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Article: Folic acid consumption reduces resistin level and restores blunted acetylcholine-induced aortic relaxation in obese/diabetic mice

TitleFolic acid consumption reduces resistin level and restores blunted acetylcholine-induced aortic relaxation in obese/diabetic mice
Authors
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
Citation
Journal Of Nutritional Biochemistry, 2010, v. 21 n. 9, p. 872-880 How to Cite?
Abstract
Folic 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.
Persistent Identifierhttp://hdl.handle.net/10722/137484
ISSN
2013 Impact Factor: 4.592
2013 SCImago Journal Rankings: 1.627
ISI Accession Number ID
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.

References

 

Author Affiliations
  1. The University of Hong Kong
  2. University of Macau
  3. Hong Kong Polytechnic University
  4. Chinese University of Hong Kong
DC FieldValueLanguage
dc.contributor.authorSeto, SWen_HK
dc.contributor.authorLam, TYen_HK
dc.contributor.authorOr, PMYen_HK
dc.contributor.authorLee, WYWen_HK
dc.contributor.authorAu, ALSen_HK
dc.contributor.authorPoon, CCWen_HK
dc.contributor.authorLi, RWSen_HK
dc.contributor.authorChan, SWen_HK
dc.contributor.authorYeung, JHKen_HK
dc.contributor.authorLeung, GPHen_HK
dc.contributor.authorLee, SMYen_HK
dc.contributor.authorNgai, SMen_HK
dc.contributor.authorKwan, YWen_HK
dc.date.accessioned2011-08-26T14:26:03Z-
dc.date.available2011-08-26T14:26:03Z-
dc.date.issued2010en_HK
dc.identifier.citationJournal Of Nutritional Biochemistry, 2010, v. 21 n. 9, p. 872-880en_HK
dc.identifier.issn0955-2863en_HK
dc.identifier.urihttp://hdl.handle.net/10722/137484-
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.en_HK
dc.languageengen_US
dc.publisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/jnutbioen_HK
dc.relation.ispartofJournal of Nutritional Biochemistryen_HK
dc.subject+db/+db miceen_HK
dc.subjectAcetylcholineen_HK
dc.subjectENOSen_HK
dc.subjectFolic aciden_HK
dc.subjectPTENen_HK
dc.subjectRelaxationen_HK
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.titleFolic acid consumption reduces resistin level and restores blunted acetylcholine-induced aortic relaxation in obese/diabetic miceen_HK
dc.typeArticleen_HK
dc.identifier.emailLeung, GPH: gphleung@hkucc.hku.hken_HK
dc.identifier.authorityLeung, GPH=rp00234en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/j.jnutbio.2009.06.015en_HK
dc.identifier.pmid19879746en_HK
dc.identifier.scopuseid_2-s2.0-77955847141en_HK
dc.identifier.hkuros189170en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-77955847141&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume21en_HK
dc.identifier.issue9en_HK
dc.identifier.spage872en_HK
dc.identifier.epage880en_HK
dc.identifier.isiWOS:000281710700012-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridSeto, SW=9941482400en_HK
dc.identifier.scopusauthoridLam, TY=18134321000en_HK
dc.identifier.scopusauthoridOr, PMY=13606043200en_HK
dc.identifier.scopusauthoridLee, WYW=23035345800en_HK
dc.identifier.scopusauthoridAu, ALS=7005391144en_HK
dc.identifier.scopusauthoridPoon, CCW=26656895800en_HK
dc.identifier.scopusauthoridLi, RWS=7404722884en_HK
dc.identifier.scopusauthoridChan, SW=7404255670en_HK
dc.identifier.scopusauthoridYeung, JHK=7006803824en_HK
dc.identifier.scopusauthoridLeung, GPH=35963668200en_HK
dc.identifier.scopusauthoridLee, SMY=35233892600en_HK
dc.identifier.scopusauthoridNgai, SM=7006074219en_HK
dc.identifier.scopusauthoridKwan, YW=7005662153en_HK
dc.identifier.citeulike6198270-

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