High-fat diet induces mouse liver steatosis with a concomitant decline in energy metabolism: attenuation by eicosapentaenoic acid (EPA) or hydroxytyrosol (HT) supplementation and the additive effects upon EPA and HT co-administration

2019 ◽  
Vol 10 (9) ◽  
pp. 6170-6183 ◽  
Author(s):  
Francisca Echeverría ◽  
Rodrigo Valenzuela ◽  
Andrés Bustamante ◽  
Daniela Álvarez ◽  
Macarena Ortiz ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Fatty Acid ◽  
Energy Metabolism ◽  
High Fat Diet ◽  
Mouse Liver ◽  
Liver Steatosis ◽  
Chain Polyunsaturated Fatty Acid ◽  
Additive Effects ◽  
High Fat ◽  
Long Chain

High-fat-diet (HFD) feeding is associated with liver oxidative stress (OS), n-3 long-chain polyunsaturated fatty acid (n-3 LCPUFA) depletion, hepatic steatosis and mitochondrial dysfunction.

scholarly journals N-3 Long-Chain Polyunsaturated Fatty Acid Supplementation Significantly Reduces Liver Oxidative Stress in High Fat Induced Steatosis

PLoS ONE ◽  
2012 ◽  
Vol 7 (10) ◽  
pp. e46400 ◽  
Author(s):  
Rodrigo Valenzuela ◽  
Alejandra Espinosa ◽  
Daniel González-Mañán ◽  
Amanda D'Espessailles ◽  
Virginia Fernández ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Fatty Acid ◽  
Polyunsaturated Fatty Acid ◽  
Chain Polyunsaturated Fatty Acid ◽  
High Fat ◽  
Fatty Acid Supplementation ◽  
Acid Supplementation ◽  
Long Chain

scholarly journals High Fat Diet Stimulates Beta-Oxidation, Alters Electrical Properties and Induces Adipogenicity of Atria in Obese Mice

2020 ◽  
Author(s):  
Nadine Suffee ◽  
Elodie Baptista ◽  
Jérôme Piquereau ◽  
Maharajah Ponnaiah ◽  
Nicolas Doisne ◽  
...  
Keyword(s):  
Atrial Fibrillation ◽  
Adipose Tissue ◽  
Fatty Acid ◽  
Free Fatty Acid ◽  
High Fat Diet ◽  
Potassium Current ◽  
Obese Mice ◽  
High Fat ◽  
Beta Oxidation ◽  
Long Chain

SUMMARYMetabolic disorders such as obesity are risk factors of atrial fibrillation, not only by sharing comorbidities but likely through their direct impact on atria, notably its adipogenicity. Here, we submitted mice that lack cardiac adipose tissue to a high fat diet and first studied the atrial metabolomic and lipidomic phenotypes using liquid chromatography-mass spectrometry. We found an increased consumption of free fatty acid by the beta-oxidation and an accumulation of long-chain lipids in atria of obese mice. Free fatty acid was the main substrate of mitochondrial respiration studied in the saponin-permeabilized atrial muscle. Conducted action potential recorded in atrial trabeculae was short, and ATP-sensitive potassium current was increased in perforated patch-clamp atrial myocytes of obese mice. There was histological and phenotypical evidence for an accumulation of adipose tissue in obese mice atria. Thus, an obesogenic diet transforms the energy metabolism, causes fat accumulation and induces electrical remodeling of atria myocardium.HIGHLIGHTS- Untargeted metabolomic and lipidomic analysis revealed that a high fat diet induces profound transformation of atrial energy metabolism with beta-oxidation activation and long-chain lipid accumulation.- Mitochondria respiration studied in atrial myocardial trabecula preferentially used Palmitoyl-CoA as energy substrate in obese mice.- Atria of obese mice become vulnerable to atrial fibrillation and show short action potential due to the activation of K-ATP dependent potassium current.- Adipocytes and fat molecular markers were detected in atria of obese mice together with an inflammatory profile consistence with a myocardial accumulation of fat.

scholarly journals Integrated Transcriptomic and Translatomic Inquiry of the Role of Betaine on Lipid Metabolic Dysregulation Induced by a High-Fat Diet

2021 ◽  
Vol 8 ◽  
Author(s):  
Tengda Huang ◽  
Lin Yu ◽  
Hongyuan Pan ◽  
Zeqiang Ma ◽  
Tian Wu ◽  
...  
Keyword(s):  
Fatty Acid ◽  
High Fat Diet ◽  
Liver Lipid ◽  
Liver Steatosis ◽  
Enrichment Analysis ◽  
Gene Set Enrichment Analysis ◽  
Translational Efficiency ◽  
High Fat ◽  
Alcoholic Fatty Liver ◽  
Translational Level

