Increase in dietary protein content exacerbates colonic inflammation and tumorigenesis in azoxymethane-induced mouse colon carcinogenesis
1
조회
0
다운로드
3
인용
0
참고문헌
키워드
초록
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.
Abstract
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.
참고문헌 (46)
- Food, Nutrition, Physical Activity, and the Prevention of Cancer: a Global Perspective, "World Cancer Research Fund", WCRF, 2007
- Haggar FA, "Colorectal cancer epidemiology: incidence, mortality, survival, and risk factors", Clin Colon Rectal Surg, 22, pp.191~197 (2009)
- Boyle P, "ABC of colorectal cancer: epidemiology", BMJ, 321, pp.805~808 (2000)
- Armstrong B, "Environmental factors and cancer incidence and mortality in different countries, with special reference to dietary practices", Int J Cancer, 15, pp.617~631 (1975)
- Chao A, "Meat consumption and risk of colorectal cancer", JAMA, 293, pp.172~182 (2005)
- Young GP, "Preventing cancer: dietary lifestyle or clinical intervention?", Asia Pac J Clin Nutr, 11(Suppl 3), pp.S618~S631 (2002)
- Kim E, "Review of the association between meat consumption and risk of colorectal cancer", Nutr Res, 33, pp.983~994 (2013)
- Toden S, "Resistant starch attenuates colonic DNA damage induced by higher dietary protein in rats", Nutr Cancer, 51, pp.45~51 (2005)
- Toden S., "Resistant starch prevents colonic DNA damage induced by high dietary cooked red meat or casein in rats", Cancer Biol Ther, 5, pp.267~272 (2006)
- Toden S, "Differential effects of dietary whey, casein and soya on colonic DNA damage and large bowel SCFA in rats fed diets low and high in resistant starch", Br J Nutr, 97, pp.535~543 (2007)
- Andriamihaja M, "Colon luminal content and epithelial cell morphology are markedly modified in rats fed with a high-protein diet", Am J Physiol Gastrointest Liver Physiol, 299, pp.G1030~G1037 (2010)
- Terzić J, "Inflammation and colon cancer", Gastroenterology, 138, pp.2101~2114 (2010)
- Eaden JA, "The risk of colorectal cancer in ulcerative colitis: a meta-analysis", Gut, 48, pp.526~535 (2001)
- Danese S, "Inflammatory bowel disease and intestinal cancer: a paradigm of the Yin-Yang interplay between inflammation and cancer", Oncogene, 29, pp.3313~3323 (2010)
- Becker C, "TGF-beta suppresses tumor progression in colon cancer by inhibition of IL-6 trans-signaling", Immunity, 21, pp.491~501 (2004)
- Mazzucchelli L, "Differential in situ expression of the genes encoding the chemokines MCP-1 and RANTES in human inflammatory bowel disease", J Pathol, 178, pp.201~206 (1996)
- Noguchi M, "Secretion imbalance between tumour necrosis factor and its inhibitor in inflammatory bowel disease", Gut, 43, pp.203~209 (1998)
- Mantovani A, "Cancer-related inflammation", Nature, 454, pp.436~444 (2008)
- Byun SY, "Curcumin ameliorates the tumor-enhancing effects of a high-protein diet in an azoxymethane-induced mouse model of colon carcinogenesis.", Nutr Res, 35, pp.726~735 (2015)
- Cooper HS, "Clinicopathologic study of dextran sulfate sodium experimental murine colitis", Lab Invest, 69, pp.238~249 (1993)
- Okayasu, I., "A novel method in the induction of reliable experimental acute and chronic ulcerative colitis in mice", Gastroenterology, 98, pp.694~702 (1990)
- Okayasu I, "Promotion of colorectal neoplasia in experimental murine ulcerative colitis", Gut, 39, pp.87~92 (1996)
- Okayasu I, "Dysplasia and carcinoma development in a repeated dextran sulfate sodium-induced colitis model", J Gastroenterol Hepatol, 17, pp.1078~1083 (2002)
