Acerola polysaccharides ameliorate high-fat diet-induced non-alcoholic fatty liver disease through reduction of lipogenesis and improvement of mitochondrial functions in mice.
Identifieur interne : 000060 ( Main/Exploration ); précédent : 000059; suivant : 000061Acerola polysaccharides ameliorate high-fat diet-induced non-alcoholic fatty liver disease through reduction of lipogenesis and improvement of mitochondrial functions in mice.
Auteurs : Yuanyuan Hu [République populaire de Chine] ; Fawen Yin ; Zhongyuan Liu ; Hongkai Xie ; Yunsheng Xu ; Dayong Zhou ; Beiwei ZhuSource :
- Food & function [ 2042-650X ] ; 2020.
Descripteurs français
- KwdFr :
- Alimentation riche en graisse (effets indésirables), Animaux (MeSH), Antioxydants (pharmacologie), Lipogenèse (MeSH), Malpighiaceae (composition chimique), Mitochondries (métabolisme), Mâle (MeSH), Oxydoréduction (MeSH), Polyosides (pharmacologie), Protéine-1 de liaison à l'élément de régulation des stérols (métabolisme), Souris (MeSH), Souris de lignée C57BL (MeSH), Stress oxydatif (effets des médicaments et des substances chimiques), Stéatose hépatique non alcoolique (métabolisme), Stéatose hépatique non alcoolique (thérapie).
- MESH :
- composition chimique : Malpighiaceae.
- effets des médicaments et des substances chimiques : Stress oxydatif.
- effets indésirables : Alimentation riche en graisse.
- métabolisme : Mitochondries, Protéine-1 de liaison à l'élément de régulation des stérols, Stéatose hépatique non alcoolique.
- pharmacologie : Antioxydants, Polyosides.
- thérapie : Stéatose hépatique non alcoolique.
- Animaux, Lipogenèse, Mâle, Oxydoréduction, Souris, Souris de lignée C57BL.
English descriptors
- KwdEn :
- Animals (MeSH), Antioxidants (pharmacology), Diet, High-Fat (adverse effects), Lipogenesis (MeSH), Male (MeSH), Malpighiaceae (chemistry), Mice (MeSH), Mice, Inbred C57BL (MeSH), Mitochondria (metabolism), Non-alcoholic Fatty Liver Disease (metabolism), Non-alcoholic Fatty Liver Disease (therapy), Oxidation-Reduction (MeSH), Oxidative Stress (drug effects), Polysaccharides (pharmacology), Sterol Regulatory Element Binding Protein 1 (metabolism).
- MESH :
- chemical , metabolism : Sterol Regulatory Element Binding Protein 1.
- chemical , pharmacology : Antioxidants, Polysaccharides.
- adverse effects : Diet, High-Fat.
- chemistry : Malpighiaceae.
- drug effects : Oxidative Stress.
- metabolism : Mitochondria, Non-alcoholic Fatty Liver Disease.
- therapy : Non-alcoholic Fatty Liver Disease.
- Animals, Lipogenesis, Male, Mice, Mice, Inbred C57BL, Oxidation-Reduction.
Abstract
Acerola polysaccharides (ACPs) were purified from acerola (Malpighia emarginata DC.), a tropical fruit with strong antioxidant and anti-inflammatory activities. However, the biological activities of ACPs have barely been investigated. The present study was designed to investigate the efficacy of ACPs in the treatment of high-fat diet (HFD)-induced nonalcoholic fatty liver disease (NAFLD) in C57BL/6 mice. Male C57BL/6 mice were fed with a high-fat diet and treated with different doses of ACPs for 9 continuous weeks. NAFLD was examined in terms of body weight, lipid profiles, liver function markers, and histology. Gene expression was determined by using both qRT-PCR and western blot. Our results showed that administration of ACPs significantly reduced HFD-induced hyperlipidemia and hepatic lipid deposition by inhibiting the SREBP1c pathway in mice. ACP treatment normalized oxidative stress by activating nuclear factor (erythroid-derived-2)-like 2 (Nrf2) and reduced the expressions of pro-inflammatory cytokines in HFD fed mice. Furthermore, ACPs reduced uncoupling protein 2 (UCP2) expression, restored mitochondrial ATP content, increased mitochondrial complex I, IV, and V activity, and increased mitochondrial beta-oxidation by stimulating peroxisomal proliferator-activated receptor-gamma coactivator-1α (PGC-1α) in the liver of HFD-fed mice. Our study indicated that ACPs may be an effective dietary supplement for preventing HFD-induced NAFLD by regulating lipogenesis, reducing inflammation and oxidative stress, and promoting the mitochondrial function.
