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Nutrition and Cancer

Dietary Sodium Gluconate Protects Rats from Large Bowel Cancer by Stimulating Butyrate Production

Chiyoko Kameue^*, Takamitsu Tsukahara^*,, Kouji Yamada, Hironari Koyama^**,1, Yoshie Iwasaki, Keizo Nakayama^, and Kazunari Ushida^*,2

^* Laboratory of Animal Science, Kyoto Prefectural University, Shimogamo, Kyoto 606-8522, Japan; KYODOKEN Institute, Kyoto 612-8073, Japan; ^** Chemical Products Research Laboratories, Fujisawa Pharmaceutical Company, Ibaraki 300-2698, Japan; and Japan Cytology Research, Kyoto 612-8219, Japan

²To whom correspondence should be addressed. E-mail: k_ushida{at}kpu.ac.jp.

Butyrate has an antitumorigenic effect on colorectal cancer cell lines. Dietary sodium gluconate (GNA) promotes butyrate production in the large intestine. Accordingly, we examined the effect of dietary GNA on tumorigenesis in the large intestine in rats. Male Fisher-344 rats (n = 32) were divided into 4 groups: 2 diets (with or without 50 g GNA/kg basal diet) x 2 treatments (with or without carcinogen administration). Colonic tumors were induced by 3 intraperitoneal injections of azoxymethane (15 mg/kg body wt, 1 time/wk) and dietary deoxycholic acid (2 g/kg basal diet). The experiment was conducted for 33 wk except for a few rats. Ingestion of GNA increased cecal butyrate concentration at the end of experiment (P < 0.01). No tumor development occurred in the untreated groups. Ingestion of GNA decreased the incidence of tumors in rats administered the carcinogen (37.5 vs. 100%, P < 0.05). Ingestion of GNA also decreased the mean number of tumors per rat (0.5 ± 0.8 vs. 2.8 ± 1.5, P < 0.01). ß-Catenin accumulation and TdT-mediated dUTP nick end labeling (TUNEL) positive cells in tumors were histochemically examined. The results of this study suggested that the antitumorigenic effect of GNA may involve the stimulation of apoptosis through enhanced butyrate production in the large intestine.

KEY WORDS: • sodium gluconate • butyrate • colorectal cancer prevention • apoptosis • rat

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