scholarly journals Correlation between increased atrial expression of genes related to fatty acid metabolism and autophagy in patients with chronic atrial fibrillation

PLoS ONE ◽  
2020 ◽  
Vol 15 (4) ◽  
pp. e0224713 ◽  
Author(s):  
Yasushige Shingu ◽  
Shingo Takada ◽  
Takashi Yokota ◽  
Ryosuke Shirakawa ◽  
Akira Yamada ◽  
...  
Keyword(s):  
Atrial Fibrillation ◽  
Fatty Acid ◽  
Fatty Acid Metabolism ◽  
Acid Metabolism ◽  
Chronic Atrial Fibrillation ◽  
Expression Of Genes

scholarly journals Correlation between increased atrial expression of genes related to fatty acid metabolism and autophagy in patients with chronic atrial fibrillation

2019 ◽  
Author(s):  
Yasushige Shingu ◽  
Shingo Takada ◽  
Takashi Yokota ◽  
Ryosuke Shirakawa ◽  
Akira Yamada ◽  
...  
Keyword(s):  
Gene Expression ◽  
Atrial Fibrillation ◽  
Fatty Acid ◽  
Fatty Acid Metabolism ◽  
Acid Metabolism ◽  
Right Atrial ◽  
Fatty Acid Transport ◽  
Acid Uptake ◽  
Fatty Acid Binding ◽  
Expression Of Genes

AbstractAtrial metabolic disturbance contributes to the onset and development of atrial fibrillation (AF). Autophagy plays a role in maintaining the cellular energy balance. We examined whether the altered atrial expression of genes related to fatty acid metabolism is linked to that related to autophagy in chronic AF. Right atrial tissue was obtained during heart surgery from 51 patients with sinus rhythm (SR, n=38) or chronic AF (n=13). Preoperative fasting serum free-fatty-acid levels were significantly higher in the AF patients. The atrial gene expression of fatty acid binding protein 3 (FABP3), which is involved in the cells’ fatty acid uptake and intracellular fatty acid transport, was significantly increased in AF patients compared to SR patients; in the SR patients it was positively correlated with the right atrial diameter and intra-atrial EMD, parameters of structural and electrical atrial remodeling that was evaluated by an echocardiography. In contrast, the two groups’ atrial contents of diacylglycerol (DAG), a toxic fatty acid metabolite, were comparable. Importantly, the atrial gene expression of microtubule-associated protein light chain 3 (LC3) was significantly increased in the AF patients, and autophagy-related genes including LC3 were positively correlated with the atrial expression of FABP3. In conclusion, in chronic AF patients, the atrial expression of FABP3 was upregulated in association with autophagy-related genes without altered atrial DAG content. Our findings may support the hypothesis that dysregulated cardiac fatty acid metabolism contributes to the progression of AF and induction of autophagy has a cardioprotective effect against cardiac lipotoxicity in chronic AF.

scholarly journals Coordinated multitissue transcriptional and plasma metabonomic profiles following acute caloric restriction in mice

2006 ◽  
Vol 27 (3) ◽  
pp. 187-200 ◽  
Author(s):  
Colin Selman ◽  
Nicola D. Kerrison ◽  
Anisha Cooray ◽  
Matthew D. W. Piper ◽  
Steven J. Lingard ◽  
...  
Keyword(s):  
Gene Expression ◽  
Fatty Acid ◽  
Caloric Restriction ◽  
Fatty Acid Metabolism ◽  
Acid Metabolism ◽  
Proton Nuclear Magnetic Resonance ◽  
Cellular Transport ◽  
Expression Of Genes ◽  
Transcriptional Changes

Caloric restriction (CR) increases healthy life span in a range of organisms. The underlying mechanisms are not understood but appear to include changes in gene expression, protein function, and metabolism. Recent studies demonstrate that acute CR alters mortality rates within days in flies. Multitissue transcriptional changes and concomitant metabolic responses to acute CR have not been described. We generated whole genome RNA transcript profiles in liver, skeletal muscle, colon, and hypothalamus and simultaneously measured plasma metabolites using proton nuclear magnetic resonance in mice subjected to acute CR. Liver and muscle showed increased gene expressions associated with fatty acid metabolism and a reduction in those involved in hepatic lipid biosynthesis. Glucogenic amino acids increased in plasma, and gene expression for hepatic gluconeogenesis was enhanced. Increased expression of genes for hormone-mediated signaling and decreased expression of genes involved in protein binding and development occurred in hypothalamus. Cell proliferation genes were decreased and cellular transport genes increased in colon. Acute CR captured many, but not all, hepatic transcriptional changes of long-term CR. Our findings demonstrate a clear transcriptional response across multiple tissues during acute CR, with congruent plasma metabolite changes. Liver and muscle switched gene expression away from energetically expensive biosynthetic processes toward energy conservation and utilization processes, including fatty acid metabolism and gluconeogenesis. Both muscle and colon switched gene expression away from cellular proliferation. Mice undergoing acute CR rapidly adopt many transcriptional and metabolic changes of long-term CR, suggesting that the beneficial effects of CR may require only a short-term reduction in caloric intake.

