• Journal of Nutrition and Health
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• v.27 no.6
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• pp.552-562
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• 1994

The study was designed to observe the effect of different dietary fats on the incidence of colorectal tumor and in vivo cell proliferation in colon carcinogenesis. Male Sprague Dawley rats were intrarectally infused with chemical carcinogen(methylnitrosourea, MNU) and fed 16%(w/w) fat diet containing one of dietary fats(beef tallow, corn oil, perilla oil) for 30 weeks. To measure in vivo cell proliferation, the incorporation of 5-bromo-2-deoxyuridine(BrdU) into DNA was localized using the monoclonal anti-BrdU antibody. Large number of tumors were found in the distal colon and tumor incidence was increased in the order of perilla oil(57.7%)$\alpha$-linolenic acid rich in perilla oil could have a protective effect against colon cancer compared to saturated fatty acid or n-6 linoleic acid.

• Journal of Nutrition and Health
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• v.31 no.4
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• pp.697-707
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• 1998

This study was designed to observe the effect of dietary fiber and fat on colon tumor incidence and cell proliferation. Male Sqraue Dawley rats(n=225) at 7 weeks of age, were divided into 3 groups depending on the type of fat b(beef tallow, corn oil and DHA-rich fish oil) and each group was again divided into 3 groups depending on type of fiber(fiber-free, perctin and cellulose) . The experimental diet containing dietary fat at 15%(w/w) and fiber at 6%(w/w) levels was fed for 25 weeks. At the same time, each rats was intramuscularly injected with DMH two times a week for 6 weeks to geive total dose of 180mg/kg body weight. Cell proliferation was measured by in vivo incroporation of bromodeoxyuridine (BrdU) into DNA. Fish oil decreased the tumor incidence (9.67%) compared with beef talow (33.39%) and corn oil (21.21%). Tumor incidence was decreased in all groups that fed cellulose (11.67%) compared with those of fiber-free(21.74%) and pectic(19.70%). Most of tumors was distributed at the site of the distal colon. The rats fed both fish oil and cellulose significantly decreased th enumber of tumors and tumor incidence compared to other groups. Fish oil was more effective in preventing cell prolofieration by decreasing crypt length and labeling index(LI) compared with beef tallow(p<0.05). Cell proliferation in distal colon was more developed to the upper part of the crypt compared to proximal colon. Overall tumor incidence and cell proliferation were more affected by dietary fat. But the effect of dietary fiber was different depending on type of fat in the experimental diet. These results suggest that a DHA -rich fish oil may has more decisive effect in inhibiting the cell proliferation in colon.

• Nutritional Sciences
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• v.4 no.2
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• pp.73-78
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• 2001

This study investigated the effect of different dietary fats and fibers on colon tumor incidence and cell proliferation, the levels of eicosanoids and polyamines in colonic mucosa of DMH-treated rats. The experiment was conducted on male Sprague Dawley rats using a 2 $\times$3 factorial design with two fats (corn oil and DHA-rich fish oil) and two fibers (cellulose and pectin) and a fiber-free control. The rats were find an experimental diet containing 15% (w/w) dietary fat and 6% (w/w) fiber for 25 weeks. Tumor incidence was Bower in rats fed fish oil as opposed to corn oil. The levels of arachidonic acid (AA) and eicosanoids ($PGE_2, and TXB_2$) in normal colonic mucosa were significantly lower in rats fed fish oil and there was a concomitant increase of docosahexaenoic acid (DHA). The levels of eicosanoids and AA in tumor tissues were significantly higher than those of normal colonic mucosa. The level of polyamines in normal colonic mucosa was not affected by dietary fats but was significantly lower than that in rumor tissues. Dietary fiber did not have a significant effect on rumor incidence and the levels of AA, eicosanoids and polyamines. Overall, fish oil rich in DHA reduced cell prolifiration and thus inhibited colon carcinogenesis through its effect on the distribution of AA and production of eicosanoids in normal colonic mucosa. However, its effect on colon carcinogenesis revealed a lack of consistency depending on the type of dietary fiber in diet.

