From: Doug Skrecky (oberon@vcn.bc.ca)
Date: Sun May 21 2000 - 04:50:51 MDT
Authors
Wilmink HW. Stroes ES. Erkelens WD. Gerritsen WB. Wever R. Banga JD.
Rabelink TJ.
Institution
Divisions of Internal Medicine , University Hospital Utrecht, The
Netherlands.
Title
Influence of folic acid on postprandial endothelial dysfunction.
Source
Arteriosclerosis, Thrombosis &
Vascular Biology. 20(1):185-8, 2000 Jan.
Abstract
Triglyceride-rich lipoproteins that circulate postprandially are increasingly
being recognized as potentially atherogenic. These particles also have been
shown to cause endothelial dysfunction. We recently demonstrated that acute
parenteral administration of folic acid restores endothelial function in vivo
in patients with increased LDL cholesterol levels. In vitro data suggested
that this effect could be mediated by a reduction of radical stress. In the
present study, therefore, we evaluated the effect of an acute oral fat load
on both endothelial function and oxygen radical production. Next, we studied
whether 2 weeks of pretreatment with 10 mg folic acid PO could prevent these
fat-induced changes. We conducted a prospective, randomized,
placebo-controlled study to evaluate the effect of oral folic acid
administration (10 mg/d for 2 weeks) on basal endothelial function as well as
endothelial function on an acute fat load in 20 healthy volunteers 18 to 33
years old. Endothelial function was assessed as flow-mediated dilatation
(FMD). Endothelium-independent dilatation was measured after sublingual
nitroglycerin spray. Oxygen radical stress was assessed by measurement of the
urinary excretion of the stable radical-damage end product malondialdehyde.
During administration of placebo, FMD decreased significantly after an acute
oral fat load, with a median from 10.6% (8.3% to 12.2%) to 5.8% (3.0% to
10.2%), P<0.05. During folic acid administration, FMD was unaffected by a fat
load, with a median from 9.6% (7.1% to 12.8%) to 9.9% (7.5% to 14.1%), P=NS.
The increase in malondialdehyde excretion in the urine after fat loading was
also prevented during folic acid administration (absolute increase after an
acute fat load during placebo, 0.11+/-0.1 micromol/L versus folic acid,
0.02+/-0.1 micromol/L, P<0.05). The response to the endothelium-independent
vasodilator nitroglycerin remained unaltered throughout the study.
Pretreatment with oral folic acid prevents the lipid-induced decrease in FMD
as well as the lipid-induced increase in urinary radical-damage end products.
Because these observations were made in healthy volunteers with normal folate
and homocysteine levels, it is suggested that a higher folate intake in the
general population may have vasculoprotective effects.
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