|Title:||Magnolol-mediated regulation of plasma triglyceride through affecting lipoprotein lipase activity in apolipoprotein A5 knock-in mice||Authors:||Chang C.-K.
|Issue Date:||2018||Journal Volume:||13||Journal Issue:||2||Start page/Pages:||e0192740||Source:||PLoS ONE||Abstract:||
Hyperlipidemia is a risk factor of arteriosclerosis, stroke, and other coronary heart disease, which has been shown to correlate with single nucleotide polymorphisms of genes essential for lipid metabolism, such as lipoprotein lipase (LPL) and apolipoprotein A5 (APOA5). In this study, the effect of magnolol, the main active component extracted from Magnolia officinalis, on LPL activity was investigated. A dose-dependent up-regulation of LPL activity, possibly through increasing LPL mRNA transcription, was observed in mouse 3T3-L1 pre-adipocytes cultured in the presence of magnolol for 6 days. Subsequently, a transgenic knock-in mice carrying APOA5 c.553G>T variant was established and then fed with corn oil with or without magnolol for four days. The baseline plasma triglyceride levels in transgenic knock-in mice were higher than those in wild-type mice, with the highest increase occurred in homozygous transgenic mice (106 mg/dL vs 51 mg/dL, p<0.01). After the induction of hyperglyceridemia along with the administration of magnolol, the plasma triglyceride level in heterozygous transgenic mice was significantly reduced by half. In summary, magnolol could effectively lower the plasma triglyceride levels in APOA5 c.553G>T variant carrier mice and facilitate the triglyceride metabolism in postprandial hypertriglyceridemia. ? 2018 Chang et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
|URI:||https://scholars.lib.ntu.edu.tw/handle/123456789/507679||ISSN:||1932-6203||DOI:||10.1371/journal.pone.0192740||metadata.dc.subject.other:||apolipoprotein A5; corn oil; lipoprotein lipase; magnolol; messenger RNA; triacylglycerol; apolipoprotein A5; biphenyl derivative; lignan; lipoprotein lipase; magnolol; triacylglycerol; 3T3-L1 cell line; animal cell; animal cell culture; animal experiment; animal model; APOA5 gene; Article; controlled study; female; gene activity; gene expression regulation; genetic variation; homozygosity; hypertriglyceridemia; in vitro study; in vivo study; lipid metabolism; LPL gene; Magnolia officinalis; male; mouse; nonhuman; proadipocyte; regulatory mechanism; RNA transcription; transgenic mouse; triacylglycerol blood level; upregulation; animal; blood; gene knock-in; genetics; heterozygote; human; hypertriglyceridemia; Magnolia; metabolism; 3T3-L1 Cells; Animals; Apolipoprotein A-V; Biphenyl Compounds; Gene Knock-In Techniques; Heterozygote; Humans; Hypertriglyceridemia; Lignans; Lipoprotein Lipase; Magnolia; Mice; Mice, Transgenic; Triglycerides; Up-Regulation
|Appears in Collections:||醫學檢驗暨生物技術學系|
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