PMID- 16132957
OWN - NLM
STAT- MEDLINE
DCOM- 20051220
LR  - 20181113
IS  - 0012-186X (Print)
IS  - 0012-186X (Linking)
VI  - 48
IP  - 10
DP  - 2005 Oct
TI  - The inflammatory properties of electronegative low-density lipoprotein from type 
      1 diabetic patients are related to increased platelet-activating factor 
      acetylhydrolase activity.
PG  - 2162-9
AB  - AIMS/HYPOTHESIS: Chemical and biological characteristics of LDL(-) from type 1 
      diabetic subjects were analysed. The diabetic patients were studied during poor 
      and optimised glycaemic control. MATERIALS AND METHODS: Total LDL was 
      subfractionated into electropositive LDL(+) and electronegative LDL(-) by anion 
      exchange chromatography and the lipid and protein composition of the two 
      determined. RESULTS: LDL(-) differed from LDL(+) in that it had higher 
      triglyceride, non-esterified fatty acids, apoE, apoC-III and platelet-activating 
      factor acetylhydrolase (PAF-AH), as well as lower apoB relative content. No 
      evidence of increased oxidation was observed in LDL(-). LDL(-) increased two-fold 
      the release of interleukin 8 (IL-8) and monocyte chemotactic protein 1 (MCP-1) in 
      endothelial cells, suggesting an inflammatory role. Optimisation of glycaemic 
      control after insulin therapy decreased the proportion of LDL(-), but did not 
      modify the composition of LDL subfractions, except for a decrease in PAF-AH 
      activity in LDL(-). The possibility that LDL(-) could be generated by 
      non-enzymatic glycosylation was studied. Fructosamine and glycated LDL content in 
      LDL subfractions from type 1 diabetic patients was greater than in LDL 
      subfractions isolated from normoglycaemic subjects, and decreased after glycaemic 
      optimisation in both subfractions. However, no difference was observed between 
      LDL(+) and LDL(-) before and after insulin therapy. CONCLUSIONS/INTERPRETATION: 
      These results provide evidence that LDL(-) is not produced by glycosylation. 
      Nevertheless, LDL(-) from diabetic patients displays inflammatory potential 
      reflected by the induction of chemokine release in endothelial cells. This 
      proatherogenic effect could be related to the high PAF-AH activity in LDL(-).
FAU - Sanchez-Quesada, J L
AU  - Sanchez-Quesada JL
AD  - Department of Biochemistry, Hospital de la Santa Creu i Sant Pau, Barcelona, 
      Spain.
FAU - Benitez, S
AU  - Benitez S
FAU - Perez, A
AU  - Perez A
FAU - Wagner, A M
AU  - Wagner AM
FAU - Rigla, M
AU  - Rigla M
FAU - Carreras, G
AU  - Carreras G
FAU - Vila, L
AU  - Vila L
FAU - Camacho, M
AU  - Camacho M
FAU - Arcelus, R
AU  - Arcelus R
FAU - Ordonez-Llanos, J
AU  - Ordonez-Llanos J
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20050818
PL  - Germany
TA  - Diabetologia
JT  - Diabetologia
JID - 0006777
RN  - 0 (Apoproteins)
RN  - 0 (Blood Glucose)
RN  - 0 (Chemokines)
RN  - 0 (Lipids)
RN  - 0 (Lipoproteins, LDL)
RN  - 0 (Transcription Factors)
RN  - 4Y8F71G49Q (Malondialdehyde)
RN  - EC 3.1.1.47 (1-Alkyl-2-acetylglycerophosphocholine Esterase)
SB  - IM
MH  - 1-Alkyl-2-acetylglycerophosphocholine Esterase/*metabolism
MH  - Apoproteins/chemistry
MH  - Blood Glucose/metabolism
MH  - Cells, Cultured
MH  - Chemical Phenomena
MH  - Chemistry, Physical
MH  - Chemokines/metabolism
MH  - Diabetes Mellitus, Type 1/*metabolism/pathology
MH  - Electrophoresis, Polyacrylamide Gel
MH  - Endothelial Cells/drug effects
MH  - Humans
MH  - Inflammation/*chemically induced/pathology
MH  - Lipids/blood
MH  - Lipoproteins, LDL/*chemistry/*toxicity
MH  - Malondialdehyde/metabolism
MH  - Oxidation-Reduction
MH  - Transcription Factors
EDAT- 2005/09/01 09:00
MHDA- 2005/12/21 09:00
CRDT- 2005/09/01 09:00
PHST- 2005/04/07 00:00 [received]
PHST- 2005/05/31 00:00 [accepted]
PHST- 2005/09/01 09:00 [pubmed]
PHST- 2005/12/21 09:00 [medline]
PHST- 2005/09/01 09:00 [entrez]
AID - 10.1007/s00125-005-1899-8 [doi]
PST - ppublish
SO  - Diabetologia. 2005 Oct;48(10):2162-9. doi: 10.1007/s00125-005-1899-8. Epub 2005 
      Aug 18.