PMID- 24988089
OWN - NLM
STAT- MEDLINE
DCOM- 20140822
LR  - 20220311
IS  - 1827-1669 (Electronic)
IS  - 0026-4806 (Linking)
VI  - 105
IP  - 3
DP  - 2014 Jun
TI  - Paraoxonase, oxidized low density lipoprotein, monocyte chemoattractant protein-1 
      and adhesion molecules are associated with macrovascular complications in 
      patients with type 2 diabetes mellitus.
PG  - 237-44
AB  - AIM: The aim of this paper was to evaluate the association between blood glucose, 
      oxidative stress, inflammation, endothelial dysfunction and paraoxonase activity 
      as contributors to the accelerated atherosclerosis seen in type 2 diabetic 
      patients. METHODS: Plasma malondialdehyde (MDA), oxidized LDL (oxLDL), monocyte 
      chemoattractant protein-1 (MCP-1), intercellular adhesion molecule-1 (ICAM-1), 
      and vascular cellular adhesion molecule-1 (VCAM-1) levels and paraoxonase-1 
      (PON1) activity were measured in sixty type 2 diabetic patients, 30 of whom had 
      macrovascular complications, and 30 controls. RESULTS: Diabetics with 
      macrovascular complications had higher levels of MDA, oxLDL, MCP-1, ICAM-1, 
      VCAM-1 than those without, and the difference was significant for all molecules 
      except for ICAM-1. PON1 activity and ApoA1 levels of the controls were 
      significantly higher than that of the patients, while PON1 activity and ApoA1 
      levels in the patients with macrovascular complications were significantly lower 
      than that in patients without. Ambient plasma glucose concentration showed a 
      significant positive association with plasma MDA, oxLDL, MCP-1, and VCAM, and a 
      significant inverse association with PON1 and ApoA1 in diabetic patients. A 
      significant positive correlation between oxLDL and MDA, a negative correlation 
      between oxLDL and PON1; a significant inverse association between MDA and PON1; a 
      positive correlation between MDA and MCP-1 and VCAM while a negative correlation 
      between PON1 and MCP-1 and VCAM were detected in patients. CONCLUSION: 
      Hyperglycemia might play a significant role in generating increased oxidative 
      stress, and decreased PON1 activity, resulting in elevated oxLDL, MCP-1 and VCAM 
      levels. This might be one of the causal pathogenic factors initiating accelerated 
      atherosclerosis in patients with type 2 diabetes mellitus. The implication of 
      these findings are unclear and therefore further studies are required.
FAU - Sozer, V
AU  - Sozer V
AD  - Department of Biochemistry Yildiz Technical University, Istanbul, Turkey - 
      huzun59@hotmail.com.
FAU - Himmetoglu, S
AU  - Himmetoglu S
FAU - Korkmaz, G G
AU  - Korkmaz GG
FAU - Kaya, S
AU  - Kaya S
FAU - Aydin, S
AU  - Aydin S
FAU - Yumuk, V
AU  - Yumuk V
FAU - Hatemi, H
AU  - Hatemi H
FAU - Uzun, H
AU  - Uzun H
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Italy
TA  - Minerva Med
JT  - Minerva medica
JID - 0400732
RN  - 0 (APOA1 protein, human)
RN  - 0 (Apolipoprotein A-I)
RN  - 0 (Blood Glucose)
RN  - 0 (CCL2 protein, human)
RN  - 0 (Cell Adhesion Molecules)
RN  - 0 (Chemokine CCL2)
RN  - 0 (ICAM1 protein, human)
RN  - 0 (Lipoproteins, LDL)
RN  - 0 (oxidized low density lipoprotein)
RN  - 126547-89-5 (Intercellular Adhesion Molecule-1)
RN  - 4Y8F71G49Q (Malondialdehyde)
RN  - EC 3.1.8.1 (Aryldialkylphosphatase)
RN  - EC 3.1.8.1 (PON1 protein, human)
SB  - IM
MH  - Adult
MH  - Aged
MH  - Apolipoprotein A-I/blood
MH  - Aryldialkylphosphatase/*blood
MH  - Atherosclerosis/blood/enzymology/*etiology/physiopathology
MH  - Blood Glucose/*metabolism
MH  - Cell Adhesion Molecules
MH  - Chemokine CCL2/*blood
MH  - Diabetes Mellitus, Type 2/*blood/complications/enzymology/physiopathology
MH  - Diabetic Angiopathies/*blood/complications/enzymology/physiopathology
MH  - Endothelium, Vascular/physiopathology
MH  - Female
MH  - Humans
MH  - Inflammation/blood/physiopathology
MH  - Intercellular Adhesion Molecule-1/*blood
MH  - Lipoproteins, LDL/*blood
MH  - Male
MH  - Malondialdehyde/*blood
MH  - Middle Aged
EDAT- 2014/07/06 06:00
MHDA- 2014/08/26 06:00
CRDT- 2014/07/03 06:00
PHST- 2014/07/03 06:00 [entrez]
PHST- 2014/07/06 06:00 [pubmed]
PHST- 2014/08/26 06:00 [medline]
AID - R10Y2014N03A0237 [pii]
PST - ppublish
SO  - Minerva Med. 2014 Jun;105(3):237-44.