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Article: Folic acid consumption reduces resistin level and restores blunted acetylcholine-induced aortic relaxation in obese/diabetic mice
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TitleFolic acid consumption reduces resistin level and restores blunted acetylcholine-induced aortic relaxation in obese/diabetic mice
 
AuthorsSeto, SW4
Lam, TY4
Or, PMY4
Lee, WYW4
Au, ALS4
Poon, CCW4
Li, RWS1
Chan, SW3
Yeung, JHK4
Leung, GPH1
Lee, SMY2
Ngai, SM4
Kwan, YW4 4 4
 
Keywords+db/+db mice
Acetylcholine
ENOS
Folic acid
PTEN
Relaxation
 
Issue Date2010
 
PublisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/jnutbio
 
CitationJournal Of Nutritional Biochemistry, 2010, v. 21 n. 9, p. 872-880 [How to Cite?]
DOI: http://dx.doi.org/10.1016/j.jnutbio.2009.06.015
 
AbstractFolic acid supplementation provides beneficial effects on endothelial functions in patients with hyperhomocysteinemia. However, its effects on vascular functions under diabetic conditions are largely unknown. Therefore, the effect(s) of folic acid (5.7 and 71 μg/kg/day for 4 weeks) on aortic relaxation was investigated using obese/diabetic (+db/+db) mice and lean littermate (+db/+m) mice. Acetylcholine-induced relaxation in +db/+db mice was less than that observed in +db/+m mice. The reduced relaxation in +db/+db mice was restored by consumption of 71 μg/kg folic acid. Acetylcholine-induced relaxation (with and without folic acid treatment) was sensitive to N G-nitro-l-arginine methyl ester, 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one, geldanamycin and triciribine. In addition, acetylcholine-induced relaxation was attenuated by resistin. The plasma level of resistin in +db/+db mice was sevenfold higher than that measured in +db/+m mice, and the elevated plasma level of resistin in +db/+db mice was reduced by 25% after treatment with 71 μg/kg folic acid. Folic acid slightly increased the ratio of reduced glutathione to oxidized glutathione in +db/+db mice. Moreover, folic acid caused a reduction in PTEN (phosphatase and tensin homolog deleted on chromosome 10) expression, an increase in the phosphorylation of endothelial nitric oxide synthase (eNOS Ser1177) and Akt Ser473, and an enhanced interaction of heat shock protein 90 (HSP90) with eNOS in both strains, with greater magnitude observed in +db/+db mice. In conclusion, folic acid consumption improved blunted acetylcholine-induced relaxation in +db/+db mice. The mechanism may be, at least partly, attributed to enhancement of PI3K/HSP90/eNOS/Akt cascade, reduction in plasma resistin level, down-regulation of PTEN and slight modification of oxidative state. © 2010 Elsevier Inc.
 
ISSN0955-2863
2012 Impact Factor: 4.552
2012 SCImago Journal Rankings: 1.262
 
DOIhttp://dx.doi.org/10.1016/j.jnutbio.2009.06.015
 
ISI Accession Number IDWOS:000281710700012
Funding AgencyGrant Number
Li Ka Shing Institute of Health Sciences
Institute of Vascular Medicine (Faculty of Medicine, The Chinese University of Hong Kon
RGC Earmarked Grants of Hong Kong SAR, People's Republic of China4107/01M
4166/02M
2140565
Chinese University of Hong Kong2401149
2041231
2401296
Department of Pharmacology (The Chinese University Hong Kong)
Funding Information:

We are grateful to the Li Ka Shing Institute of Health Sciences and the Institute of Vascular Medicine (Faculty of Medicine, The Chinese University of Hong Kong) for financial support (to Y.W. Kwan). This project was financially supported by the RGC Earmarked Grants of Hong Kong SAR, People's Republic of China (reference nos. 4107/01M and 4166/02M, project code 2140565), and Direct Grants for Research (The Chinese University of Hong Kong) (reference no. 2401149; project code.; 2041231 and 2401296). Mr. S.W. Seto, Ms. T.Y. Lam, Ms. Alice LS. Au and Mr. Wayne Y.W. Lee are recipients of postgraduate studentships from the Department of Pharmacology (The Chinese University Hong Kong). We thank Ms. Jian Hong Wu (State Key Laboratory of Chinese Medicine and Molecular Pharmacology, Department of Applied Biology and Chemical Technology, The Hong Kong Polytechnic University) for technical assistance in measuring cholesterol and lipoproteins levels. Provision of the Student Campus Work Scheme by the Chou's Foundation Fund and the Student Campus Work Scheme (Shaw College, The Chinese University of Hong Kong) is also. appreciated. Proofreading of the manuscript by Mr. Ho Yeung Lam is also acknowledged.

