GEO DataSets

Analysis of livers of transgenics overexpressing lipin 1-beta, an alternative form of lipin 1 containing a 33 amino acid insertion. Mutations in the gene encoding lipin 1 cause hepatic steatosis in fld animals, a genetic model of lipodystrophy. Results provide insight into the function of lipin 1.

Organism:

Mus musculus

Type:

Expression profiling by array, count, 2 genotype/variation sets

Platform:

GPL339

Series:

GSE5538

4 Samples

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(Submitter supplied) Mutations in the gene encoding lipin 1 cause hepatic steatosis in fld mice, a genetic model of lipodystrophy. Lipin 1 appears to be highly involved in the control of fatty acid metabolism. Lipin 1 is most often located in the nucleus, but other studies suggest that lipin also has effects in the cytoplasm. However, the molecular function of lipin 1 is unclear. To evaluate the effects of activation of the lipin 1 system in liver, lipin 1beta was overexpressed in mouse liver using an adenoviral vector. more...

Organism:

Mus musculus

Type:

Expression profiling by array

Dataset:

GDS2291

Platform:

GPL339

4 Samples

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(Submitter supplied) To identify Nrf1-dependent and Nrf2-dependent genes in the liver, we examined the gene expression profiles of Nrf1 Alb-CKO, Nrf2 knockout and Keap1 knockdown mouse livers by microarray analyses.

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL4134

18 Samples

Download data: TXT

(Submitter supplied) Impaired mitochondrial function has been implicated in the pathogenesis of type 2 diabetes, heart failure and neurodegeneration as well as during aging. Studies with the PGC-1 transcriptional coactivators have demonstrated that these factors are key components of the regulatory network that controls mitochondrial function in mammalian cells. Here we describe a genome-wide coactivation assay to globally identify the transcriptional partners for PGC-1α. more...

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL1261

2 Samples

Download data: CEL

(Submitter supplied) Hepatic metabolic derangements are key components in the development of fatty liver, insulin resistance, and atherosclerosis. SIRT1, a NAD+-dependent protein deacetylase, is an important regulator of energy homeostasis in response to nutrient availability. Here we demonstrate that hepatic SIRT1 regulates fatty acid metabolism by positively regulating PPAR-alpha. Hepatocyte-specific deletion of SIRT1 impairs PPAR-alpha signaling and decreased fatty acid beta-oxidation in the liver. more...

Organism:

Mus musculus

Type:

Expression profiling by array

Dataset:

GDS3666

Platform:

GPL7202

6 Samples

Download data: TIFF, TXT

Analysis of liver deficient for SIRT1. SIRT1, a NAD+-dependent protein deacetylase, is an important regulator of energy homeostasis in response to nutrient availability. Results provide insight into the role of hepatic SIRT1 in fatty acid metabolsim.

Organism:

Mus musculus

Type:

Expression profiling by array, count, 2 genotype/variation sets

Platform:

GPL7202

Series:

GSE14921

6 Samples

Download data: TIFF, TXT

(Submitter supplied) These arrays contain data from the livers of 10 week old L-Pex5 -/- male mice

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL1261

6 Samples

Download data: CEL

(Submitter supplied) Mitochondrial oxidative function is tightly controlled to maintain energy homeostasis in response to nutrient and hormonal signals. An important cellular component in the energy sensing response is the target of rapamycin (TOR) kinase pathway; however whether and how mTOR controls mitochondrial oxidative activity is unknown. Here, we show that mTOR kinase activity stimulates mitochondrial gene expression and oxidative function. more...

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL1261

12 Samples

Download data: CEL

(Submitter supplied) Huntington’s Disease (HD) is an inherited neurodegenerative disease caused by a glutamine repeat expansion in huntingtin protein. Transcriptional deregulation and altered energy metabolism have been implicated in HD pathogenesis. We report here that mutant huntingtin causes disruption of mitochondrial function by inhibiting expression of PGC-1a, a transcriptional coactivator that regulates several metabolic processes including mitochondrial biogenesis and respiration. more...

Organism:

Mus musculus

Type:

Expression profiling by array

Dataset:

GDS2391

Platform:

GPL1261

6 Samples

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Analysis of brain striatum of PGC-1alpha transcriptional coactivator null mutants. PGC-1alpha regulates several metabolic processes. Altered energy metabolism is implicated in Huntington's disease (HD). Results provide insight into the role of PGC-1alpha in HD pathogenesis.

Organism:

Mus musculus

Type:

Expression profiling by array, count, 2 genotype/variation sets

Platform:

GPL1261

Series:

GSE5786

6 Samples

Download data

(Submitter supplied) Subcutaneous abdominal adipose tissue was obtained from female subjects undergoing plastic surgery in agreement with French laws on biomedical research. Stromal cells prepared from WAT were cultured for 13 days in a chemically defined medium. At day 13, 60–80% of cells were differentiated into lipid droplet-containing adipocytes. The cells were infected at a m.o.i. of 200 for 6 h. The day after infection, cells were treated with the following drugs at 1 µM unless otherwise indicated: rosiglitazone (BRL49653, Smith Kline and French, Harlow, UK) and 9-cis-RA (Sigma). more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Platforms:

GPL3941 GPL3942

16 Samples

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(Submitter supplied) *Objectives:* In addition to their well-known role in the control of cellular proliferation and cancer, cell cycle regulators are increasingly identified as important metabolic modulators. Genome wide association studies identified SNPs near the cell cycle regulator CDKN2A/p16INK4a (p16) as strongly associated with risk of developing type 2 diabetes (T2D). T2D is associated with numerous perturbations of hepatic lipid and glucose metabolism. more...