• Journal of Nutrition and Health
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• v.33 no.6
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• pp.632-638
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• 2000

This study was designed to observe the effect of green tea on colon tumor incidence and biomarkers of colon carcinogenesis in 1, 2-dimethlhydrazine-treated rats. Male Sprague Dawley rats at 7 weeks of age were divided into two groups: control and green tea(GT) groups. Control rats had distilled water as drinking water but GT group received green tea extracts(2.5%, w/v water) as drinking water throughout the experiment periods. All rats were fed the experimental diet containing 15% fat by weight for 20 weeks. and were i.m. injected with DMH for 6 weeks to give total dose of 180mg/kg body weight. Tumor incidence was reduced in GT group (39%) compared with control group (56%) Green tea significantly reduced cell proliferation (total cells per crypt, crypt length and proliferative zone) in colonic mucosa and also significantly reduced the levels of preformed prostalandin E2(PGE2) and thromboxance B2(TXB2) in colonic mucosa but the fatty acid profile of total lipid in colonic mucosa was not significantly influenced by green tea. However the relative percent of C20:4 and the levels f preformed PGE2 and TXB2. were significantly higher in tumor tissue compared with normal surrounding mucosa.Green tea increased the fecal excretion of total bile acid but not scondary bile acid which is known as one of promoters for colon cancer,. These results suggest that green tea could have preventive effect against colon cancer when consumed daily by influencing on antioxidant effect and the metabolism of arachidonic acid.

• Nutritional Sciences
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• v.2 no.2
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• pp.71-75
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• 1999

Epidemiologic studies consistently demonstrate an inverse relationship between risk for colon canter and consumption of fruits and vegetables. Wheat bran, flax and soy contain dietary fiber and phytochemicals, such as lignans and isoflavones, that may inhibit colon carcinogenesis. Orange juice contains hesperidin, a flavanone glucoside that protects against colon carcinogenesis. This study determined if feeding orange juice, wheat bran, soy and flaxseed (combined diet) would inhibit azoxymethane (AOM) induced colon cancer. Cancer was initiated in male Fisher 344 rats by injecting 15 mg AOM/kg of weight at 22 and 29 days of age. One week after the second AOM injection, rats (N = 30) in the combined diet group received dry diet containing wheat bran (4%), soy with ethanol soluble phytochemirals(13%) and flaxseed (8%) and orange juice replaced drinking water. The control group remained on the control diet and received distilled water to drink. The rats were killed 28 weeks later, and colon tissues and tumors were removed for histologic analysis. Feeding the combined diet significantly reduced tumor incidence (p < 0.05), however tumor multiplicity was not changed (p > 0.05, 0.9 tumors/rat fed the combined diet vs 1.2 for controls). Also, tumor burden was only marginally reduced in rats fed the combined diet vs control rats (65 vs 210 mg of tumor/rats, respectively). The reduction in tumor incidence was associated with a decreased labeling index and proliferation zone in normal appearing colon mucosa. Therefore, this study shows that phytochemicals in wheat bran, soy, flax and orange juice reduce colon carcinogenesis, presumably by decreasing cell proliferation and enhancing cell differentiation.

• Journal of Nutrition and Health
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• v.35 no.10
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• pp.1038-1044
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• 2002

