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The effect of glutathione S-transferase M1 and T1 polymorphisms on ascorbic acid plasma levels in diabetic patients

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dc.contributor.authorValente, A.
dc.contributor.authorBicho, M.
dc.contributor.authorSantos, A.C.
dc.contributor.authorMatos, A.
dc.contributor.authorDuarte, R.
dc.contributor.authorRaposo, J.F.
dc.contributor.authorCosta, H.S.
dc.date.accessioned2019-03-08T19:52:11Z
dc.date.available2019-03-08T19:52:11Z
dc.date.issued2018-05
dc.description.abstractIntroduction: Type 2 diabetes mellitus have been associated with excessive production of reactive oxygen species. Glutathione S-transferase (GST) polymorphisms result in decreased or absent enzyme activity and altered oxidative stress. Meta-analyses have indicated that deletion of either GSTM1 or GSTT1 is associated with a significant increased risk of coronary heart disease. The aim of this study was to evaluated if ascorbic acid (AA) plasma levels differ by GST genotype in diabetic patients with and without angiopathy. Methods: An observational analytical case-control study in 123 Caucasians type 2 diabetic patients was performed. GI - 65 diabetics with angiopathy, GII - 58 diabetics without angiopathy. Plasma levels of AA were measured by a validated HPLC method. The genotyping of GSTT1 and GSTM1 it was determined simultaneously by PCRMultiplex technique. Results: The frequency of GSTM1 and GSTT1 single-null genotypes was 42.9% and 30.8% in group I and 43.9% and 31.0% among in group II. The percentage of diabetics patients who had both GSTM1 and GSTT1 functional genotypes was GI:46.0% and GII:42.9%, who had one of the present genotypes was GI:33.4% and GII:37.5% and who had both null genotypes was GI:20.6% and GII:19.6%. Plasma AA concentrations were lower in those with the GSTT1 null genotype than in those with the GSTT1 functional genotype. GSTM1 null genotypes had higher plasma AA levels than those with functional GSTM1 allele. Suboptimal AA plasma concentrations (<4.93 μmol/L) were more frequent in GSTT1 deletion genotype (76.3%) compared to GSTT1-1 (69.4%). Inversely, the percentage of patients with functional GSTM1 allele (72.1%) was higher than null genotype (67.3%). Conclusion: Plasmatic levels of AA differ by GSTM1 and GSTT1 polymorphisms in Caucasians diabetic patients with or without angiopathy. The upper and lower regulation of AA plasma levels in subjects with nonfunctional GSTT1 or GSTM1 could be partially understood to compensate the lack of functionality.pt_PT
dc.description.sponsorshipThis study was funded by PIC/IC/82957/2007 from Fundação para a Ciência e a Tecnologia and Ana Valente is grateful for PhD grant SFRH/BD/16166/2004/5E4M and research grant.pt_PT
dc.description.versioninfo:eu-repo/semantics/publishedVersionpt_PT
dc.identifier.urihttp://hdl.handle.net/10400.18/6161
dc.language.isoengpt_PT
dc.peerreviewedyespt_PT
dc.relationNUTRIÇÃO E AS DOENÇAS CARDIOVASCULARES EM DIABÉTICOS
dc.subjectType 2 diabetes mellituspt_PT
dc.subjectGlutathione S-transferase polymorphismspt_PT
dc.subjectNutrição Aplicadapt_PT
dc.titleThe effect of glutathione S-transferase M1 and T1 polymorphisms on ascorbic acid plasma levels in diabetic patientspt_PT
dc.typeconference object
dspace.entity.typePublication
oaire.awardTitleNUTRIÇÃO E AS DOENÇAS CARDIOVASCULARES EM DIABÉTICOS
oaire.awardURIinfo:eu-repo/grantAgreement/FCT/5646-ICCMS/PIC%2FIC%2F82957%2F2007/PT
oaire.awardURIinfo:eu-repo/grantAgreement/FCT//SFRH%2FBD%2F16166%2F2004/PT
oaire.citation.conferencePlaceBarcelona, Espanhapt_PT
oaire.citation.title20th European Congress of Endocrinology (ECE 2018), 19-22 maio 2018pt_PT
oaire.fundingStream5646-ICCMS
project.funder.identifierhttp://doi.org/10.13039/501100001871
project.funder.identifierhttp://doi.org/10.13039/501100001871
project.funder.nameFundação para a Ciência e a Tecnologia
project.funder.nameFundação para a Ciência e a Tecnologia
rcaap.rightsrestrictedAccesspt_PT
rcaap.typeconferenceObjectpt_PT
relation.isProjectOfPublicationfe6af5b5-1538-4602-b13a-c8916b4b229a
relation.isProjectOfPublication5bfbe1d3-549c-4941-acb2-7468ccc66f44
relation.isProjectOfPublication.latestForDiscoveryfe6af5b5-1538-4602-b13a-c8916b4b229a

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