<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Farbstein D</submitter><funding>BSF</funding><funding>NIDDK NIH HHS</funding><funding>NIH</funding><funding>JDRF</funding><pagination>240-4</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC3200506</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>219(1)</volume><pubmed_abstract>&lt;h4>Objective&lt;/h4>Vitamin E provides cardiovascular protection to individuals with diabetes and the haptoglobin 2-2 genotype but appears to increase cardiovascular risk in individuals with diabetes and the haptoglobin 2-1 genotype. We have previously demonstrated that the haptoglobin protein is associated with HDL and that HDL function and its oxidative modification are haptoglobin genotype dependent. We set out to test the hypothesis that the pharmacogenetic interaction between the haptoglobin genotype on cardiovascular risk might be secondary to a parallel interaction between the haptoglobin genotype and vitamin E on HDL function.&lt;h4>Research design and methods&lt;/h4>Fifty-nine individuals with diabetes and the haptoglobin 2-1 or 2-2 genotypes were studied in a double-blind placebo control</pubmed_abstract><journal>Atherosclerosis</journal><pubmed_title>Vitamin E therapy results in a reduction in HDL function in individuals with diabetes and the haptoglobin 2-1 genotype.</pubmed_title><pmcid>PMC3200506</pmcid><funding_grant_id>R01 DK085226</funding_grant_id><funding_grant_id>RO1DK085226</funding_grant_id><funding_grant_id>R01DK085226</funding_grant_id><pubmed_authors>Laor A</pubmed_authors><pubmed_authors>Levy Y</pubmed_authors><pubmed_authors>Abbas N</pubmed_authors><pubmed_authors>Asaf R</pubmed_authors><pubmed_authors>Anbinder Y</pubmed_authors><pubmed_authors>Tavori H</pubmed_authors><pubmed_authors>Farbstein D</pubmed_authors><pubmed_authors>Pollak M</pubmed_authors><pubmed_authors>Vardi M</pubmed_authors><pubmed_authors>Star M</pubmed_authors><pubmed_authors>Vaya J</pubmed_authors><pubmed_authors>Miller-Lotan R</pubmed_authors><pubmed_authors>Moskovich D</pubmed_authors><pubmed_authors>Ozeri D</pubmed_authors><pubmed_authors>Lache O</pubmed_authors><pubmed_authors>Perry N</pubmed_authors><pubmed_authors>Levy AP</pubmed_authors><pubmed_authors>Asleh R</pubmed_authors><pubmed_authors>Blum S</pubmed_authors><pubmed_authors>Viener HL</pubmed_authors><pubmed_authors>Barkay I</pubmed_authors><pubmed_authors>Schwartz A</pubmed_authors><pubmed_authors>Kalet-Littman S</pubmed_authors><pubmed_authors>Bucher SE</pubmed_authors></additional><is_claimable>false</is_claimable><name>Vitamin E therapy results in a reduction in HDL function in individuals with diabetes and the haptoglobin 2-1 genotype.</name><description>&lt;h4>Objective&lt;/h4>Vitamin E provides cardiovascular protection to individuals with diabetes and the haptoglobin 2-2 genotype but appears to increase cardiovascular risk in individuals with diabetes and the haptoglobin 2-1 genotype. We have previously demonstrated that the haptoglobin protein is associated with HDL and that HDL function and its oxidative modification are haptoglobin genotype dependent. We set out to test the hypothesis that the pharmacogenetic interaction between the haptoglobin genotype on cardiovascular risk might be secondary to a parallel interaction between the haptoglobin genotype and vitamin E on HDL function.&lt;h4>Research design and methods&lt;/h4>Fifty-nine individuals with diabetes and the haptoglobin 2-1 or 2-2 genotypes were studied in a double-blind placebo control</description><dates><release>2011-01-01T00:00:00Z</release><publication>2011 Nov</publication><modification>2026-05-04T22:15:38.168Z</modification><creation>2019-03-26T23:05:21Z</creation></dates><accession>S-EPMC3200506</accession><cross_references><pubmed>21722898</pubmed><doi>10.1016/j.atherosclerosis.2011.06.005</doi></cross_references></HashMap>