PMID- 21119093
OWN - NLM
STAT- MEDLINE
DCOM- 20120126
LR  - 20131121
IS  - 1552-4604 (Electronic)
IS  - 0091-2700 (Linking)
VI  - 51
IP  - 10
DP  - 2011 Oct
TI  - Effect of bezafibrate on monocyte cytokine release and systemic inflammation in 
      patients with impaired fasting glucose.
PG  - 1459-67
LID - 10.1177/0091270010382914 [doi]
AB  - This study assessed the effect of bezafibrate on monocyte secretory function and 
      systemic inflammation in patients with impaired fasting glucose (IFG), comparing 
      this effect with that produced by bezafibrate in mixed dyslipidemic subjects. The 
      study included 28 patients with IFG, 29 individuals with mixed dyslipidemia, and 
      24 age-, sex- and weight-matched control subjects without lipid and glucose 
      metabolism abnormalities. Compared with the control group, in both IFG and mixed 
      dyslipidemic subjects, monocyte release of monocyte chemoattractant protein-1 
      (MCP-1), interleukin-6, tumor necrosis factor-alpha (TNF-alpha), and interleukin-1beta was 
      increased, which was accompanied by higher plasma levels of high-sensitivity 
      C-reactive protein (hsCRP). Despite affecting plasma lipids in both treatment 
      groups, bezafibrate administration (200 mg twice daily for 90 days) reduced 
      fasting plasma glucose levels, the homeostasis model assessment index, and 
      glycated hemoglobin only in IFG subjects. Bezafibrate treatment normalized 
      monocyte release of MCP-1, interleukin-6, TNF-alpha, and interleukin-1beta and also 
      normalized plasma hsCRP levels in mixed dyslipidemic subjects, whereas in IFG 
      individuals the drug reduced only MCP-1 and interleukin-6 release. This study 
      shows that IFG is associated with the presence of systemic inflammation and 
      abnormal monocyte secretory function. Compared with patients with mixed 
      dyslipidemia, IFG patients who are administered bezafibrate experience a stronger 
      effect on glucose metabolism and weaker anti-inflammatory and 
      monocyte-suppressing actions.
FAU - Krysiak, Robert
AU  - Krysiak R
AD  - Department of Internal Medicine and Clinical Pharmacology, Medical University of 
      Silesia, Medykow 18, PL 40-752 Katowice, Poland. r.krysiak@interia.pl
FAU - Okopien, Boguslaw
AU  - Okopien B
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20101130
PL  - England
TA  - J Clin Pharmacol
JT  - Journal of clinical pharmacology
JID - 0366372
RN  - 0 (Blood Glucose)
RN  - 0 (Cytokines)
RN  - Y9449Q51XH (Bezafibrate)
SB  - IM
MH  - Bezafibrate/*pharmacology
MH  - Blood Glucose/*drug effects
MH  - Case-Control Studies
MH  - Cytokines/*metabolism
MH  - Dyslipidemias/metabolism
MH  - Female
MH  - Humans
MH  - Inflammation/*drug therapy
MH  - Male
MH  - Middle Aged
MH  - Models, Biological
MH  - Monocytes/*metabolism
EDAT- 2010/12/02 06:00
MHDA- 2012/01/27 06:00
CRDT- 2010/12/02 06:00
PHST- 2010/12/02 06:00 [entrez]
PHST- 2010/12/02 06:00 [pubmed]
PHST- 2012/01/27 06:00 [medline]
AID - 0091270010382914 [pii]
AID - 10.1177/0091270010382914 [doi]
PST - ppublish
SO  - J Clin Pharmacol. 2011 Oct;51(10):1459-67. doi: 10.1177/0091270010382914. Epub 
      2010 Nov 30.