Linked Life Data

17903340

Source:http://linkedlifedata.com/resource/pubmed/id/17903340

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
2008-3-6
pubmed:abstractText
The objective of the study was to determine whether Plasminogen Activator Inhibitor Type 1 (PAI-1) -675 4G/5G polymorphism is associated with the response of functional plasma PAI-1 concentrations to changes in the amount and quality of dietary fat in healthy subjects. PAI-1 is the major inhibitor of fibrinolysis, and a lower level of fibrinolytic activity could be implicated in an increased risk of IHD. Fifty-nine healthy Spanish volunteers (ten 4G/4G homozygotes, twenty-eight heterozygotes 4G/5G and twenty-one 5G/5G homozygotes) consumed three diets for periods of 4 weeks each: a SFA-rich diet (38 % fat, 20 % SFA), followed by a carbohydrate-rich diet (30 % fat, 55 % carbohydrate) and a MUFA-rich diet (38 % fat, 22 % MUFA) according to a randomized crossover design. At the end of each dietary period plasma lipid and functional plasma PAI-1 concentrations were determined. Subjects carrying the 4G allele (4G/4G and 4G/5G) showed a significant decrease in PAI-1 concentrations after the MUFA diet, compared with the SFA-rich and carbohydrate-rich diets (genotype x diet interaction: P = 0.028). 5G/5G homozygotes had the lowest plasma PAI-1 concentrations compared with 4G/4G and 4G/5G subjects (genotype: P = 0.002), without any changes as a result of the amount and the quality of the dietary fat. In summary, no differences in plasma PAI-1 concentration response were found after changes in dietary fat intake in 5G/5G homozygotes, although these subjects displayed the lowest concentrations of PAI-1. On the other hand, carriers of the 4G allele are more likely to hyper-respond to the presence of MUFA in the diet because of a greater decrease in PAI-1 concentrations.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0007-1145
pubmed:author
pubmed:issnType
Print
pubmed:volume
99
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
699-702
pubmed:meshHeading
pubmed-meshheading:17903340-Adult, pubmed-meshheading:17903340-Analysis of Variance, pubmed-meshheading:17903340-Cardiovascular Diseases, pubmed-meshheading:17903340-Cross-Over Studies, pubmed-meshheading:17903340-Dietary Carbohydrates, pubmed-meshheading:17903340-Dietary Fats, pubmed-meshheading:17903340-Fatty Acids, Monounsaturated, pubmed-meshheading:17903340-Fatty Acids, Volatile, pubmed-meshheading:17903340-Female, pubmed-meshheading:17903340-Fibrinolysis, pubmed-meshheading:17903340-Genotype, pubmed-meshheading:17903340-Heterozygote, pubmed-meshheading:17903340-Homozygote, pubmed-meshheading:17903340-Humans, pubmed-meshheading:17903340-Lipids, pubmed-meshheading:17903340-Male, pubmed-meshheading:17903340-Plasminogen Activator Inhibitor 1, pubmed-meshheading:17903340-Polymorphism, Genetic, pubmed-meshheading:17903340-Postprandial Period
pubmed:year
2008
pubmed:articleTitle
The -675 4G/5G polymorphism at the Plasminogen Activator Inhibitor 1 (PAI-1) gene modulates plasma Plasminogen Activator Inhibitor 1 concentrations in response to dietary fat consumption.
pubmed:affiliation
Lipids and Atherosclerosis Research Unit, Hospital Universitario Reina Sofia, CIBER, Fisiopatologia, Obesidad y Nutricion, Avda. Menendez Pidal, s/n. 14004 Cordoba, Spain. pablopermar@yahoo.es
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, Non-P.H.S., Randomized Controlled Trial, Research Support, Non-U.S. Gov't, Research Support, N.I.H., Extramural