title: High serum apolipoprotein E determines hypertriglyceridemic dyslipidemias, coronary disease and apoA-I dysfunctionality.
abstract: The relevance of serum apolipoprotein E (apoE) levels to two hypertriglyceridemic dyslipidemias has not been clarified. We explored, in a cross-sectional (and short-term prospective) evaluation, the independent relationship of serum apoE to the atherogenic dyslipidemia, hypertriglyceridemia with elevated apoB (HtgB) and to apoA-I dysfunctionality, previously shown in Turkish adults to be independent of apoE genotype. Serum apoE concentrations were measured by immunonephelometry in 1,127 middle-aged adults. In multivariable regression analysis, apoE concentrations showed log-linear associations with apoB and apoA-I levels, waist circumference, independent of C-reactive protein (CRP), homeostatic model assessment (HOMA) index and other confounders. The likelihood of atherogenic dyslipidemia and of HtgB roughly tripled per 1-SD increment in apoE concentrations, additively to apoE genotype, HOMA, apoA-I, CRP concentrations and waist circumference; yet apoA-I, protective against atherogenic dyslipidemia, appeared to promote HtgB, a finding consistent with apoA-I dysfunctionality in this setting. Each 1-SD increment in the apoE level was moreover, associated in both genders with MetS (at OR 1.5), after adjustment for sex, age, apoB, apoA-I and CRP, or for apoE genotypes. Circulating apoE predicted in both genders age-adjusted prevalent and incident coronary heart disease (CHD), independent of apoE genotype and CRP (OR 1.32 [95 % CI 1.11; 1.58]). To conclude, in a general population prone to MetS, elevated apoE concentrations are strongly linked to HtgB and atherogenic dyslipidemia, irrespective of apoE genotype, are associated with MetS and CHD. Excess apoE reflects pro-inflammatory state and likely autoimmune activation.
authors.affiliation: Turkish Society of Cardiology, Istanbul, Turkey. alt_onat@yahoo.com.tr
authors.forename: Altan
authors.initials: A
authors.lastname: Onat
authors.forename: Günay
authors.initials: G
authors.lastname: Can
authors.forename: Ender
authors.initials: E
authors.lastname: Ornek
authors.forename: Erkan
authors.initials: E
authors.lastname: Ayhan
authors.forename: Nihan
authors.initials: N
authors.lastname: Erginel-Ünaltuna
authors.forename: Sani N
authors.initials: SN
authors.lastname: Murat
mesh_terms: D000328:Adult; D000368:Aged; D016632:Apolipoprotein A-I / Q000097:blood*; D001055:Apolipoproteins B / Q000097:blood; D001057:Apolipoproteins E / Q000097:blood*; D002097:C-Reactive Protein / Q000032:analysis; D003327:Coronary Disease / Q000097:blood* / Q000150:complications; D003430:Cross-Sectional Studies; D050171:Dyslipidemias / Q000097:blood* / Q000150:complications; D005260:Female; D006801:Humans; D015228:Hypertriglyceridemia / Q000097:blood*; D008297:Male; D024821:Metabolic Syndrome / Q000097:blood; D008875:Middle Aged; D011446:Prospective Studies
chemical_list: D016632:Apolipoprotein A-I; D001055:Apolipoproteins B; D001057:Apolipoproteins E; D002097:C-Reactive Protein