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Vol. 302, Issue 1, 232-239, July 2002
Expression and Decreased Plasma Nonesterified Fatty Acids
and Liver Triglyceride in Fructose-Fed Rats
Unidad de Farmacología y Farmacognosia, Facultad de
Farmacia, Universidad de Barcelona, Barcelona, Spain (N.R., E.S., C.P.,
M.A., M.V., T.A., J.C.L., R.M.S.); and División Médica,
Pfizer S.A. Avda Europa, Madrid, Spain (C.D., G.H.)
We aimed to investigate the effect of atorvastatin (5 and 30 mg/kg/day
for 2 weeks) on hepatic lipid metabolism in a well established model of
dietary hypertriglyceridemia, the fructose-fed rat. Fructose feeding
(10% fructose in drinking water for 2 weeks) induced hepatic
lipogenesis and reduced peroxisome proliferator-activated receptor 
(PPAR) expression and fatty acid oxidation. As a result, plasma and
liver triglyceride and plasma apolipoprotein B (apoB) levels were
increased. Atorvastatin, 5 and 30 mg/kg during 2 weeks, markedly
reduced plasma triglyceride, but decreased apoB levels only at the
highest dose tested (50%). Triglyceride biosynthetic enzymes and
microsomal triglyceride transfer protein were unchanged, whereas
liver PPAR, acyl-CoA oxidase, and carnitine palmitoyltransferase I
mRNA levels (1.9-, 1.25-, and 3.4-fold, respectively) and hepatic fatty
acid 
-oxidation activity (1.25-fold) were increased by atorvastatin
at 30 mg/kg. Furthermore, hepatic triglyceride content (45%) and
plasma nonesterified fatty acids (NEFAs) (49%) were reduced. These
results show for the first time that liver triglyceride increase in
fructose-fed rats is linked to decreased expression of PPAR, which
is prevented by atorvastatin treatment. The increase in PPAR
expression caused by atorvastatin was associated with reduced liver
triglyceride and plasma NEFA levels.
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