Dietary fat modulation of apoA-II metabolism and prevention of senile amyloidosis in the senescence- accelerated mouse

Senescence-accelerated mouse-prone (SAMP1; SAMP1@Umz) is an animal model of senile amyloidosis with apolipoprotein A-II (apoA-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...

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Main Authors: Makiko Umezawa, Kenjiro Tatematsu, Tatsumi Korenaga, Xiaoying Fu, Takatoshi Matushita, Harumi Okuyama, Masanori Hosokawa, Toshio Takeda, Keiichi Higuchi
Format: Article
Language:English
Published: Elsevier 2003-04-01
Series:Journal of Lipid Research
Subjects:
Online Access:http://www.sciencedirect.com/science/article/pii/S0022227520311664
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author Makiko Umezawa
Kenjiro Tatematsu
Tatsumi Korenaga
Xiaoying Fu
Takatoshi Matushita
Harumi Okuyama
Masanori Hosokawa
Toshio Takeda
Keiichi Higuchi
author_facet Makiko Umezawa
Kenjiro Tatematsu
Tatsumi Korenaga
Xiaoying Fu
Takatoshi Matushita
Harumi Okuyama
Masanori Hosokawa
Toshio Takeda
Keiichi Higuchi
author_sort Makiko Umezawa
collection DOAJ
description Senescence-accelerated mouse-prone (SAMP1; SAMP1@Umz) is an animal model of senile amyloidosis with apolipoprotein A-II (apoA-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 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). ApoA-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.
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spelling doaj.art-7f2bfb19e710485a8870e25c8ce428132022-12-21T18:55:46ZengElsevierJournal of Lipid Research0022-22752003-04-01444762769Dietary fat modulation of apoA-II metabolism and prevention of senile amyloidosis in the senescence- accelerated mouseMakiko Umezawa0Kenjiro Tatematsu1Tatsumi Korenaga2Xiaoying Fu3Takatoshi Matushita4Harumi Okuyama5Masanori Hosokawa6Toshio Takeda7Keiichi Higuchi8Department of Nutrition, Koshien University, 10-1 Momijigaoka, Takarazuka, Hyogo 665-0006, Japan; Department of Preventive Nutraceutical Sciences, Graduate School of Pharmaceutical Biological Chemistry, Nagoya City University, Nagoya 467-8603, Japan; Field of Regeneration Control, Institute for Frontier Medical Sciences, Kyoto University, Kyoto 606-8397, Japan; Department of Aging Angiology, Research Center on Aging and Adaptation, Shinshu University School of Medicine, Matsumoto 390-8621, JapanDepartment of Nutrition, Koshien University, 10-1 Momijigaoka, Takarazuka, Hyogo 665-0006, Japan; Department of Preventive Nutraceutical Sciences, Graduate School of Pharmaceutical Biological Chemistry, Nagoya City University, Nagoya 467-8603, Japan; Field of Regeneration Control, Institute for Frontier Medical Sciences, Kyoto University, Kyoto 606-8397, Japan; Department of Aging Angiology, Research Center on Aging and Adaptation, Shinshu University School of Medicine, Matsumoto 390-8621, JapanDepartment of Nutrition, Koshien University, 10-1 Momijigaoka, Takarazuka, Hyogo 665-0006, Japan; Department of Preventive Nutraceutical Sciences, Graduate School of Pharmaceutical Biological Chemistry, Nagoya City University, Nagoya 467-8603, Japan; Field of Regeneration Control, Institute for Frontier Medical Sciences, Kyoto University, Kyoto 606-8397, Japan; Department of Aging Angiology, Research Center on Aging and Adaptation, Shinshu University School of Medicine, Matsumoto 390-8621, JapanDepartment of Nutrition, Koshien University, 10-1 Momijigaoka, Takarazuka, Hyogo 665-0006, Japan; Department of Preventive Nutraceutical Sciences, Graduate School of Pharmaceutical Biological Chemistry, Nagoya City University, Nagoya 467-8603, Japan; Field of Regeneration Control, Institute for Frontier Medical Sciences, Kyoto University, Kyoto 606-8397, Japan; Department of Aging Angiology, Research Center on Aging and Adaptation, Shinshu University School of Medicine, Matsumoto 390-8621, JapanDepartment of Nutrition, Koshien University, 10-1 Momijigaoka, Takarazuka, Hyogo 665-0006, Japan; Department of Preventive Nutraceutical Sciences, Graduate School of Pharmaceutical Biological Chemistry, Nagoya City