[Lipids-lowering effects of equol on low density lipoprotein receptor knockout hamsters].

equol ezetimibe gene knockout hamster genistein lipid metabolism low density lipoprotein receptor

Journal

Wei sheng yan jiu = Journal of hygiene research
ISSN: 1000-8020
Titre abrégé: Wei Sheng Yan Jiu
Pays: China
ID NLM: 9426367

Informations de publication

Date de publication:
Sep 2021
Historique:
entrez: 9 11 2021
pubmed: 10 11 2021
medline: 11 11 2021
Statut: ppublish

Résumé

Used low density lipoprotein receptor knockout(LDLR KO) hamster as the model similar to human dyslipidemia to observe the lipid-lowering effect of equol on heterozygotes. With soy-free high cholesterol high fat diet, 12-week-old LDLR KO female heterozygous hamsters were randomly divided into negative control group(no addition), positive control group(add 0.004% ezetimibe), genistein group(add 0.1%), and low, medium and high-dose groups of equol(add 0.025%, 0.05%, 0.1% respectively). Body weight, food consumption and blood lipid were continuously monitored for 12 weeks after feeding each group. Finally, liver morphology and lipid metabolism related genes expressions were checked. There was no significant difference in body weight and average weekly food intake among the groups. The blood lipids in negative control group increased over time, and the cholesterol and triglyceride levels of LDLR KO heterozygous hamsters were significantly reduced by ezetimibe in the second week, while the high-density lipoprotein cholesterol was also significantly decreased. The lipid-lowering effects of genistein and equol were weaker than ezetimibe, and there was significant difference between the two groups after 12 weeks, but the decrease of HDL-c was not as significant as ezetimibe. Compared with genistein, the effect of medium and high dose equol was stronger. At 12 weeks, the liver weight ratio also decreased significantly, and the liver lipid accumulation was inhibited, especially in the high dose of equol. The expression of ApoAI, SREBP-2 and HMGCR were significantly up-regulated by equol and genistein. Equol could reduce female LDLR KO hamster blood lipid. It may play a role in lipid lowering by inhibiting cholesterol absorption besides estrogen receptor pathway, but it is weaker than NPC1 L1 inhibitor. At the same time, up-regulation of ApoAI inhibits the decrease of high-density lipoprotein and reduces lipid accumulation in liver.

Identifiants

pubmed: 34749871
doi: 10.19813/j.cnki.weishengyanjiu.2021.05.012
doi:

Substances chimiques

Cholesterol, HDL 0
Lipids 0
Receptors, LDL 0
Equol 531-95-3
Cholesterol 97C5T2UQ7J

Types de publication

Journal Article

Langues

chi

Sous-ensembles de citation

IM

Pagination

775-780

Auteurs

Yuqi Dou (Y)

School of Public Health, Peking University, Beijing 100191, China.

Gonglie Chen (G)

Institute of Cardiovascular Research, Peking University, Key Laboratory of Molecular Cardiology, Ministry of Education, Beijing 100191, China.

Yuanfa Cai (Y)

School of Public Health, Peking University, Beijing 100191, China.

Xiao Lin (X)

Institute of Cardiovascular Research, Peking University, Key Laboratory of Molecular Cardiology, Ministry of Education, Beijing 100191, China.

Zekun Chen (Z)

School of Public Health, Peking University, Beijing 100191, China.

Xue Yu (X)

School of Public Health, Peking University, Beijing 100191, China.

Ying Wang (Y)

School of Public Health, Peking University, Beijing 100191, China.

Ling Zhang (L)

Institute of Cardiovascular Research, Peking University, Key Laboratory of Molecular Cardiology, Ministry of Education, Beijing 100191, China.

Yuhui Wang (Y)

Institute of Cardiovascular Research, Peking University, Key Laboratory of Molecular Cardiology, Ministry of Education, Beijing 100191, China.

Defu Ma (D)

School of Public Health, Peking University, Beijing 100191, China.

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Classifications MeSH