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Postnatal PPARa-dependent gene expression in two-days old mouse liver

ABSTRACT: Inborn errors of lipid metabolism illustrate the importance of proper milk fat oxidation in newborn mammals. In the liver, a remarkable lipid catabolic competence is present at birth; however, it is unclear how this critical trait is acquired and regulated. In this work, we found that the genes required for milk lipid catabolism are already transcribed before birth in the term fetus (E19.5) and controlled by the peroxisome-proliferator activated receptor alpha (PPARα) in mouse liver. The developmental activity of PPARα strongly regulates fatty acid oxidation genes. Two days after birth (P2), during milk suckling, PPARα-null mice develop a congenital steatosis and milk protein oxidation is de-repressed to fuel an alternative energy pathway that maintains glucose homeostasis and postnatal growth. Our results demonstrate for the first time, the developmental role of PPARα in regulating the metabolic ability to use maternal milk as fuel in the early days of life.

ORGANISM(S): Mus musculus

PROVIDER: GSE39670 | GEO | 2016/06/01

SECONDARY ACCESSION(S): PRJNA171358

REPOSITORIES: GEO

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Prenatal PPARa-dependent gene expression in fetal mouse liver just before birth (E19.5)

Project description:Inborn errors of lipid metabolism illustrate the importance of proper milk fat oxidation in newborn mammals. In the liver, a remarkable lipid catabolic competence is present at birth; however, it is unclear how this critical trait is acquired and regulated. In this work, we found that the genes required for milk lipid catabolism are already transcribed before birth in the term fetus (E19.5) and controlled by the peroxisome-proliferator activated receptor alpha (PPARα) in mouse liver. The developmental activity of PPARα strongly regulates fatty acid oxidation genes. Two days after birth (P2), during milk suckling, PPARα-null mice develop a congenital steatosis and milk protein oxidation is de-repressed to fuel an alternative energy pathway that maintains glucose homeostasis and postnatal growth. Our results demonstrate for the first time, the developmental role of PPARα in regulating the metabolic ability to use maternal milk as fuel in the early days of life.

2016-06-01 | GSE39669 | GEO

Postnatal PPARa-dependent gene expression in two-days old mouse liver

Project description:Inborn errors of lipid metabolism illustrate the importance of proper milk fat oxidation in newborn mammals. In the liver, a remarkable lipid catabolic competence is present at birth; however, it is unclear how this critical trait is acquired and regulated. In this work, we found that the genes required for milk lipid catabolism are already transcribed before birth in the term fetus (E19.5) and controlled by the peroxisome-proliferator activated receptor alpha (PPARÎ±) in mouse liver. The developmental activity of PPARÎ± strongly regulates fatty acid oxidation genes. Two days after birth (P2), during milk suckling, PPARÎ±-null mice develop a congenital steatosis and milk protein oxidation is de-repressed to fuel an alternative energy pathway that maintains glucose homeostasis and postnatal growth. Our results demonstrate for the first time, the developmental role of PPARÎ± in regulating the metabolic ability to use maternal milk as fuel in the early days of life. Expression profile difference between PPARalpha wild-type (3 males and 3 females) and knock-out (3 males and 3 females) mouse liver in suckling mice. Two days after birth, pups were killed and their liver promptly removed and frozen in liquid nitrogen.

2016-06-01 | E-GEOD-39670 | biostudies-arrayexpress

Prenatal PPARa-dependent gene expression in fetal mouse liver just before birth (E19.5)