University, Nagoya 467-8603, Japan; Field of Regeneration Control, Institute for Frontier Medical Sciences, Kyoto University, Kyoto 606-8397, Japan; Department of Aging Angiology, Research Center on Aging and Adaptation, Shinshu University School of Medicine, Matsumoto 390-8621, JapanDepartment of Nutrition, Koshien University, 10-1 Momijigaoka, Takarazuka, Hyogo 665-0006, Japan; Department of Preventive Nutraceutical Sciences, Graduate School of Pharmaceutical Biological Chemistry, Nagoya City University, Nagoya 467-8603, Japan; Field of Regeneration Control, Institute for Frontier Medical Sciences, Kyoto University, Kyoto 606-8397, Japan; Department of Aging Angiology, Research Center on Aging and Adaptation, Shinshu University School of Medicine, Matsumoto 390-8621, JapanDepartment of Nutrition, Koshien University, 10-1 Momijigaoka, Takarazuka, Hyogo 665-0006, Japan; Department of Preventive Nutraceutical Sciences, Graduate School of Pharmaceutical Biological Chemistry, Nagoya City University, Nagoya 467-8603, Japan; Field of Regeneration Control, Institute for Frontier Medical Sciences, Kyoto University, Kyoto 606-8397, Japan; Department of Aging Angiology, Research Center on Aging and Adaptation, Shinshu University School of Medicine, Matsumoto 390-8621, JapanDepartment of Nutrition, Koshien University, 10-1 Momijigaoka, Takarazuka, Hyogo 665-0006, Japan; Department of Preventive Nutraceutical Sciences, Graduate School of Pharmaceutical Biological Chemistry, Nagoya City University, Nagoya 467-8603, Japan; Field of Regeneration Control, Institute for Frontier Medical Sciences, Kyoto University, Kyoto 606-8397, Japan; Department of Aging Angiology, Research Center on Aging and Adaptation, Shinshu University School of Medicine, Matsumoto 390-8621, JapanDepartment of Nutrition, Koshien University, 10-1 Momijigaoka, Takarazuka, Hyogo 665-0006, Japan; Department of Preventive Nutraceutical Sciences, Graduate School of Pharmaceutical Biological Chemistry, Nagoya City University, Nagoya 467-8603, Japan; Field of Regeneration Control, Institute for Frontier Medical Sciences, Kyoto University, Kyoto 606-8397, Japan; Department of Aging Angiology, Research Center on Aging and Adaptation, Shinshu University School of Medicine, Matsumoto 390-8621, JapanSenescence-accelerated mouse-prone (SAMP1; SAMP1@Umz) is an animal model of senile amyloidosis with apolipoprotein A-II (apoA-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 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). ApoA-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.http://www.sciencedirect.com/science/article/pii/S0022227520311664apolipoprotein A-IIapolipoprotein A-II amyloid fibrilhigh density lipoprotein
spellingShingle Makiko Umezawa
Kenjiro Tatematsu
Tatsumi Korenaga
Xiaoying Fu
Takatoshi Matushita
Harumi Okuyama
Masanori Hosokawa
Toshio Takeda
Keiichi Higuchi
Dietary fat modulation of apoA-II metabolism and prevention of senile amyloidosis in the senescence- accelerated mouse
Journal of Lipid Research
apolipoprotein A-II
apolipoprotein A-II amyloid fibril
high density lipoprotein
title Dietary fat modulation of apoA-II metabolism and prevention of senile amyloidosis in the senescence- accelerated mouse
title_full Dietary fat modulation of apoA-II metabolism and prevention of senile amyloidosis in the senescence- accelerated mouse
title_fullStr Dietary fat modulation of apoA-II metabolism and prevention of senile amyloidosis in the senescence- accelerated mouse
title_full_unstemmed Dietary fat modulation of apoA-II metabolism and prevention of senile amyloidosis in the senescence- accelerated mouse
title_short Dietary fat modulation of apoA-II metabolism and prevention of senile amyloidosis in the senescence- accelerated mouse
title_sort dietary fat modulation of apoa ii metabolism and prevention of senile amyloidosis in the senescence accelerated mouse
topic apolipoprotein A-II
apolipoprotein A-II amyloid fibril
high density lipoprotein
url http://www.sciencedirect.com/science/article/pii/S0022227520311664
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