Title of article :
LDL composition in E2/2 subjects and LDL distribution by Apo E genotype in type 1 diabetes
Author/Authors :
Susan J. Murdoch، نويسنده , , Andrew P. Boright، نويسنده , , Andrew D. Paterson، نويسنده , , Bernard Zinman، نويسنده , , Michael Steffes، نويسنده , , Patricia Cleary، نويسنده , , Karen Edwards، نويسنده , , Santica S. Marcovina، نويسنده , , Jonathan Q. Purnell، نويسنده , , John D. Brunzell and the DCCT/EDIC Research Group، نويسنده ,
Issue Information :
روزنامه با شماره پیاپی سال 2007
Pages :
10
From page :
138
To page :
147
Abstract :
Apo E plays an important role in chylomicron and VLDL remnant processing, uptake or conversion to LDL. The type of lipoprotein that isolates in the LDL density of E2/2 subjects was investigated and the effect of the apo E isoforms on LDL mass was determined in all genotypes in a large group of Type 1 diabetics. Analysis of the LDL composition of E2/2 homozygotes (n = 6) compared to subjects with the common E3/3 isoform (n = 6) demonstrated an enrichment in apo E, unesterified cholesterol, phospholipid and triglyceride relative to apo B in E2/2 subjects, more typical of a dense IDL remnant than of LDL. Although diabetics were studied, these findings are considered to reflect those of the general population. Comparison of the lipoprotein distribution of homozygous and heterozygous subjects revealed that, as genotype changed from E4/4 (n = 22) to E3/4 (n = 262), E3/3 (n = 710) = E2/4 (n = 30), E2/3 (n = 151), E2/2 (n = 6), LDL cholesterol decreased significantly in a stepwise manner. The decrease was not in a specific subgroup of LDL. In conclusion, for E2/2 subjects, lipoproteins isolated in the LDL density range appear to be composed mainly of dense IDL remnants and some Lp(a). The apo E isoform also has a significant effect on LDL concentration in both homozygotes and heterozygotes.
Keywords :
Apo E genotype , E2/2 , LDL , VLDL remnants , LDL composition
Journal title :
Atherosclerosis
Serial Year :
2007
Journal title :
Atherosclerosis
Record number :
632352
Link To Document :
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