Fatty acid oxidation and related gene expression in heart depleted of carnitine by mildronate treatment in the rat

2004 ◽  
Vol 258 (1/2) ◽  
pp. 171-182 ◽  
Author(s):  
Pascal Degrace ◽  
Laurent Demizieux ◽  
Joseph Gresti ◽  
Marcelline Tsoko ◽  
Agnès André ◽  
...  
Keyword(s):  
Gene Expression ◽  
Fatty Acid ◽  
Fatty Acid Oxidation ◽  
Acid Oxidation ◽  
Related Gene

scholarly journals Effects of conjugated linoleic acid on growth, non-specific immunity, antioxidant capacity, lipid deposition and related gene expression in juvenile large yellow croaker (Larmichthys crocea) fed soyabean oil-based diets

2013 ◽  
Vol 110 (7) ◽  
pp. 1220-1232 ◽  
Author(s):  
Rantao Zuo ◽  
Qinghui Ai ◽  
Kangsen Mai ◽  
Wei Xu
Keyword(s):  
Gene Expression ◽  
Fatty Acid ◽  
Antioxidant Capacity ◽  
Fatty Acid Oxidation ◽  
Acid Oxidation ◽  
Large Yellow Croaker ◽  
Lipid Deposition ◽  
Related Gene ◽  
Specific Immunity ◽  
Acyl Coa Oxidase

The effects of conjugated linoleic acid (CLA) on growth performance, non-specific immunity, antioxidant capacity, lipid deposition and related gene expression were investigated in the large yellow croaker (Larmichthys crocea). Fish (7·56 (sem 0·60) g) were fed soyabean oil-based diets with graded levels of CLA (0, 0·42, 0·83, 1·70 %) for 70 d. Quantitative PCR was used to assess the effects of CLA on the transcription of inflammation- and fatty acid oxidation-related genes. Growth in fish fed the diet with 0·42 % CLA was significantly higher. Also, phagocytic index and respiratory burst activity were significantly higher in fish fed the diets containing 0·42 and 0·83 % CLA, respectively. Hepatic total antioxidative capacity and catalase activities increased significantly when CLA increased from 0 to 0·83 %, and then decreased with further increase of CLA. However, hepatic malondialdehyde content decreased significantly as dietary CLA increased. Lipid concentration in the whole body and muscle increased significantly with increasing dietary CLA. Transcription of genes related to inflammation (cyclo-oxygenase-2 and IL-β) in the liver and kidney and fatty acid oxidation (carnitine palmitoyl transferase I and acyl CoA oxidase) in the kidney decreased significantly as dietary CLA increased. PPARα and acyl CoA oxidase expression in the liver decreased significantly as CLA increased from 0·42 to 1·70 %. These results strongly suggest that dietary CLA could significantly affect growth performance, non-specific immunity, antioxidant capacity, lipid deposition and transcription of inflammation- and fatty acid oxidation-related genes of the large yellow croaker. This may contribute to our understanding of the mechanisms related to the physiological effects of dietary CLA in fish.

scholarly journals Tang-Nai-Kang Alleviates Pre-diabetes and Metabolic Disorders and Induces a Gene Expression Switch toward Fatty Acid Oxidation in SHR.Cg-Leprcp/NDmcr Rats

PLoS ONE ◽  
2015 ◽  
Vol 10 (4) ◽  
pp. e0122024 ◽  
Author(s):  
Linyi Li ◽  
Hisae Yoshitomi ◽  
Ying Wei ◽  
Lingling Qin ◽  
Jingxin Zhou ◽  
...  
Keyword(s):  
Gene Expression ◽  
Fatty Acid ◽  
Fatty Acid Oxidation ◽  
Metabolic Disorders ◽  
Acid Oxidation

scholarly journals SIRT4 Regulates Fatty Acid Oxidation and Mitochondrial Gene Expression in Liver and Muscle Cells

2010 ◽  
Vol 285 (42) ◽  
pp. 31995-32002 ◽  
Author(s):  
Nargis Nasrin ◽  
Xiaoping Wu ◽  
Eric Fortier ◽  
Yajun Feng ◽  
Olivia Claire Bare' ◽  
...  
Keyword(s):  
Gene Expression ◽  
Fatty Acid ◽  
Fatty Acid Oxidation ◽  
Mitochondrial Gene ◽  
Muscle Cells ◽  
Acid Oxidation ◽  
Mitochondrial Gene Expression

Fatty Acid Oxidation Enzyme Gene Expression Is Downregulated in the Failing Heart

Circulation ◽  
1996 ◽  
Vol 94 (11) ◽  
pp. 2837-2842 ◽  
Author(s):  
Michael N. Sack ◽  
Toni A. Rader ◽  
Sonhee Park ◽  
Jean Bastin ◽  
Sylvia A. McCune ◽  
...  
Keyword(s):  
Gene Expression ◽  
Fatty Acid ◽  
Fatty Acid Oxidation ◽  
Acid Oxidation ◽  
Enzyme Gene ◽  
Failing Heart ◽  
Fatty Acid Oxidation Enzyme ◽  
Oxidation Enzyme

scholarly journals Estrogen-Related Receptor α Directs Peroxisome Proliferator-Activated Receptor α Signaling in the Transcriptional Control of Energy Metabolism in Cardiac and Skeletal Muscle

2004 ◽  
Vol 24 (20) ◽  
pp. 9079-9091 ◽  
Author(s):  
Janice M. Huss ◽  
Inés Pineda Torra ◽  
Bart Staels ◽  
Vincent Giguère ◽  
Daniel P. Kelly
Keyword(s):  
Gene Expression ◽  
Skeletal Muscle ◽  
Fatty Acid ◽  
Fatty Acid Oxidation ◽  
Target Genes ◽  
Cellular Fatty Acid ◽  
Acid Oxidation ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferator Activated Receptor ◽  
Oxidation Rates

ABSTRACT Estrogen-related receptors (ERRs) are orphan nuclear receptors activated by the transcriptional coactivator peroxisome proliferator-activated receptor γ (PPARγ) coactivator 1α (PGC-1α), a critical regulator of cellular energy metabolism. However, metabolic target genes downstream of ERRα have not been well defined. To identify ERRα-regulated pathways in tissues with high energy demand such as the heart, gene expression profiling was performed with primary neonatal cardiac myocytes overexpressing ERRα. ERRα upregulated a subset of PGC-1α target genes involved in multiple energy production pathways, including cellular fatty acid transport, mitochondrial and peroxisomal fatty acid oxidation, and mitochondrial respiration. These results were validated by independent analyses in cardiac myocytes, C2C12 myotubes, and cardiac and skeletal muscle of ERRα−/− mice. Consistent with the gene expression results, ERRα increased myocyte lipid accumulation and fatty acid oxidation rates. Many of the genes regulated by ERRα are known targets for the nuclear receptor PPARα, and therefore, the interaction between these regulatory pathways was explored. ERRα activated PPARα gene expression via direct binding of ERRα to the PPARα gene promoter. Furthermore, in fibroblasts null for PPARα and ERRα, the ability of ERRα to activate several PPARα targets and to increase cellular fatty acid oxidation rates was abolished. PGC-1α was also shown to activate ERRα gene expression. We conclude that ERRα serves as a critical nodal point in the regulatory circuitry downstream of PGC-1α to direct the transcription of genes involved in mitochondrial energy-producing pathways in cardiac and skeletal muscle.

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