DOI: 10.1039/c9fo01611b
PubMed: 31819934
Affiliations:
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last="Yin">Fawen Yin</name></author><author><name sortKey="Liu, Zhongyuan" sort="Liu, Zhongyuan" uniqKey="Liu Z" first="Zhongyuan" last="Liu">Zhongyuan Liu</name></author><author><name sortKey="Xie, Hongkai" sort="Xie, Hongkai" uniqKey="Xie H" first="Hongkai" last="Xie">Hongkai Xie</name></author><author><name sortKey="Xu, Yunsheng" sort="Xu, Yunsheng" uniqKey="Xu Y" first="Yunsheng" last="Xu">Yunsheng Xu</name></author><author><name sortKey="Zhou, Dayong" sort="Zhou, Dayong" uniqKey="Zhou D" first="Dayong" last="Zhou">Dayong Zhou</name></author><author><name sortKey="Zhu, Beiwei" sort="Zhu, Beiwei" uniqKey="Zhu B" first="Beiwei" last="Zhu">Beiwei Zhu</name></author></analytic><series><title level="j">Food & function</title><idno type="eISSN">2042-650X</idno><imprint><date when="2020" type="published">2020</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals (MeSH)</term><term>Antioxidants (pharmacology)</term><term>Diet, High-Fat (adverse effects)</term><term>Lipogenesis (MeSH)</term><term>Male (MeSH)</term><term>Malpighiaceae (chemistry)</term><term>Mice (MeSH)</term><term>Mice, Inbred C57BL (MeSH)</term><term>Mitochondria (metabolism)</term><term>Non-alcoholic Fatty Liver Disease (metabolism)</term><term>Non-alcoholic Fatty Liver Disease (therapy)</term><term>Oxidation-Reduction (MeSH)</term><term>Oxidative Stress (drug effects)</term><term>Polysaccharides (pharmacology)</term><term>Sterol Regulatory Element Binding Protein 1 (metabolism)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Alimentation riche en graisse (effets indésirables)</term><term>Animaux (MeSH)</term><term>Antioxydants (pharmacologie)</term><term>Lipogenèse (MeSH)</term><term>Malpighiaceae (composition chimique)</term><term>Mitochondries (métabolisme)</term><term>Mâle (MeSH)</term><term>Oxydoréduction (MeSH)</term><term>Polyosides (pharmacologie)</term><term>Protéine-1 de liaison à l'élément de régulation des stérols (métabolisme)</term><term>Souris (MeSH)</term><term>Souris de lignée C57BL (MeSH)</term><term>Stress oxydatif (effets des médicaments et des substances chimiques)</term><term>Stéatose hépatique non alcoolique (métabolisme)</term><term>Stéatose hépatique non alcoolique (thérapie)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Sterol Regulatory Element Binding Protein 1</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Antioxidants</term><term>Polysaccharides</term></keywords><keywords scheme="MESH" qualifier="adverse effects" xml:lang="en"><term>Diet, High-Fat</term></keywords><keywords scheme="MESH" qualifier="chemistry" xml:lang="en"><term>Malpighiaceae</term></keywords><keywords scheme="MESH" qualifier="composition chimique" xml:lang="fr"><term>Malpighiaceae</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Oxidative Stress</term></keywords><keywords scheme="MESH" qualifier="effets des médicaments et des substances chimiques" xml:lang="fr"><term>Stress oxydatif</term></keywords><keywords scheme="MESH" qualifier="effets indésirables" xml:lang="fr"><term>Alimentation riche en graisse</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Mitochondria</term><term>Non-alcoholic Fatty Liver Disease</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Mitochondries</term><term>Protéine-1 de liaison à l'élément de régulation des stérols</term><term>Stéatose hépatique non alcoolique</term></keywords><keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Antioxydants</term><term>Polyosides</term></keywords><keywords scheme="MESH" qualifier="therapy" xml:lang="en"><term>Non-alcoholic Fatty Liver Disease</term></keywords><keywords scheme="MESH" qualifier="thérapie" xml:lang="fr"><term>Stéatose hépatique non alcoolique</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Lipogenesis</term><term>Male</term><term>Mice</term><term>Mice, Inbred C57BL</term><term>Oxidation-Reduction</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Lipogenèse</term><term>Mâle</term><term>Oxydoréduction</term><term>Souris</term><term>Souris de lignée C57BL</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Acerola polysaccharides (ACPs) were purified from acerola (Malpighia emarginata DC.), a tropical fruit with strong antioxidant and anti-inflammatory activities. However, the biological activities of ACPs have barely been investigated. The present study was designed to investigate the efficacy of ACPs in the treatment of high-fat diet (HFD)-induced nonalcoholic fatty liver disease (NAFLD) in C57BL/6 mice. Male C57BL/6 mice were fed with a high-fat diet and treated with different doses of ACPs for 9 continuous weeks. NAFLD was examined in terms of body weight, lipid profiles, liver function markers, and histology. Gene expression was determined by using both qRT-PCR and western blot. Our results showed that administration of ACPs significantly reduced HFD-induced hyperlipidemia and hepatic lipid deposition by inhibiting the SREBP1c pathway in mice. ACP treatment normalized oxidative stress by activating nuclear factor (erythroid-derived-2)-like 2 (Nrf2) and reduced the expressions of pro-inflammatory cytokines in HFD fed mice. Furthermore, ACPs reduced uncoupling protein 2 (UCP2) expression, restored mitochondrial ATP content, increased mitochondrial complex I, IV, and V activity, and increased mitochondrial beta-oxidation by stimulating peroxisomal proliferator-activated receptor-gamma coactivator-1α (PGC-1α) in the liver of HFD-fed mice. Our study indicated that ACPs may be an effective dietary supplement for preventing HFD-induced NAFLD by regulating lipogenesis, reducing inflammation and oxidative stress, and promoting the mitochondrial function.