Please use this identifier to cite or link to this item: https://hdl.handle.net/20.500.12530/37202
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dc.contributor.authorSan Mauro Martín, Ismael
dc.contributor.authorBlumenfeld Olivares, Javier Andrés
dc.contributor.authorPérez Arruche, Eva
dc.contributor.authorArce Delgado, Esperanza
dc.contributor.authorCiudad Cabañas, María José
dc.contributor.authorGaricano Vilar, Elena
dc.contributor.authorCollado Yurrita, Luis
dc.date.accessioned2019-06-28T18:27:33Z-
dc.date.available2019-06-28T18:27:33Z-
dc.date.issued2018-04-03
dc.identifier.citationDiseases.2018 Apr;(6)2:
dc.identifier.issn2079-9721
dc.identifier.urihttps://hdl.handle.net/20.500.12530/37202-
dc.description.abstractRaised serum cholesterol concentration is a well-established risk factor in cardiovascular disease. In addition, genetic load may have an indirect influence on cardiovascular risk. Plant-based sterol-supplemented foods are recommended to help reduce the serum low-density lipoprotein cholesterol level. The objective was to analyse the influence of different polymorphisms in hypercholesterolemia patients following a dietary treatment with plant sterols. A randomised double-blind cross-over controlled clinical trial was carried out in 45 people (25 women). Commercial milk, containing 2.24 g of sterols, was ingested daily during a 3-week period, and then the same amount of skim milk, without sterols, was consumed daily during the 3-week placebo phase. Both phases were separated by a washout period of 2 weeks. At the beginning and end of each phase, blood draws were performed. Genes LIPC C-514T and APOA5 C56G are Ser19Trp carriers and greatly benefit from sterol intake in the diet. LIPC C-514T TT homozygous carriers had lower low-density lipoprotein cholesterol (LDL-c) levels than CC homozygote and CT heterozygote carriers after the ingestion of plant sterols (p = 0.001). These two genes also showed statistically significant changes in total cholesterol levels (p = 0.025; p = 0.005), and no significant changes in high-density lipoprotein (HDL) cholesterol levels (p = 0.032; p = 0.003), respectively. No statistically significant differences were observed for other genes. Further studies are needed to establish which genotype combinations would be the most protective against hypercholesterolemia.
dc.language.isoeng
dc.rightsopenAccess-
dc.subjectcardiovascular disease
dc.subjectcholesterol
dc.subjectgenetic
dc.subjectlow-density lipoprotein cholesterol
dc.subjectnutrigenetics
dc.subjectsterol
dc.titleGenomic Influence in the Prevention of Cardiovascular Diseases with a Sterol-Based Treatment.
dc.typeArtículo
dc.identifier.pubmedID29614023
dc.format.volume6
dc.identifier.journalDiseases (Basel, Switzerland)
dc.identifier.doi10.3390/diseases6020024
dc.format.number2
dc.identifier.pmcPMC6023396
dc.pubmedtypeJournal Article
Appears in Collections:Hospitales > H. El Escorial > Artículos

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