Promoting effects of high-fat corn oil and high-fat mixed lipid diets on 7,12-dimethylbenz[a]anthracene-induced mammary tumorigenesis in F344 rats.
Epidemiological studies and laboratory animal model assays suggest that a high intake of dietary fat promotes mammary carcinogenesis as well as colon tumorigenesis. Fat intake in the United States traditionally includes high amounts (30% of total caloric intake) of saturated fatty acids (SFAs) compared to polyunsaturated fatty acids (PUFAs). A recent study suggested that a high-fat mixed-lipid diet (HFML), which simulates the mixed-lipid and high SFAs composition of the average American diet, strongly promotes rat colon carcinogenesis, even when compared to another high-fat diet containing PUFA-rich corn oil. On the other hand, some reports suggest that a high-fat diet rich in n-6 PUFAs promotes mammary carcinogenesis more strongly than a high-fat diet rich in SFAs. Therefore, the present study was designed to compare the effects of HFML, high-fat corn oil diet (HFCO) that is rich in n-6 PUFAs, and a low-fat corn oil diet (LFCO) on 7,12-dimethylbenz[a]anthracene (DMBA)-induced mammary carcinogenesis in female F344 rats. At 7 weeks of age, female F344 rats intended for carcinogen treatment received a gavage of DMBA at a dose level of 65 mg/kg of body weight. Beginning 1 week after carcinogen treatment, groups of rats were then maintained on experimental diets containing LFCO, HFCO or HFML. All rats were evaluated weekly by palpation of mammary tumors and sacrificed 20 weeks after the DMBA treatment. Palpable tumors of mammary glands were detected at the 8, 11, and 19 weeks in the HFCO, HFML and LFCO groups, respectively. Histopathological observation revealed that the incidence and number of mammary tumors in the HFCO group were significantly higher than in the LFCO group. Rats on the HFML diet tended towards a higher incidence and number of mammary tumors compared with the LFCO group, although the correlation was not statistically significant. These results suggest that, for this animal model, both the HFCO and HFML diets promote DMBA-induced mammary carcinogenesis when compared to the LFCO diet, and that the HFCO diet is more tumor-promotional than the HFML diet.
Kuno
Toshiya
T
Department of Pathology, Gifu University School of Medicine, 40 Tsukasa-Machi, Gifu 500-8705, Japan. tkuno@cc.gifu-u.ac.jp
Hirose
Yoshinobu
Y
Yamada
Yasuhiro
Y
Yoshida
Koujirou
K
Qiao
Zheng
Z
Katayama
Masaki
M
Sakata
Keiko
K
Hara
Akira
A
Sugie
Shigeyuki
S
Mori
Hideki
H
D015127:9,10-Dimethyl-1,2-benzanthracene / Q000633:toxicity; D000818:Animals; D001835:Body Weight / Q000187:drug effects; D003043:Cocarcinogenesis; D003314:Corn Oil / Q000009:adverse effects*; D004041:Dietary Fats / Q000009:adverse effects*; D005260:Female; D008055:Lipids / Q000009:adverse effects*; D008325:Mammary Neoplasms, Experimental / Q000139:chemically induced* / Q000473:pathology; D051381:Rats; D011916:Rats, Inbred F344
D004041:Dietary Fats; D008055:Lipids; D015127:9,10-Dimethyl-1,2-benzanthracene; D003314:Corn Oil