Journal of Lipid Research, Vol 38, 295-300, Copyright © 1997 by Lipid Research, Inc.
Incorporation of [U-14C]palmitate into rat brain: effect of an inhibitor of beta-oxidation
MC Chang, E Grange, O Rabin and JM Bell
Laboratory of Neurosciences, National Institutes on Aging, National Institutes of Health, Bethesda, MD 20892, USA.
We examined the effect of a clinically therapeutic dose of methyl 2-
tetradecylglycidate (McN-3716, methyl palmoxirate, MEP) (2.5 mg/kg), an
inhibitor of beta-oxidation of fatty acids, on incorporation of
radiolabeled palmitic acid ([U-14C]PAM) from plasma into brain lipids of
awake rats. Four hour pretreatment with 2.5 mg/kg MEP significantly
increased the incorporation of [U-14C]PAM into brain lipids and
substantially decreased aqueous radiolabeled metabolites in brain that can
constitute unwanted background signal when analyzed by quantitative
autoradiography. MEP treatment increased the lipid to aqueous background
radioactivity from 0.8 to 3.0. Net rate of incorporation, k*, was
significantly increased (60%) by MEP and was attributed to incorporation of
[U-14C]PAM into phospholipid and triglyceride brain compartments. MEP
treatment did not affect the size of the fatty acyl- CoA pool or the
distribution of the various molecular acyl-CoA species. These results
indicate that MEP, at a dose of 2.5 mg/kg (per os), can be used to increase
incorporation of [1-(11C)]PAM for studying brain lipid metabolism in humans
by positron emission tomography (PET).
CiteULike 
Complore 
Connotea 
Del.icio.us 
Digg 
Reddit 
Technorati What's this?