Project description:Inborn errors of lipid metabolism illustrate the importance of proper milk fat oxidation in newborn mammals. In the liver, a remarkable lipid catabolic competence is present at birth; however, it is unclear how this critical trait is acquired and regulated. In this work, we found that the genes required for milk lipid catabolism are already transcribed before birth in the term fetus (E19.5) and controlled by the peroxisome-proliferator activated receptor alpha (PPARÎ±) in mouse liver. The developmental activity of PPARÎ± strongly regulates fatty acid oxidation genes. Two days after birth (P2), during milk suckling, PPARÎ±-null mice develop a congenital steatosis and milk protein oxidation is de-repressed to fuel an alternative energy pathway that maintains glucose homeostasis and postnatal growth. Our results demonstrate for the first time, the developmental role of PPARÎ± in regulating the metabolic ability to use maternal milk as fuel in the early days of life. Expression profile difference between PPARalpha wild-type (n=6) and knock-out (n=6) mouse liver at fetal day E19.5. Term fetuses were collected by cesarean section, their liver promptly dissected and frozen in liquid nitrogen.

2016-06-01 | E-GEOD-39669 | biostudies-arrayexpress

Real-time quantitative PCR analysis of fatty acid metabolism genes of liver tissue from wild-type and PPARa (-/-) mice exposed to 2,4-dinitrotoluene (PPARa)

Project description:2,4-dinitrotoluene (2,4-DNT), a nitroaromatic used in industrial and explosive manufacturing processes, is known to contaminate artillery ranges, demilitarization areas and munitions manufacturing facilities. Previous transcriptomic and lipidomic studies identified energy metabolism as a principle biochemical process affected by 2,4-DNT where up-stream effects on PPARα signaling were hypothesized as themolecular initiating event for these effects. Here, the validity of this hypothetical adverse outcome pathway (AOP) was assessed by testing the hypothesis that 2,4-DNT-induced perturbations in PPARα signaling and resultant downstream deficits in energy metabolism, especially from lipids, would result in organism-level impacts on exercise endurance. PPARα knock-out (-/-) and wild-type (WT) mice were exposed for 14 days to vehicle or 2,4-DNT at a dose (134 mg/kg/day) that did not exhibit overt systemic toxicity. Mice performed an exercise challenge (forced swim) 1 day after the last dose. 2,4-DNT decreased swim times in WT and PPARα (-/-) mice, but the effect was significantly less in PPARα (-/-) mice indicating the critical of PPARα in mediating 2,4-DNT-induced energy metabolism deficits. 2,4-DNT caused down-regulation of transcripts involved in fatty acid metabolism, gluconeogenesis, triacylglycerol catabolism, and the pentose phosphate pathway, and 2,4-DNT treated wild-type mice had decreased serum trigylcerides and increased serum glucose versus 2,4-DNT treated PPARα (-/-) mice. Our results support the hypothesis that 2,4-DNT perturbs PPARα signaling as a molecular initiating event therefore impacting energy metabolism, especially lipid metabolism, producing reduced exercise endurance in mice. RNA was isolated from liver tissue of vehicle or 2,4-DNT treated wild-type or PPARα (-/-) mice (n=6) and RT-PCR performed to analyze genes involved in fatty acid metabolism

2014-06-30 | E-GEOD-50167 | biostudies-arrayexpress

Ppara and fatty acid oxidation coordinate hepatic transcriptional architecture (ATAC-Seq)

Project description:Mice harboring a liver-specific carnitine palmityltransferase 2 (Cpt2) knockout exhibit drastic lipid accumulation following a 24hr fast. Crossing Cpt2L-/- mice with Pparα-/- mice provides a model to drive ligand-activated Pparα signaling in liver. We use this to investigate unique patterns of Pparα target gene transcription and demonstrate the requirement for ligand-activated Pparα in maintaining transcriptionally permissive genomic architecture in liver, including regulation of promoters and enhancer elements during periods of nutrient deprivation.

2021-06-29 | GSE179050 | GEO

Ppara and fatty acid oxidation coordinate hepatic transcriptional architecture (ChIP-Seq)

Project description:Mice harboring a liver-specific carnitine palmityltransferase 2 (Cpt2) knockout exhibit drastic lipid accumulation following a 24hr fast. Crossing Cpt2L-/- mice with Pparα-/- mice provides a model to drive ligand-activated Pparα signaling in liver. We use this to investigate unique patterns of Pparα target gene transcription and demonstrate the requirement for ligand-activated Pparα in maintaining transcriptionally permissive genomic architecture in liver including regulation of promoters and enhancer elements during periods of acute nutrient deprivation.

