatty acid degradation and fatty acid elongation—and included 7 proteins. Conclusion: GO and KEGG analyses showed that differentially expressed HADHA, HADHB, ACSL1, ACADS, ACAT1 and ACAA2 in the mitochondrion act via fatty acid metabolism, fatty acid degradation and fatty acid elongation to influence the metabolism and synthesis of long-, short- and medium-chain fatty acids and influence IMF anabolism and catabolism. Protein-protein interaction (PPI) network analysis showed that IMF accumulation in different muscle tissues of Aerbasi cashmere goat was affected by not only 5 key enzymes or proteins involved in fatty acid synthesis and metabolism but also 5 DEPs (SUCLG1, SUCLG2, CS, DLST, ACO2) in the TCA cycle. Our results provide new insights into IMF deposition in goat and improve our understanding of the molecular mechanisms underlying IMF anabolism and catabolism.
2020-12-04 | PXD022901 |