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Dietary Soybean Protein Compared with Casein Retards Senescence in the Senescence Accelerated Mouse1, 2,

Makiko Umezawa3, Masanori Hosokawa*, Atsuko Kohno{dagger}, Shintaro Ishikawa*, Kaori Kitagawa* and Toshio Takeda*

Department of Nutrition, Koshien University, Hyogo 665 * Department of Senescence Biology, Chest Disease Research Institute, Kyoto University, Kyoto 606 {dagger} Department of Food and Nutrition, Seinan-Jogakuin College, Fukuoka 803, Japan

The effects of replacing dietary casein with soybean protein on mean life span, mean life span of the last one-tenth of a group, grading scores of senescence and deposition of senile amyloid were investigated in senescence accelerated mice (SAM-P/1) compared with a control strain (SAM-R/1). SAM-R/1 mice fed the soybean protein-containing diet had mean life spans of 618 ± 42 d (males) and 578 ± 62 d (females), 58% (males) and 44% (females) longer than those of corresponding casein fed mice (P < 0.01). Similarly, in SAM-P/1 mean life-spans were 265 ± 16 d (males) and 307 ± 23 d (females) in the soybean diet group, 27% (males) and 30% (females) longer than in the casein diet groups (P < 0.01). The mean life span of the last one-tenth of each group fed soybean protein was significantly longer than the corresponding group fed casein. In SAM-R/1 mice, pathological studies revealed that severe secondary amyloid deposition (amyloid A protein) in the kidneys, spleen, stomach and liver was significantly suppressed, in males only, by replacing casein with soybean protein (P < 0.01). The occurrence of contracted kidneys caused by the infiltration of amyloid A protein was suppressed in SAM-R/1 mice fed the soybean protein-containing diet (P < 0.05). The deposition of senile amyloid in SAM-P/1 mice with aging was retarded by replacing casein with soybean protein (P < 0.01). These results indicate that dietary protein source is important in modulating the advance of senescence in SAM Mice.


KEY WORDS: • senescence accelerated mouse • life span • dietary protein • senile amyloid • secondary amyloid

1 This work was supported by grants from the Ministry of Education, Science and Culture and the Ministry of Health and Welfare of Japan, and the Fuji Oil Co., Ltd.

2 The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 USC section 1734 solely to indicate this fact.

3 To whom correspondence and reprint requests should be addressed at: The Department of Nutrition, Koshien University, 10-1 Momijigaoka, Takarazuka, Hyogo 665, Japan.

Manuscript received 19 October 1992. Revision accepted 25 June 1993.







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