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL16570

8 Samples

Download data: CEL

(Submitter supplied) Apolipoprotein E-knock out (apoE-KO) mouse is known as a model animal for atherosclerosis accompanied by spontaneous hypercholesterolemia. When apoE-KO mice were fed a chow supplemented with 1.25% cholesterol (high-Chol diet), cholesterol and bile acids were highly increased in the liver within a week. However, the amount of triacylglycerol (TG) in very low-density lipoprotein (VLDL), but not in the liver, was reduced by 78%. more...

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL7202

2 Samples

Download data: TXT

(Submitter supplied) 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. more...

Organism:

Mus musculus

Type:

Expression profiling by array

Dataset:

GDS4823

Platform:

GPL1261

12 Samples

Download data: CEL, TXT

Analysis of livers from sirtuin 4 (SIRT4)-null, 129SV males. Fatty acid oxidation rates are higher in SIRT4 knockout hepatocytes than in wildtype cells. Results provide insight into the role of SIRT4 in hepatic lipid metabolism.

Organism:

Mus musculus

Type:

Expression profiling by array, count, 2 genotype/variation sets

Platform:

GPL1261

Series:

GSE56321

12 Samples

Download data: CEL

(Submitter supplied) Purpose: MetS consist of five risk factors: elevated blood pressure and fasting glucose, visceral obesity, dyslipidemia and hypercholesterinemia. The physiological impact of lipid metabolism indicated as visceral obesity and hepatic lipid accumulation is still under debate. One major cause of disturbed lipid metabolism might be dysfunction of cellular organelles controlling energy homeostasis, i.e. mitochondria and peroxisomes. Experimental design: The New Zealand Obese (NZO) mouse model exhibits a polygenic syndrome of obesity, insulin resistance, triglyceridemia and hypercholesterolemia that resembles human metabolic syndrome. We applied a combinatorial approach of lipidomics with liver transcriptomics, 2D-DIGETM and mass spectroscopy based organelle proteomics of highly purified mitochondria and peroxisomes in male mice, to investigate molecular mechanisms related to the impact of lipid metabolism in the pathophysiology of the metabolic syndrome. Conclusions and clinical relevance: Proteome analyses of liver organelles indicated differences in fatty acid metabolism, oxidative stress and response, mainly influenced by PG-C1α/PPARα mediated pathways. These results were in accordance with serum lipid profiles and elevated organelle functionality. These data emphasize that metabolic syndrome is accompanied with increased mitochondria and peroxisomal activity controlling directly cellular energy homeostasis to cope with dyslipidemia and hypercholesterinemia driven hepatic lipid overflow in developing a fatty liver.

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL1261

6 Samples

Download data: CEL, CHP

(Submitter supplied) In the present study we have studied the mechanistic and functional aspects of NCoR1 function in mouse skeletal muscle. NCoR1 muscle-specific knockout mice exhibited an increased oxidative metabolism. Global gene expression analysis revealed a high overlap between the effects of NCoR1 deletion and peroxisome proliferator-activated receptor (PPAR) gamma coactivator 1alpha (PGC-1alpha) overexpression on oxidative metabolism in skeletal muscle. more...

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL6246

20 Samples

Download data: CEL

(Submitter supplied) Mouse FGF15 and human FGF19 are orthologous proteins that regulate bile acid metabolism. However, other hepatic functions of FGF15/19 are not well characterized.

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL8321

6 Samples

Download data: CEL, CHP

(Submitter supplied) Mitochondrial biogenesis and metabolism recently emerged as critical modulators of stemness properties and differentiation programmes. The increase in mitochondrial biogenesis and metabolic shift toward increased oxidative phosphorylations (OXPHOS) appear as hallmarks of stem cell differentiation processes. While several mechanisms support the involvement of mitochondrial biogenesis and function in the regulation of stem cell differentiation, the mechanisms triggering mitochondrial biogenesis in the context of cell differentiation remain elusive. more...

Organism:

Homo sapiens

Type:

Expression profiling by high throughput sequencing

Platform:

GPL16791

6 Samples

Download data: TXT

(Submitter supplied) PGC-1a is a transcriptional coactivator known to regulate a broad gene program of nutrient and mitochondrial metabolism. Many splice variants of this protein have been identified, but their functions were unknown. This experiment was designed to delineate the downstream targets of two different PGC-1alpha isoforms (PGC-1a1 and PGC-1a4) in hepatocytes, and to determine whether inflammatory signaling (via TNFR activation) modulated these targets Liver is exposed to constantly changing metabolic and inflammatory environments. more...

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL1261

18 Samples

Download data: CEL, CHP