Correction: Quercetin Induces Hepatic Lipid Omega-Oxidation and Lowers Serum Lipid Levels in Mice

Abstract

Elevated circulating lipid levels are known risk factors for cardiovascular diseases (CVD). In order to examine the effects of quercetin on lipid metabolism, mice received a mild-high-fat diet without (control) or with supplementation of 0.33% (w/w) quercetin for 12 weeks. Gas chromatography and 1 H nuclear magnetic resonance were used to quantitatively measure serum lipid profiles. Whole genome microarray analysis of liver tissue was used to identify possible mechanisms underlying altered circulating lipid levels. Body weight, energy intake and hepatic lipid accumulation did not differ significantly between the quercetin and the control group. In serum of quercetin-fed mice, triglycerides (TG) were decreased with 14% (p,0.001) and total poly unsaturated fatty acids (PUFA) were increased with 13% (p,0.01). Palmitic acid, oleic acid, and linoleic acid were all decreased by 9-15% (p,0.05) in quercetin-fed mice. Both palmitic acid and oleic acid can be oxidized by omega (v)-oxidation. Gene expression profiling showed that quercetin increased hepatic lipid metabolism, especially voxidation. At the gene level, this was reflected by the up-regulation of cytochrome P450 (Cyp) 4a10, Cyp4a14, Cyp4a31 and Acyl-CoA thioesterase 3 (Acot3). Two relevant regulators, cytochrome P450 oxidoreductase (Por, rate limiting for cytochrome P450s) and the transcription factor constitutive androstane receptor (Car; official symbol Nr1i3) were also upregulated in the quercetin-fed mice. We conclude that quercetin intake increased hepatic lipid v-oxidation and lowered corresponding circulating lipid levels, which may contribute to potential beneficial effects on CVD.

Omega-3 Phospholipids from Krill Oil Enhance Intestinal Fatty Acid Oxidation More Effectively than Omega-3 Triacylglycerols in High-Fat Diet-Fed Obese Mice

“…Thus, these data support the idea that malic enzyme is the producer of nicotinamide adenine dinucleotide phosphate (NADPH) needed for CYP4A function [52]. Activation of FA ω-oxidation is important in preventing lipotoxicity during periods of substrate overload, e.g., in the case of high-fat feeding or insufficient mitochondrial FA β-oxidation [53,54]. Moreover, members of the CYP4A family can alleviate obesity-related inflammation, mainly through the anabolism and catabolism of critical anti-inflammatory and pro-resolving lipid mediators [55,56].…”

Dihydroquercetin Supplementation Improved Hepatic Lipid Dysmetabolism Mediated by Gut Microbiota in High-Fat Diet (HFD)-Fed Mice

“…Furthermore, various genes, including ACADL, CPT1A, EHHADH, CYP4A10, CYP4A14, and CYP4A31, were down-regulated in mice fed with a HFD, whereas DHQ supplementation inhibited these changes. CPT1A, EHHADH, and ACADL are implicated in β-oxidation of fatty acid, while CYP4A10, CYP4A14, and CYP4A31 were involved in ω-oxidation of fatty acid [43][44][45]. Of note, CPT1A is the ratelimiting enzyme in fatty acid oxidation, which is responsible for transporting fatty acids from cytoplasm to mitochondria for oxidative decomposition.…”

White Adipose Tissue Response of Obese Mice to Ambient Oxygen Restriction at Thermoneutrality: Response Markers Identified, but no WAT Inflammation

“…After hybridization and washing, arrays were covered with ozone-barrier slides and scanned. Signals were quantified using Feature Extraction version 10.7.3 (Agilent), followed by quality control and normalization as published [32]. Microarray data are deposited in Gene Expression Omnibus under accession number GSE53802.…”