 
ReferencesReferences in Scopus
 
DC FieldValue
dc.contributor.authorSeto, SW
 
dc.contributor.authorLam, TY
 
dc.contributor.authorOr, PMY
 
dc.contributor.authorLee, WYW
 
dc.contributor.authorAu, ALS
 
dc.contributor.authorPoon, CCW
 
dc.contributor.authorLi, RWS
 
dc.contributor.authorChan, SW
 
dc.contributor.authorYeung, JHK
 
dc.contributor.authorLeung, GPH
 
dc.contributor.authorLee, SMY
 
dc.contributor.authorNgai, SM
 
dc.contributor.authorKwan, YW
 
dc.date.accessioned2011-08-26T14:26:03Z
 
dc.date.available2011-08-26T14:26:03Z
 
dc.date.issued2010
 
dc.description.abstractFolic acid supplementation provides beneficial effects on endothelial functions in patients with hyperhomocysteinemia. However, its effects on vascular functions under diabetic conditions are largely unknown. Therefore, the effect(s) of folic acid (5.7 and 71 μg/kg/day for 4 weeks) on aortic relaxation was investigated using obese/diabetic (+db/+db) mice and lean littermate (+db/+m) mice. Acetylcholine-induced relaxation in +db/+db mice was less than that observed in +db/+m mice. The reduced relaxation in +db/+db mice was restored by consumption of 71 μg/kg folic acid. Acetylcholine-induced relaxation (with and without folic acid treatment) was sensitive to N G-nitro-l-arginine methyl ester, 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one, geldanamycin and triciribine. In addition, acetylcholine-induced relaxation was attenuated by resistin. The plasma level of resistin in +db/+db mice was sevenfold higher than that measured in +db/+m mice, and the elevated plasma level of resistin in +db/+db mice was reduced by 25% after treatment with 71 μg/kg folic acid. Folic acid slightly increased the ratio of reduced glutathione to oxidized glutathione in +db/+db mice. Moreover, folic acid caused a reduction in PTEN (phosphatase and tensin homolog deleted on chromosome 10) expression, an increase in the phosphorylation of endothelial nitric oxide synthase (eNOS Ser1177) and Akt Ser473, and an enhanced interaction of heat shock protein 90 (HSP90) with eNOS in both strains, with greater magnitude observed in +db/+db mice. In conclusion, folic acid consumption improved blunted acetylcholine-induced relaxation in +db/+db mice. The mechanism may be, at least partly, attributed to enhancement of PI3K/HSP90/eNOS/Akt cascade, reduction in plasma resistin level, down-regulation of PTEN and slight modification of oxidative state. © 2010 Elsevier Inc.
 
dc.description.natureLink_to_subscribed_fulltext
 
dc.identifier.citationJournal Of Nutritional Biochemistry, 2010, v. 21 n. 9, p. 872-880 [How to Cite?]
DOI: http://dx.doi.org/10.1016/j.jnutbio.2009.06.015
 
dc.identifier.citeulike6198270
 
dc.identifier.doihttp://dx.doi.org/10.1016/j.jnutbio.2009.06.015
 
dc.identifier.epage880
 
dc.identifier.hkuros189170
 
dc.identifier.isiWOS:000281710700012
Funding AgencyGrant Number
Li Ka Shing Institute of Health Sciences
Institute of Vascular Medicine (Faculty of Medicine, The Chinese University of Hong Kon
RGC Earmarked Grants of Hong Kong SAR, People's Republic of China4107/01M
4166/02M
2140565
Chinese University of Hong Kong2401149
2041231
2401296
Department of Pharmacology (The Chinese University Hong Kong)
Funding Information:

We are grateful to the Li Ka Shing Institute of Health Sciences and the Institute of Vascular Medicine (Faculty of Medicine, The Chinese University of Hong Kong) for financial support (to Y.W. Kwan). This project was financially supported by the RGC Earmarked Grants of Hong Kong SAR, People's Republic of China (reference nos. 4107/01M and 4166/02M, project code 2140565), and Direct Grants for Research (The Chinese University of Hong Kong) (reference no. 2401149; project code.; 2041231 and 2401296). Mr. S.W. Seto, Ms. T.Y. Lam, Ms. Alice LS. Au and Mr. Wayne Y.W. Lee are recipients of postgraduate studentships from the Department of Pharmacology (The Chinese University Hong Kong). We thank Ms. Jian Hong Wu (State Key Laboratory of Chinese Medicine and Molecular Pharmacology, Department of Applied Biology and Chemical Technology, The Hong Kong Polytechnic University) for technical assistance in measuring cholesterol and lipoproteins levels. Provision of the Student Campus Work Scheme by the Chou's Foundation Fund and the Student Campus Work Scheme (Shaw College, The Chinese University of Hong Kong) is also. appreciated. Proofreading of the manuscript by Mr. Ho Yeung Lam is also acknowledged.

 
dc.identifier.issn0955-2863
2012 Impact Factor: 4.552
2012 SCImago Journal Rankings: 1.262
 
dc.identifier.issue9
 
dc.identifier.pmid19879746
 
dc.identifier.scopuseid_2-s2.0-77955847141
 
dc.identifier.spage872
 
dc.identifier.urihttp://hdl.handle.net/10722/137484
 
dc.identifier.volume21
 
dc.languageeng
 
dc.publisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/jnutbio
 
dc.publisher.placeUnited States
 
dc.relation.ispartofJournal of Nutritional Biochemistry
 
dc.relation.referencesReferences in Scopus
 
dc.subject.meshAcetylcholine - pharmacology
 
dc.subject.meshDiabetes Mellitus - metabolism
 
dc.subject.meshFolic Acid - metabolism - pharmacology
 
dc.subject.meshResistin - metabolism
 
dc.subject.meshVasodilation - drug effects
 
dc.subject+db/+db mice
 
dc.subjectAcetylcholine
 
dc.subjectENOS
 
dc.subjectFolic acid
 
dc.subjectPTEN
 
dc.subjectRelaxation
 
dc.titleFolic acid consumption reduces resistin level and restores blunted acetylcholine-induced aortic relaxation in obese/diabetic mice
 
dc.typeArticle
 
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<contributor.author>Au, ALS</contributor.author>
<contributor.author>Poon, CCW</contributor.author>
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Author Affiliations
  1. The University of Hong Kong
  2. University of Macau
  3. Hong Kong Polytechnic University
  4. Chinese University of Hong Kong