J. Lipid Res.
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A more recent version of this article appeared on April 1, 2003

Papers In Press, published online ahead of print February 1, 2003
J. Lipid Res., doi:10.1194/jlr.M200405-JLR200
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Submitted on October 15, 2002
Revised on December 31, 2002
Accepted on January 17, 2003

Dietary fat modulation of ApoA-II metabolism and prevention of senile amyloidosis in the senescence accelerated mouse (SAMP1)

Makiko Umezawa, Kenjiri Tatematsu, Tatsumi Korenaga, Xiaoyong Fu, Takatoshi Matushita, Harumi Okuyama, Masanori Hosokawa, Toshio Takeda, and Keiichi Higuchi

Department of Nutrition, Koshien University, Takarazuka, Hyogo 665-0006

Corresponding Author: umezawa{at}koshien.ac.jp

SAMP1(SAMP1@Umz) is an animal model of senile amyloidosis, with Apolipoprotein A-II amyloid fibril (AApoAII) deposits. This study was undertaken to investigate the effects of dietary fats on AApoAII deposits in SAMP1 mice, when purified diets containing 4% fat as either butter, safflower oil or fish oil were fed to male mice for 26 weeks. The serum HDL cholesterol was significantly lower (P<0.01) in mice on the diet containing fish oil (7.4?3.0 mg/dl), than in mice on the butter diet (38.7?12.5 mg/dl) which in turn had significantly lower (P<0.01) HDL levels than mice on the safflower oil diet (51.9?5.6 mg/dl). Apolipoprotein A-II was also significantly lower (P<0.01) in mice on the fish oil diet (7.6?2.7 mg/dl) than on the butter (26.9?7.3 mg/dl) or safflower oil (21.6?3.7 mg/dl) diets. The mice fed fish oil had a significantly greater ratio (P<0.01) of ApoA-I to ApoA-II and a smaller HDL particle size than those fed butter and safflower oil. Severe AApoAII deposits in the spleen, heart, skin, liver and stomach were shown in the fish oil group compared with those in the butter and safflower oil groups (fish oil > butter > safflower oil group, P<0.05). These findings suggest that dietary fats differ in their effects on serum lipoprotein metabolism and that dietary lipids may modulate amyloid deposition in SAMP1 mice. Key words: dietary fats, senile amyloidosis, apolipoprotein A-II, senescence accelerated mouse (SAM)


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