An excessive high-fat/energy diet is a major cause of obesity and linked complications, such as non-alcoholic fatty liver disease (NAFLD). Betaine has been shown to effectively improve hepatic lipid metabolism. However, the mechanistic basis for this improvement is largely unknown. Herein, integration of mRNA sequencing and ribosome footprints profiling (Ribo-seq) was used to investigate the means by which betaine alleviates liver lipid metabolic disorders induced by a high-fat diet. For the transcriptome, gene set enrichment analysis demonstrated betaine to reduce liver steatosis by up-regulation of fatty acid beta oxidation, lipid oxidation, and fatty acid catabolic processes. For the translatome, 574 differentially expressed genes were identified, 17 of which were associated with the NAFLD pathway. By combined analysis of transcriptome and translatome, we found that betaine had the greater effect on NAFLD at the translational level. Further, betaine decreased translational efficiency (TE) for IDI1, CYP51A1, TM7SF2, and APOA4, which are related to lipid biosynthesis. In summary, this study demonstrated betaine alleviating lipid metabolic dysfunction at the translational level. The transcriptome and translatome data integration approach used herein provides for a new understanding of the means by which to treat NAFLD.

High-Fat Diet Elevates Liver Docosahexaenoic Acid Possibly through Over-Expression of Very Long-Chain Fatty Acid Elongase 2 in C57BL/6J Mice

2019 ◽  
Vol 89 (1-2) ◽  
pp. 62-72
Author(s):  
Mooli Raja Gopal Reddy ◽  
Gundluri Venkata Asha ◽  
Sravan Kumar Manchiryala ◽  
Uday Kumar Putcha ◽  
Ayyalasomayajula Vajreswari ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Lipid Metabolism ◽  
High Fat Diet ◽  
Chain Fatty Acid ◽  
High Fat ◽  
Long Chain Fatty Acid ◽  
Fatty Acid Elongase ◽  
Over Expression ◽  
Long Chain

Abstract. The liver is the main site of lipid metabolism and vitamin A storage. Dietary factors are known to affect liver function, thereby leading to metabolic abnormalities. Here, we assessed the impact of long-term feeding of a high-fat diet on hepatic vitamin A status and lipid metabolism. For this purpose, 14 male and 14 female 35-day-old mice (strain C57BL/6J) were each divided into 2 groups of 7 animals and fed either a stock diet or a high-fat (HF) diet for 26 weeks. In addition to increased body weight/weight gain, the HF diet induced hypertriglyceridemia in both (p < 0.01). However, liver triglyceride levels were comparable among groups, which could be partly explained by unaltered expression of various lipogenic pathway proteins such as sterol regulatory element binding protein 1 (SREBP1), fatty acid synthase (FAS), microsomal triglyceride transfer protein (MTTP), and glycerol 3-phosphate acyl transferase (GPAT). On the other hand, hepatic retinol stores increased significantly in both sexes, whereas males displayed elevated circulatory retinol levels. Notably, long-term feeding of a HF diet elevated n-3 polyunsaturated fatty acid (PUFA) and docosahexaenoic acid (DHA, C22:6) levels in the liver (p ≤ 0.001), which is in line with the over-expression of very long-chain fatty acid elongase 2 (ELOVL2) protein in both sexes of mice (p < 0.01). In conclusion, very long-term feeding of a HF diet increased hepatic retinol stores and induced hypertriglyceridemia. However, it had no effect on hepatic triglyceride accumulation, possibly due to increased DHA levels arising from the ELOVL2-mediated elongation pathway.

Supplementation with antioxidant-rich extra virgin olive oil prevents hepatic oxidative stress and reduction of desaturation capacity in mice fed a high-fat diet: Effects on fatty acid composition in liver and extrahepatic tissues

Nutrition ◽  
2016 ◽  
Vol 32 (11-12) ◽  
pp. 1254-1267 ◽  
Author(s):  
Miguel Angel Rincón-Cervera ◽  
Rodrigo Valenzuela ◽  
María Catalina Hernandez-Rodas ◽  
Macarena Marambio ◽  
Alejandra Espinosa ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Fatty Acid Composition ◽  
Fatty Acid ◽  
Olive Oil ◽  
Acid Composition ◽  
High Fat Diet ◽  
Virgin Olive Oil ◽  
Extra Virgin Olive Oil ◽  
High Fat ◽  
Extrahepatic Tissues
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