- Fiocchi C., "Inflammatory bowel disease: etiology and pathogenesis", Gastroenterology, 115, pp.182~205 (1998)
- Kwon HS, "Glabridin, a functional compound of liquorice, attenuates colonic inflammation in mice with dextran sulphate sodium-induced colitis", Clin Exp Immunol, 151, pp.165~173 (2008)
- Huang YF, "Anti-inflammatory effects of Brucea javanica oil emulsion by suppressing NFkappaB activation on dextran sulfate sodium-induced ulcerative colitis in mice", J Ethnopharmacol, 198, pp.389~398 (2017)
- Wang D, "Eicosanoids and cancer", Nat Rev Cancer, 10, pp.181~193 (2010)
- Philip M, "Inflammation as a tumor promoter in cancer induction", Semin Cancer Biol, 14, pp.433~439 (2004)
- Itzkowitz SH, "Inflammation and cancer IV. Colorectal cancer in inflammatory bowel disease: the role of inflammation", Am J Physiol Gastrointest Liver Physiol, 287, pp.G7~G17 (2004)
- Tatsuta M, "Enhanced induction of colon carcinogenesis by azoxymethane in Wistar rats fed a low-protein diet", Int J Cancer, 50, pp.108~111 (1992)
- Fleming SE, "Intestinal cell proliferation is influenced by intakes of protein and energy, aflatoxin, and whole-body radiation", Nutr Cancer, 22, pp.11~30 (1994)
- Toden S, "High red meat diets induce greater numbers of colonic DNA double-strand breaks than white meat in rats: attenuation by high-amylose maize starch", Carcinogenesis, 28, pp.2355~2362 (2007)
- Daniel CR, "Prospective investigation of poultry and fish intake in relation to cancer risk", Cancer Prev Res (Phila), 4, pp.1903~1911 (2011)
- Windey K, "Relevance of protein fermentation to gut health", Mol Nutr Food Res, 56, pp.184~196 (2012)
- Liu X, "High-protein diet modifies colonic microbiota and luminal environment but not colonocyte metabolism in the rat model: the increased luminal bulk connection", Am J Physiol Gastrointest Liver Physiol, 307, pp.G459~G470 (2014)
- Lan A, "Dual effects of a high-protein diet on DSS-treated mice during colitis resolution phase", Am J Physiol Gastrointest Liver Physiol, 311, pp.G624~G633 (2016)
- McConnell BB, "The role of inflammation in the pathogenesis of colorectal cancer", Curr Colorectal Cancer Rep, 5, pp.69~74 (2009)
- Sinicrope FA, "Role of cyclooxygenase-2 in colorectal cancer", Cancer Metastasis Rev, 23, pp.63~75 (2004)
- Lala PK, "Role of nitric oxide in carcinogenesis and tumour progression", Lancet Oncol, 2, pp.149~156 (2001)
- Takahashi M, "Increased expression of inducible and endothelial constitutive nitric oxide synthases in rat colon tumors induced by azoxymethane", Cancer Res, 57, pp.1233~1237 (1997)
- Eberhart CE, "Up-regulation of cyclooxygenase 2 gene expression in human colorectal adenomas and adenocarcinomas", Gastroenterology, 107, pp.1183~1188 (1994)
- Cianchi F, "Inducible nitric oxide synthase expression in human colorectal cancer: correlation with tumor angiogenesis", Am J Pathol, 162, pp.793~801 (2003)
- Sun Y, "Cyclooxygenase-2overexpression reduces apoptotic susceptibility by inhibiting the cytochrome c-dependent apoptotic pathway in human colon cancer cells", Cancer Res, 62, pp.6323~6328 (2002)
- Li G, "Cyclooxygenase-2 increased the angiogenic and metastatic potential of tumor cells", Biochem Biophys Res Commun, 299, pp.886~890 (2002)
- Tsujii M, "Cyclooxygenase regulates angiogenesis induced by colon cancer cells", Cell, 93, pp.705~716 (1998)
- Rao CV, "Nitric oxide signaling in colon cancer chemoprevention", Mutat Res, 555, pp.107~119 (2004)