PMID- 16634114
OWN - NLM
STAT- MEDLINE
DCOM- 20070226
LR  - 20181201
IS  - 1520-7552 (Print)
IS  - 1520-7552 (Linking)
VI  - 23
IP  - 1
DP  - 2007 Jan
TI  - Electronegative low-density lipoprotein subfraction from type 2 diabetic subjects 
      is proatherogenic and unrelated to glycemic control.
PG  - 26-34
AB  - BACKGROUND: The physicochemical and biological characteristics of electronegative 
      low-density lipoprotein (LDL) (LDL(-)) from type 2 diabetic patients (DM2), 
      before and after insulin therapy, were studied. METHODS: Total LDL was 
      subfractionated in LDL(+) (native LDL) and LDL(-) by anion-exchange 
      chromatography. RESULTS: The proportion of LDL(-) was increased in plasma from 
      DM2 patients compared to control subjects (13.8 +/- 4.6% versus 6.1 +/- 2.5, P < 
      0.05) and was not modified after glycemic optimization (14.0 +/- 5.9%). LDL(-) 
      from DM2 patients presented similar differential characteristics versus LDL(+) 
      than LDL(-) from controls; that is, decreased apoB and oxidizability, and 
      increased triglyceride, nonesterified fatty acids (NEFA), apoE, apoC-III, 
      platelet-activating factor (PAF) acetylhydrolase activity and aggregability. No 
      difference in particle size, antioxidants, malondialdehyde (MDA), fructosamine or 
      glycated low-density lipoprotein (gLDL) was observed between LDL subfractions. 
      Concerning differences between LDL subfractions isolated from DM2 and from 
      control subjects, the former showed increased MDA, fructosamine and gLDL 
      proportion and decreased LDL size and antioxidant content. The only effect of 
      glycemic optimization was a decrease in fructosamine and gLDL in LDL(+) from DM2 
      subjects. LDL(-) from DM2 patients presented low binding affinity to the 
      low-density lipoprotein receptor (LDLr) in cultured fibroblasts compared to 
      LDL(+) and two- to threefold increased ability to release interleukin-8 (IL-8) 
      and monocyte chemotactic protein 1 (MCP-1) in endothelial cells. CONCLUSION: 
      These results suggest that, although nonenzymatic glycosylation and oxidation are 
      increased in type 2 diabetes, these features would not be directly involved in 
      the generation of LDL(-). Moreover, LDL(-) properties suggest that the high 
      proportion observed in plasma could promote accelerated atherosclerosis in DM2 
      patients through increased residence time in plasma and induction of inflammatory 
      responses in artery wall cells.
FAU - Benitez, Sonia
AU  - Benitez S
AD  - Research Institute, Hospital de la Santa Creu i Sant Pau, Barcelona, Spain.
FAU - Perez, Antonio
AU  - Perez A
FAU - Sanchez-Quesada, Jose Luis
AU  - Sanchez-Quesada JL
FAU - Wagner, Ana Maria
AU  - Wagner AM
FAU - Rigla, Mercedes
AU  - Rigla M
FAU - Arcelus, Rosa
AU  - Arcelus R
FAU - Jorba, Oscar
AU  - Jorba O
FAU - Ordonez-Llanos, Jordi
AU  - Ordonez-Llanos J
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - Diabetes Metab Res Rev
JT  - Diabetes/metabolism research and reviews
JID - 100883450
RN  - 0 (Blood Glucose)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Interleukin-8)
RN  - 0 (Lipids)
RN  - 0 (Lipoproteins, LDL)
RN  - 0 (Receptors, LDL)
RN  - EC 3.1.1.47 (1-Alkyl-2-acetylglycerophosphocholine Esterase)
SB  - IM
MH  - 1-Alkyl-2-acetylglycerophosphocholine Esterase/metabolism
MH  - Aged
MH  - Blood Glucose/metabolism
MH  - Cells, Cultured
MH  - Chemical Phenomena
MH  - Chemistry, Physical
MH  - Chemokine CCL2/metabolism
MH  - Chromatography, Ion Exchange
MH  - Diabetes Mellitus, Type 2/*blood/therapy
MH  - Electrophoresis, Polyacrylamide Gel
MH  - Endothelial Cells/drug effects/metabolism
MH  - Female
MH  - Humans
MH  - Interleukin-8/metabolism
MH  - Lipids/blood
MH  - Lipoproteins, LDL/*chemistry
MH  - Male
MH  - Middle Aged
MH  - Receptors, LDL/metabolism
EDAT- 2006/04/25 09:00
MHDA- 2007/02/27 09:00
CRDT- 2006/04/25 09:00
PHST- 2006/04/25 09:00 [pubmed]
PHST- 2007/02/27 09:00 [medline]
PHST- 2006/04/25 09:00 [entrez]
AID - 10.1002/dmrr.643 [doi]
PST - ppublish
SO  - Diabetes Metab Res Rev. 2007 Jan;23(1):26-34. doi: 10.1002/dmrr.643.