Ingested cocoa can prevent high-fat diet-induced obesity by regulating the expression of genes for fatty acid metabolism

Nutrition ◽  
2005 ◽  
Vol 21 (5) ◽  
pp. 594-601 ◽  
Author(s):  
Naoko Matsui ◽  
Ryoichi Ito ◽  
Eisaku Nishimura ◽  
Mariko Yoshikawa ◽  
Masatoshi Kato ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Fatty Acid Metabolism ◽  
High Fat Diet ◽  
Acid Metabolism ◽  
High Fat ◽  
Diet Induced Obesity ◽  
Expression Of Genes

Dietary L‐carnitine affects the expression of genes involved in apoptosis and fatty acid metabolism in rooster testes

Andrologia ◽  
2020 ◽  
Vol 52 (11) ◽  
Author(s):  
Vahid Mohammadi ◽  
Seyed Davood Sharifi ◽  
Mohsen Sharafi ◽  
Abdollah Mohammadi‐Sangcheshmeh ◽  
Elham Abedheydari ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Fatty Acid Metabolism ◽  
Acid Metabolism ◽  
Expression Of Genes

scholarly journals Effects of Di-(2-Ethylhexyl) Phthalate At Environmentally Relevant Concentrations On Oxidative Stress and Lipid Metabolism in Livers of Male Xenopus Tropicalis

2021 ◽  
Author(s):  
Xinying Pan ◽  
Li Zheng ◽  
Yong Ding ◽  
Zhuo Dai ◽  
Xufeng Qi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Fatty Acid ◽  
Fatty Acid Metabolism ◽  
Acid Metabolism ◽  
Aquatic Organisms ◽  
Mitochondrial Morphology ◽  
Histopathological Analysis ◽  
Expression Of Genes ◽  
Ethylhexyl Phthalate ◽  
Dehp Exposure

Abstract Di-(2-ethylhexyl) phthalate (DEHP), used as a popular plasticizer to enhance the flexibility of plastics, is a major pollutant in aquatic environments. DEHP poses severe risks to aquatic organisms since it is an endocrine-disrupting compound. To comprehensively evaluate the toxicity of DEHP on the growth and livers of male X. tropicalis, sexually mature male X. tropicalis were exposed to environmentally relevant concentrations of DEHP, 0.2, 0.6, 1.8, 5.4 mg/L, for 49 days. The results showed that DEHP had a severe toxic effect on the livers of male X. tropicalis. Histopathological analysis of livers in all the DEHP-exposed groups showed changes in terms of vacuolization, loose cell cords, and an increasing amount of melanin. Large lipid droplets were markedly formed, and there were changes in the mitochondrial morphology upon DEHP exposure. In addition, oxidative stress was induced through the suppression of biochemical indicators and the downregulation in the mRNA expression of genes (nrf2, cat, sod, gst, and gpx) related to oxidative stress. A reduction in expression of fatty acid metabolism-related genes (pparα) was seen post-DEHP exposure. Thus, our study suggests that the hepatotoxicity induced by DEHP could be attributed to oxidative stress and disordered fatty acid metabolism. In conclusion, long-term exposure to DEHP at environmentally relevant concentrations poses ecological risks to aquatic organisms, which serves as a reminder that the application of DEHP and other plasticizers should be limited.

Abstract 14844: Ampk is Required for Maintaining Atrial Metabolism and Oxidative Stress

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Yina Ma ◽  
Xiaohong Wu ◽  
Xiaoyue Hu ◽  
Gary Cline ◽  
Fadi G Akar ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Atrial Fibrillation ◽  
Fatty Acid ◽  
Fatty Acid Metabolism ◽  
Acid Metabolism ◽  
Critical Role ◽  
Acid Oxidation ◽  
Fatty Acid Binding ◽  
And Oxidative Stress ◽  
Long Chain

Background: AMP-activated kinase (AMPK) has a critical role in cellular substrate and energy metabolism, regulating fatty acid oxidation, stimulating glucose transport and glycolysis. AMPK is crucial in the LV, preventing ischemic injury and heart failure. Atrial AMPK depletion induces atrial fibrillation in mice, but the role of AMPK in regulating atrial metabolism and oxidative stress is unknown. Methods: Atrial AMPK was selectively depleted in mice, utilizing sarcolipin-Cre mediated deletion of floxed α1 and α2 catalytic subunits (AMPKdKO). Floxed littermate mice were controls (CON). Microarray, immunoblotting, liquid chromatography-mass spectrometry (LC-MS), and electron microscope (EM) were used to access the gene, protein, metabolism, and mitochondria changes. Results: Pathway analysis of microarray data showed that fatty acid metabolism was downregulated in the AMPKdKO vs. CON atria (n=4 per group, p<0.0001). PGC1-α and downstream genes regulating fatty acid metabolism, including acyl-CoA thioesterase (ACOT), long-chain fatty acid-CoA ligase (ACSL), carnitine palmitoyltransferase 2 (CPT2), and fatty acid binding protein (FABP) were reduced in the AMPKdKO vs. CON atria (at 1 week of age). Atrial long-chain fatty acyl-CoA and acyl-carnitine levels were decreased (by LC-MS) in the AMPKdKO vs. CON atria (at 4 and 8 weeks of age) (n=3-4 per group, p<0.05). EM images showed evidence of swollen, broken and degraded mitochondrial in AMPKdKO atria (at 8 weeks age). Atrial expression of antioxidant enzymes, including SOD2 and PRDX3, was reduced (by immunoblotting) in AMPKdKO vs. CON atria (n=3-4, p<0.05). Conclusion: AMPK regulates critical mechanisms regulating atrial fatty acid metabolism and oxidative stress. Loss of atrial AMPK reduces the concentration of critical fatty acid intermediates for oxidative mitochondrial metabolism. These metabolic alterations may contribute to structural and electrical remodeling, and ensuing atrial fibrillation, that results from the loss of AMPK in the atria.

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