Magnolol-mediated regulation of plasma triglyceride through affecting lipoprotein lipase activity in apolipoprotein A5 knock-in mice.
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...
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Public Library of Science (PLoS)
2018-01-01
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Online Access: | http://europepmc.org/articles/PMC5806881?pdf=render |
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author | Chun-Kai Chang Xiu-Ru Lin Yen-Lin Lin Woei-Horng Fang Shu-Wha Lin Sui-Yuan Chang Jau-Tsuen Kao |
author_facet | Chun-Kai Chang Xiu-Ru Lin Yen-Lin Lin Woei-Horng Fang Shu-Wha Lin Sui-Yuan Chang Jau-Tsuen Kao |
author_sort | Chun-Kai Chang |
collection | DOAJ |
description | 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. |
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issn | 1932-6203 |
language | English |
last_indexed | 2024-12-12T02:12:27Z |
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spelling | doaj.art-dd1be0e6863e42c59b2914bdc9b85c1f2022-12-22T00:41:52ZengPublic Library of Science (PLoS)PLoS ONE1932-62032018-01-01132e019274010.1371/journal.pone.0192740Magnolol-mediated regulation of plasma triglyceride through affecting lipoprotein lipase activity in apolipoprotein A5 knock-in mice.Chun-Kai ChangXiu-Ru LinYen-Lin LinWoei-Horng FangShu-Wha LinSui-Yuan ChangJau-Tsuen KaoHyperlipidemia 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.http://europepmc.org/articles/PMC5806881?pdf=render |
spellingShingle | Chun-Kai Chang Xiu-Ru Lin Yen-Lin Lin Woei-Horng Fang Shu-Wha Lin Sui-Yuan Chang Jau-Tsuen Kao Magnolol-mediated regulation of plasma triglyceride through affecting lipoprotein lipase activity in apolipoprotein A5 knock-in mice. PLoS ONE |
title | Magnolol-mediated regulation of plasma triglyceride through affecting lipoprotein lipase activity in apolipoprotein A5 knock-in mice. |
title_full | Magnolol-mediated regulation of plasma triglyceride through affecting lipoprotein lipase activity in apolipoprotein A5 knock-in mice. |
title_fullStr | Magnolol-mediated regulation of plasma triglyceride through affecting lipoprotein lipase activity in apolipoprotein A5 knock-in mice. |
title_full_unstemmed | Magnolol-mediated regulation of plasma triglyceride through affecting lipoprotein lipase activity in apolipoprotein A5 knock-in mice. |
title_short | Magnolol-mediated regulation of plasma triglyceride through affecting lipoprotein lipase activity in apolipoprotein A5 knock-in mice. |
title_sort | magnolol mediated regulation of plasma triglyceride through affecting lipoprotein lipase activity in apolipoprotein a5 knock in mice |
url | http://europepmc.org/articles/PMC5806881?pdf=render |
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