The study was designed to observe the effect of conjugated linoleic acid (CLA) on tumor incidence, eicosanoid formation and antioxidant enzyme activities in colonic mucosa and the fecal excretion of deoxycholic acid and lithocholic acid in 1,2-dimethylhydrazine (DMH)-treated rats. One hundred twenty male Sprague Dawley rats were divided into 2 groups, BT (beef tallow diet) group and FO (fish oil diet) group, and each group was again subdivided into 2 groups depending on CLA supplementation, i.e.4 groups of BT, BTC, FO, FOC. All rats were fed experimental diet for 30 weeks, which contained 12% (wt/wt) total dietary fat including 1% (wt/wt) CLA, and were intramuscularly injected with DMH for 6 weeks to give total dose of 180 mg/kg body. CLA-supplemented to BT and FO diet reduced tumor incidence, eicosanoid (PGE$_2$ and TXA$_2$) level in colonic mucosa. N-3 fatty acids (mainly DHA) of fish oil diet (FO, FOC group) also reduced tumor incidence and significantly reduced eicosanoid (PGE$_2$ and TXA$_2$) level in colonic mucosa. CLA supplementation and n-3 fatty acid significantly increased colonic mucosal level of superoxide dismutase and glutathione peroxidase activities but reduced secondary bile acids (deoxycholic acid and lithocholic acid) excretion in the feces. In conclusion, CLA supplementation and n-3 fatty acid could reduce tumor incidence by reducing eicosanoids and increasing antioxidant enzyme activities in colon and decreasing the excretion of deoxycholic acid and lithocholic acid in the feces. The data might suggest that CLA supplementation and n-3 DHA rich fish oil may modulate colon carcinogenesis.termediate level of endurance exercise training for 6 weeks did not influence concentrations of most of free amino acid in soleus muscle of rats collected at an overnight fasted and rested state. In contrast, isolucine and leucine concentrations in extensor digitorum longus muscle of exercise-trained rats were significantly lower than those for control animals. These results indicate that aerobic energy metabolism had not been efficiently conducted, and thereby the utilization of BCAA for energy substrate was enhanced in fast twitch oxidative glycolytic fibers of extensor digitorum longus muscle of rats followed exercise-training protocol for 6 weeks.

• Journal of Food Hygiene and Safety
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• v.26 no.4
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• pp.388-397
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• 2011

Selenium (Se) is known to prevent from several cancers, while iron (Fe) is known to be associated with high risk of cancers. The role of Se on colon carcinogenesis was investigated in an animal model induced by azoxymethane (AOM) and dextran sodium sulfate (DSS) in low Fe mice. Six-week old ICR mice fed on a low Fe diet (4.5 ppm Fe; generally 10 times lower than normal Fe) with three different Se (0.02, 0.1 or 0.5 ppm) levels for 24 weeks. The animals received weekly three ($0{\sim}2^{nd}$ weeks) i.p. injections of AOM (10 mg/kg RW), followed by 2% DSS with drinking water for 1 week to induce the colon cancer. There were five experimental groups including vehicle, positive control (normal Fe level, AOM/DSS), Low Fe (LFe) + AOM/DSS+Low Se (LSe), LFe + AOM/DSS + medium Se (MSe) and LFe + AOM/DSS + high Se (HSe) groups. HSe group showed a 66.7% colonic tumor incidence, MSe group showed a 69.2% tumor incidence, and LSe group showed a 80.0% tumor incidence. The tumor incidence was negatively associated with Se levels of diets. Tumor multiplicity in Hse group was significantly low compared to the other groups (p < 0.05). With increasing Se levels of diets, the primary anti-proliferating cell nuclear antigen (PCNA)-positive cells were decreased and apoptotic bodies were increased in a dose-dependent manner. Se-dependent glutathione peroxidase activity and its protein level were dependent on the levels of Se of diets. Malondialdehyde level in liver was lowest in Hse group among experimental groups. These findings indicate that dietary Se is chemopreventive for colon cancer by increasing antioxidant activity and decreasing cell proliferation in Fe-deficient mice.

