Reduction in NaCl-enhanced gastric carcinogenesis in rats fed a high-protein diet

Tatsuta, Masaharu; Baba, Miyako; Uehara, Hiroyuki; Nakaizumi, Akihiko; Iseki, Kazushige

doi:10.1016/s0304-3835(97)00197-3

Cited by 8 publications

(2 citation statements)

References 15 publications

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“… 47 The protein content of the diet also influences this promotion by salt of MNNG‐induced gastric carcinogenesis. Following the administration of MNNG and salt, Wistar rats fed an isocaloric low‐protein (10% casein) diet compared with a normal‐protein (25% casein) diet showed increased gastric carcinogenesis, 48 while Wistar rats fed a high‐protein (50% casein) diet showed decreased gastric carcinogenesis compared with those on a normal‐protein (25% casein) diet 49 …”

Section: Dietary Saltmentioning

confidence: 99%

How useful are the rodent animal models of gastric adenocarcinoma?

Pritchard

Przemeck

2004

Aliment Pharmacol Ther

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SUMMARYGastric cancer is the second most common cause of cancer-related mortality world-wide. In most cases, it develops via the pre-malignant stages of atrophic gastritis, intestinal metaplasia and dysplasia, following Helicobacter pylori infection of susceptible individuals. A number of rodent models have recently provided valuable insights into the host, bacterial and environmental factors involved in gastric carcinogenesis. Wildtype rodents do not develop gastric adenocarcinoma, but early studies showed that the disease could be induced in several rodent species by chemical carcinogens. More recently, it has been demonstrated that gastric adenocarcinoma can be induced in Mongolian gerbils by H. pylori infection and in C57BL/6 mice by long-term H. felis infection. These models have allowed the importance of Helicobacter virulence genes, host factors, such as gender, strain and immune response, and environmental factors, such as dietary salt, to be explored. A number of transgenic mice with alterations in various pathways, including the immune response, gastrin biosynthesis, parietal cell development, growth factors and tumour suppressors, have also provided models of various stages of gastric carcinogenesis. One model that has proved to be particularly valuable is the hypergastrinaemic INS-GAS mouse, in which gastric carcinoma develops spontaneously in old animals, but the process is greatly accelerated by Helicobacter infection.

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Section: Dietary Saltmentioning

confidence: 99%

How useful are the rodent animal models of gastric adenocarcinoma?

Pritchard

Przemeck

2004

Aliment Pharmacol Ther

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“…Sodium chloride (NaCl) enhances both the initiation and the promotion stages of experimental gastric carcinogenesis (Takahashi et al, 1984; Tatsuta et al, 1995, 1997). We have found that dietary calcium significantly attenuates NaCl‐enhanced gastric carcinogenesis in Wistar rats (Iishi et al, 1996).…”

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Attenuation by genistein of sodium-chloride-enhanced gastric carcinogenesis induced byN-methyl-N?-nitro-N-nitrosoguanidine in Wistar rats

et al. 1999

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The effects of prolonged administration of genistein, a tyrosine‐kinase inhibitor, on sodium‐chloride‐enhanced induction of gastric carcinogenesis induced by N‐methyl‐N′‐nitro‐N‐nitrosoguanidine, and the labeling and apoptotic indices and vessel counts in the gastric mucosa and gastric cancers, were investigated in Wistar rats. After 25 weeks of the carcinogen treatment, rats were fed chow pellets containing 10% sodium chloride and were given s.c. injections of genistein at dosages of 15 mg/kg or 30 mg/kg body weight every other day. In week 52, the incidence of gastric cancers was significantly greater in rats fed sodium chloride than in untreated control rats. Prolonged administration of genistein at a dosage of 30 mg/kg, but not 15 mg/kg, body weight significantly reduced the incidence of gastric cancers, which was increased by oral treatment with sodium chloride. Genistein at the higher dose significantly decreased the labeling index and vessel counts of the antral mucosa and the gastric cancers (which were increased by treatment with sodium chloride) and significantly increased the apoptotic index of the antral mucosa and the cancers (which was lowered by the treatment with sodium chloride). These findings suggest that genistein attenuates gastric carcinogenesis promoted by sodium chloride, by inducing increased apoptosis and lower cell proliferation and angiogenesis of antral mucosa and gastric cancers. Int. J. Cancer 80:396–399, 1999. © 1999 Wiley‐Liss, Inc.

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