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">31819934</PMID><DateCompleted><Year>2020</Year><Month>10</Month><Day>07</Day></DateCompleted><DateRevised><Year>2020</Year><Month>10</Month><Day>07</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Electronic">2042-650X</ISSN><JournalIssue CitedMedium="Internet"><Volume>11</Volume><Issue>1</Issue><PubDate><Year>2020</Year><Month>Jan</Month><Day>29</Day></PubDate></JournalIssue><Title>Food & function</Title><ISOAbbreviation>Food Funct</ISOAbbreviation></Journal><ArticleTitle>Acerola polysaccharides ameliorate high-fat diet-induced non-alcoholic fatty liver disease through reduction of lipogenesis and improvement of mitochondrial functions in mice.</ArticleTitle><Pagination><MedlinePgn>1037-1048</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1039/c9fo01611b</ELocationID><Abstract><AbstractText>Acerola polysaccharides (ACPs) were purified from acerola (Malpighia emarginata DC.), a tropical fruit with strong antioxidant and anti-inflammatory activities. However, the biological activities of ACPs have barely been investigated. The present study was designed to investigate the efficacy of ACPs in the treatment of high-fat diet (HFD)-induced nonalcoholic fatty liver disease (NAFLD) in C57BL/6 mice. Male C57BL/6 mice were fed with a high-fat diet and treated with different doses of ACPs for 9 continuous weeks. NAFLD was examined in terms of body weight, lipid profiles, liver function markers, and histology. Gene expression was determined by using both qRT-PCR and western blot. Our results showed that administration of ACPs significantly reduced HFD-induced hyperlipidemia and hepatic lipid deposition by inhibiting the SREBP1c pathway in mice. ACP treatment normalized oxidative stress by activating nuclear factor (erythroid-derived-2)-like 2 (Nrf2) and reduced the expressions of pro-inflammatory cytokines in HFD fed mice. Furthermore, ACPs reduced uncoupling protein 2 (UCP2) expression, restored mitochondrial ATP content, increased mitochondrial complex I, IV, and V activity, and increased mitochondrial beta-oxidation by stimulating peroxisomal proliferator-activated receptor-gamma coactivator-1α (PGC-1α) in the liver of HFD-fed mice. Our study indicated that ACPs may be an effective dietary supplement for preventing HFD-induced NAFLD by regulating lipogenesis, reducing inflammation and oxidative stress, and promoting the mitochondrial function.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Hu</LastName><ForeName>Yuanyuan</ForeName><Initials>Y</Initials><Suffix></Suffix><AffiliationInfo><Affiliation>School of Food Science and Technology, Dalian Polytechnic University, Dalian, 116034, PR China. zdyzf1@163.com.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Yin</LastName><ForeName>Fawen</ForeName><Initials>F</Initials><Suffix></Suffix></Author><Author ValidYN="Y"><LastName>Liu</LastName><ForeName>Zhongyuan</ForeName><Initials>Z</Initials><Suffix></Suffix></Author><Author ValidYN="Y"><LastName>Xie</LastName><ForeName>Hongkai</ForeName><Initials>H</Initials><Suffix></Suffix></Author><Author 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MajorTopicYN="N">Polysaccharides</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051780" MajorTopicYN="N">Sterol Regulatory Element Binding Protein 1</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2019</Year><Month>12</Month><Day>11</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2020</Year><Month>10</Month><Day>8</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2019</Year><Month>12</Month><Day>11</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">31819934</ArticleId><ArticleId IdType="doi">10.1039/c9fo01611b</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>République populaire de Chine</li></country></list><tree><noCountry><name sortKey="Liu, Zhongyuan" sort="Liu, Zhongyuan" uniqKey="Liu Z" first="Zhongyuan" last="Liu">Zhongyuan Liu</name><name sortKey="Xie, Hongkai" sort="Xie, Hongkai" uniqKey="Xie H" first="Hongkai" last="Xie">Hongkai Xie</name><name sortKey="Xu, Yunsheng" sort="Xu, Yunsheng" uniqKey="Xu Y" first="Yunsheng" last="Xu">Yunsheng Xu</name><name sortKey="Yin, Fawen" sort="Yin, Fawen" uniqKey="Yin F" first="Fawen" last="Yin">Fawen Yin</name><name sortKey="Zhou, Dayong" sort="Zhou, Dayong" uniqKey="Zhou D" first="Dayong" last="Zhou">Dayong Zhou</name><name sortKey="Zhu, Beiwei" sort="Zhu, Beiwei" uniqKey="Zhu B" first="Beiwei" last="Zhu">Beiwei Zhu</name></noCountry><country name="République populaire de Chine"><noRegion><name sortKey="Hu, Yuanyuan" sort="Hu, Yuanyuan" uniqKey="Hu Y" first="Yuanyuan" 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