• Journal of Nutrition and Health
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• v.26 no.7
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• pp.829-838
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• 1993

This study was designed to compare the effect of different dietary fats on the incidence of colorectal tumor, the level of plasma thromboxane B2(TXB2) and fatty acid profiles of platelet and colonic mucosal lipids in N - methyl - N - nitro - N - nitrosoguanidine(MNNG) - treated rats. Male Sprague Dawley rats, at 8 weeks old, were divided into 2 groups and infused intrarectally with saline(control group) or with 2mg MNNG(carcinogen-treated group) twice a week for 3 weeks. Each group was again divided into 4 groups and fed one of four diets(BT, CO, PO, FO) containing dietary fat at 9%(w/w) level for 37 weeks, Dietary fats were beef tallow(7.2%)+corn oil(1.8%) for BT, corn oil(9.0%) for CO, perilla oil(9.0%) for PO, fish oil (6.5%)+corn oil (2.5%) for FO diets. MNNG-treated rats had colonic tumor, while no tumors(adenocarcinoma and adenoma) than others. Tumor sizes in BT-MNNG rats ranged from 2mm papillary form to 15mm of polypoid. However, the size of tumors in PO-MNNG or FO-MNNG rats could not be measured by gross examination. BT-MNNG and CO-MNNG groups were higher in the level of plasma TXB2 and the ratio of c20 : 4/c20 :5 platelet. PO-MNNG groups were lower in the ratio of c20 : 4/c20 : 5(p<0.05) in fatty acid of colonic mucosal lipids suggesting that perilla oil and fish oil could reduce the level of PGE2 and TXB2 by modifying its precursor content and restrain tumor promotion in colon. Effect of perilla oil rich in $\alpha$-linolenic acid on colon carcinogenesis was similar to that of fish oil and thus perilla oil could have a protective effect against colon cancer possibly by inhibiting the production of arachidonic acid metabolite.

• Nutrition Research and Practice
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• v.11 no.4
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• pp.281-289
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• 2017

BACKGROUND/OBJECTIVE: The incidence of colorectal cancer (CRC) has been attributed to higher intake of fat and protein. However, reports on the relationship between protein intake and CRC are inconsistent, possibly due to the complexity of diet composition. In this study, we addressed a question whether alteration of protein intake is independently associated with colonic inflammation and colon carcinogenesis. MATERIALS/METHODS: Balb/c mice were randomly divided into 4 experimental groups: 20% protein (control, 20P, 20% casein/kg diet), 10% protein (10P, 10% casein/kg diet), 30% protein (30P, 30% casein/kg diet), and 50% protein (50P, 50% casein/kg diet) diet groups and were subjected to azoxymethane-dextran sodium sulfate induced colon carcinogenesis. RESULTS: As the protein content of the diet increased, clinical signs of colitis including loss of body weight, rectal bleeding, change in stool consistency, and shortening of the colon were worsened. This was associated with a significant decrease in the survival rate of the mice, an increase in proinflammatory protein expression in the colon, and an increase in mucosal cell proliferation. Further, colon tumor multiplicity was dramatically increased in the 30P (318%) and 50P (438%) groups compared with the control (20P) group. CONCLUSIONS: These results suggest that a high protein diet stimulates colon tumor formation by increasing colonic inflammation and proliferation.

• Journal of Digestive Cancer Research
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• v.1 no.1
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• pp.6-16
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• 2013

Recent estimates for colon cancer incidence in Korea have been increased and continue to rank as the second most common in male and the third in female. Although colonoscopy has been known as the best screening tool for colon cancer, 20-25% of patients with colon cancer was diagnosed with stage IV cancer. During the past 10 years, intensive clinical studies helped to establish the value of palliative treatment for colon cancer with metastasis. The introduction of new chemotherapeutic agents such as irinotecan and oxaliplatin has led to a significant increase in tumor response and median survival. In advanced colon cancer, impressive prolongation or overall survival can be achieved through sequential application of combined systemic chemotherapy. In addition, targeted manipulation of molecular tumor mechanisms with new substances such as monoclonal antibodies against the epidermal growth factor receptor or vascular endothelial growth factor shows promising effects. Progress in the systemic treatment of colon cancer is evident, not only because of the significant increase in life expectancy in advanced colon cancer.