2021-06-29 | GSE179052 | GEO

Real-time quantitative PCR analysis of fatty acid metabolism genes of liver tissue from wild-type and PPARa (-/-) mice exposed to 2,4-dinitrotoluene (PPARa)

2014-06-30 | GSE50167 | GEO

PPARM-NM-4 activation in human myotubes increases mitochondrial fatty acid oxidative capacity and reduces glucose utilization by a switch in substrate preference.

Project description:The role of peroxisome proliferator-activated receptor M-NM-4 (PPARM-NM-4) activation on global gene expression and mitochondrial fuel utilization were investigated in human myotubes. Only 21 genes were up-regulated and 3 genes were down-regulated after activation by the PPARM-NM-4 agonist GW501516. Pathway analysis showed up-regulated mitochondrial fatty acid oxidation, TCA cycle and cholesterol biosynthesis. GW501516 increased oleic acid oxidation and mitochondrial oxidative capacity by 2-fold. Glucose uptake and oxidation were reduced, but total substrate oxidation was not affected, indicating a fuel switch from glucose to fatty acid. Cholesterol biosynthesis was increased, but lipid biosynthesis and mitochondrial content were not affected. This study confirmed that the principal effect of PPARM-NM-4 activation was to increase mitochondrial fatty acid oxidative capacity. Our results further suggest that PPARM-NM-4 activation reduced glucose utilization through a switch in mitochondrial substrate preference by up-regulating pyruvate dehydrogenase kinase isozyme 4 and genes involved in lipid metabolism and fatty acid oxidation. Keywords: Expression profiling by array Human myotubes from four donors were exposed to a PPARM-NM-4 agonist or control for 96 h after which gene expression was profiled.

2014-05-23 | E-GEOD-40789 | biostudies-arrayexpress

Expression data from WT (Pparafl/fl) mice and hepatocyte-specific PPARα disruption (Ppara△Hep) mice liver tissue at 12 hours after PHx or Sham operation

Project description:PPARα act as the master of lipid metabolism in liver, however, the changes of its target genes after PHx and the effects of PPARα on regenerative genes were unknown. At 12 to 24 hours after PHx, the mice develope marked steatosis, therefore the time point of 12 hour after PHx was choosen to perform microarray analysis. We used microarray to detail the gene expression of WT (Pparafl/fl) mice and hepatocyte-specific PPARα disruption (Ppara△Hep) mice liver tissue at 12 hour after PHx or Sham operation

2018-05-10 | GSE114223 | GEO

PPARδ activation in human myotubes increases mitochondrial fatty acid oxidative capacity and reduces glucose utilization by a switch in substrate preference.

Project description:The role of peroxisome proliferator-activated receptor δ (PPARδ) activation on global gene expression and mitochondrial fuel utilization were investigated in human myotubes. Only 21 genes were up-regulated and 3 genes were down-regulated after activation by the PPARδ agonist GW501516. Pathway analysis showed up-regulated mitochondrial fatty acid oxidation, TCA cycle and cholesterol biosynthesis. GW501516 increased oleic acid oxidation and mitochondrial oxidative capacity by 2-fold. Glucose uptake and oxidation were reduced, but total substrate oxidation was not affected, indicating a fuel switch from glucose to fatty acid. Cholesterol biosynthesis was increased, but lipid biosynthesis and mitochondrial content were not affected. This study confirmed that the principal effect of PPARδ activation was to increase mitochondrial fatty acid oxidative capacity. Our results further suggest that PPARδ activation reduced glucose utilization through a switch in mitochondrial substrate preference by up-regulating pyruvate dehydrogenase kinase isozyme 4 and genes involved in lipid metabolism and fatty acid oxidation. Keywords: Expression profiling by array

2014-05-23 | GSE40789 | GEO

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