PMID- 17011788
OWN - NLM
STAT- MEDLINE
DCOM- 20070123
LR  - 20181201
IS  - 1043-6618 (Print)
IS  - 1043-6618 (Linking)
VI  - 54
IP  - 6
DP  - 2006 Dec
TI  - Effect of atorvastatin on soluble CD14, CD40 Ligand, sE- and sP-selectins and 
      MCP-1 in patients with type 2 diabetes mellitus: relationship to cholesterol 
      turnover.
PG  - 421-8
AB  - Metabolic abnormalities frequently associated with type 2 diabetes, feature 
      besides endothelial dysfunction a novel factor of low cholesterol absorption and 
      high cholesterol synthesis. We hypothesized an association between endothelial 
      dysfunction and disturbances in cholesterol turnover, predisposing advanced 
      atherosclerosis in patients with type 2 diabetes. We studied 75 patients: 30 with 
      type 2 diabetes, 30 non-diabetic subjects with a history of cardiovascular 
      disease, and 15 healthy subjects. Plasma sterols, soluble adhesion molecules 
      sCD14, sCD40 Ligand, monocyte chemo-attractant protein-1 (MCP-1), sE- and 
      sP-selectins were measured with and without atorvastatin therapy. The diabetic 
      patients showed significantly higher levels of lathosterol and lower levels of 
      sitosterol and campesterol. Non-diabetic subjects showed no significant 
      differences in non-cholesterol based sterols. Plasma levels of hsCRP, sE- and 
      sP-selectins and MCP-1 were significantly increased in patients with diabetes. 
      The plasma levels of sCD40L correlate significantly with clinical parameters of 
      BMI and glycaemia, and the plasma levels of sP-selectin correlate significantly 
      with parameters of glycaemia and HbA(1c). The diabetic patients without statin 
      therapy showed a significant correlation of sE-selectin with the marker of 
      cholesterol absorption-sitosterol and sitosterol/cholesterol ratio. The diabetic 
      patients without statin therapy showed a significant inverse correlation of 
      sP-selectin with the marker of cholesterol synthesis-lathosterol. Both 
      relationships disappeared with statin treatment. We conclude that endothelial 
      dysfunction in obese patients with type 2 diabetes mellitus and cardiovascular 
      disease associates with obesity and glycaemic control. The relation of parameters 
      of endothelial dysfunction (such as sP-selectin and sE-selectin) with cholesterol 
      synthesis and absorption may be influenced by reverse cholesterol transport.
FAU - Blaha, Vladimir
AU  - Blaha V
AD  - Department of Metabolic Care and Gerontology, University Hospital Hradec Kralove 
      and Medical Faculty Charles University in Hradec Kralove, Sokolska 581, 50005 
      Hradec Kralove, Czech Republic. blaha@lfhk.cuni.cz
FAU - Andrys, Ctirad
AU  - Andrys C
FAU - Smahelova, Alena
AU  - Smahelova A
FAU - Knizek, Jiri
AU  - Knizek J
FAU - Hyspler, Radomir
AU  - Hyspler R
FAU - Solichova, Dagmar
AU  - Solichova D
FAU - Blaha, Milan
AU  - Blaha M
FAU - Zadak, Zdenek
AU  - Zadak Z
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20060903
PL  - Netherlands
TA  - Pharmacol Res
JT  - Pharmacological research
JID - 8907422
RN  - 0 (CCL2 protein, human)
RN  - 0 (CD40 Antigens)
RN  - 0 (Chemokine CCL2)
RN  - 0 (E-Selectin)
RN  - 0 (Heptanoic Acids)
RN  - 0 (Hydroxymethylglutaryl-CoA Reductase Inhibitors)
RN  - 0 (Ligands)
RN  - 0 (Lipopolysaccharide Receptors)
RN  - 0 (P-Selectin)
RN  - 0 (Pyrroles)
RN  - 97C5T2UQ7J (Cholesterol)
RN  - A0JWA85V8F (Atorvastatin)
SB  - IM
MH  - Atorvastatin
MH  - CD40 Antigens/*metabolism
MH  - Chemokine CCL2/*metabolism
MH  - Cholesterol/*metabolism
MH  - Diabetes Mellitus, Type 2/*metabolism
MH  - E-Selectin/*metabolism
MH  - Female
MH  - Heptanoic Acids/*pharmacology
MH  - Humans
MH  - Hydroxymethylglutaryl-CoA Reductase Inhibitors/*pharmacology
MH  - Ligands
MH  - Lipid Metabolism/drug effects
MH  - Lipopolysaccharide Receptors/*metabolism
MH  - Male
MH  - Middle Aged
MH  - P-Selectin/*metabolism
MH  - Pyrroles/*pharmacology
EDAT- 2006/10/03 09:00
MHDA- 2007/01/24 09:00
CRDT- 2006/10/03 09:00
PHST- 2005/12/18 00:00 [received]
PHST- 2006/08/25 00:00 [revised]
PHST- 2006/08/28 00:00 [accepted]
PHST- 2006/10/03 09:00 [pubmed]
PHST- 2007/01/24 09:00 [medline]
PHST- 2006/10/03 09:00 [entrez]
AID - S1043-6618(06)00162-9 [pii]
AID - 10.1016/j.phrs.2006.08.005 [doi]
PST - ppublish
SO  - Pharmacol Res. 2006 Dec;54(6):421-8. doi: 10.1016/j.phrs.2006.08.005. Epub 2006 
      Sep 3.