Effect of caloric intake on western-style diet-induced intestinal tumors in a mouse model for hereditary colon cancer

Osamu Itano, Kunhua Fan, Kan Yang, Keiich Suzuki, Fred Quimby, Zhiqian Dong, Bo Jin, Winfried Edelmann, Martin Lipkin

Research output: Contribution to journalArticle

2 Citations (Scopus)

Abstract

Increased caloric intake has been associated with increased risk for cancer of the large intestine. We studied caloric intake effect on tumor formation in Apc1638 N/+ mice, a preclinical model for human familial adenomatous polyposis. Mice were fed a controlled AIN-76A diet or a new Western-style diet (NWD). Intestinal tumor development was evaluated after 6 mo of feeding 1) AIN-76A diet (fed ad libitum) vs. AIN-76A (caloric intake reduced 30%); 2) NWD (fed ad libitum) vs. NWD (caloric intake reduced 30%); and 3) AIN-76A (fed ad libitum) vs. NWD (paired-fed with NWD providing equal caloric intakes to AIN-76A). Intestinal tumor incidences were 78-100% with intergroup variation P > 0.05; however, tumor multiplicity responded differently to dietary treatment: 1) Tumor multiplicity was unchanged after AIN-76A (caloric intake reduced 30% vs. mice fed AIN-76A ad libitum); 2) tumor multiplicity was unchanged after NWD (caloric intake reduced 30% vs. NWD ad libitum); and 3) tumor multiplicity increased 130% after NWD was paired-fed with the same caloric intake as mice fed AIN-76A ad libitum (P < 0.05). Body weights showed no association with tumor development. Findings indicated modified nutrients in NWD were mainly responsible for increased tumors in mice fed NWD vs. AIN-76A in this preclinical mouse model for human FAP.

Original languageEnglish
Pages (from-to)401-408
Number of pages8
JournalNutrition and Cancer
Volume64
Issue number3
DOIs
Publication statusPublished - 2012 Apr 1
Externally publishedYes

Fingerprint

Energy Intake
Colonic Neoplasms
Diet
Neoplasms
Intestinal Neoplasms
Adenomatous Polyposis Coli
Large Intestine
Body Weight
Food

ASJC Scopus subject areas

  • Medicine (miscellaneous)
  • Nutrition and Dietetics
  • Oncology
  • Cancer Research

Cite this

Effect of caloric intake on western-style diet-induced intestinal tumors in a mouse model for hereditary colon cancer. / Itano, Osamu; Fan, Kunhua; Yang, Kan; Suzuki, Keiich; Quimby, Fred; Dong, Zhiqian; Jin, Bo; Edelmann, Winfried; Lipkin, Martin.

In: Nutrition and Cancer, Vol. 64, No. 3, 01.04.2012, p. 401-408.

Research output: Contribution to journalArticle

Itano, O, Fan, K, Yang, K, Suzuki, K, Quimby, F, Dong, Z, Jin, B, Edelmann, W & Lipkin, M 2012, 'Effect of caloric intake on western-style diet-induced intestinal tumors in a mouse model for hereditary colon cancer', Nutrition and Cancer, vol. 64, no. 3, pp. 401-408. https://doi.org/10.1080/01635581.2012.660672
Itano, Osamu ; Fan, Kunhua ; Yang, Kan ; Suzuki, Keiich ; Quimby, Fred ; Dong, Zhiqian ; Jin, Bo ; Edelmann, Winfried ; Lipkin, Martin. / Effect of caloric intake on western-style diet-induced intestinal tumors in a mouse model for hereditary colon cancer. In: Nutrition and Cancer. 2012 ; Vol. 64, No. 3. pp. 401-408.
@article{9d15e85488b447cf80afaa697f246818,
title = "Effect of caloric intake on western-style diet-induced intestinal tumors in a mouse model for hereditary colon cancer",
abstract = "Increased caloric intake has been associated with increased risk for cancer of the large intestine. We studied caloric intake effect on tumor formation in Apc1638 N/+ mice, a preclinical model for human familial adenomatous polyposis. Mice were fed a controlled AIN-76A diet or a new Western-style diet (NWD). Intestinal tumor development was evaluated after 6 mo of feeding 1) AIN-76A diet (fed ad libitum) vs. AIN-76A (caloric intake reduced 30{\%}); 2) NWD (fed ad libitum) vs. NWD (caloric intake reduced 30{\%}); and 3) AIN-76A (fed ad libitum) vs. NWD (paired-fed with NWD providing equal caloric intakes to AIN-76A). Intestinal tumor incidences were 78-100{\%} with intergroup variation P > 0.05; however, tumor multiplicity responded differently to dietary treatment: 1) Tumor multiplicity was unchanged after AIN-76A (caloric intake reduced 30{\%} vs. mice fed AIN-76A ad libitum); 2) tumor multiplicity was unchanged after NWD (caloric intake reduced 30{\%} vs. NWD ad libitum); and 3) tumor multiplicity increased 130{\%} after NWD was paired-fed with the same caloric intake as mice fed AIN-76A ad libitum (P < 0.05). Body weights showed no association with tumor development. Findings indicated modified nutrients in NWD were mainly responsible for increased tumors in mice fed NWD vs. AIN-76A in this preclinical mouse model for human FAP.",
author = "Osamu Itano and Kunhua Fan and Kan Yang and Keiich Suzuki and Fred Quimby and Zhiqian Dong and Bo Jin and Winfried Edelmann and Martin Lipkin",
year = "2012",
month = "4",
day = "1",
doi = "10.1080/01635581.2012.660672",
language = "English",
volume = "64",
pages = "401--408",
journal = "Nutrition and Cancer",
issn = "0163-5581",
publisher = "Routledge",
number = "3",

}

TY - JOUR

T1 - Effect of caloric intake on western-style diet-induced intestinal tumors in a mouse model for hereditary colon cancer

AU - Itano, Osamu

AU - Fan, Kunhua

AU - Yang, Kan

AU - Suzuki, Keiich

AU - Quimby, Fred

AU - Dong, Zhiqian

AU - Jin, Bo

AU - Edelmann, Winfried

AU - Lipkin, Martin

PY - 2012/4/1

Y1 - 2012/4/1

N2 - Increased caloric intake has been associated with increased risk for cancer of the large intestine. We studied caloric intake effect on tumor formation in Apc1638 N/+ mice, a preclinical model for human familial adenomatous polyposis. Mice were fed a controlled AIN-76A diet or a new Western-style diet (NWD). Intestinal tumor development was evaluated after 6 mo of feeding 1) AIN-76A diet (fed ad libitum) vs. AIN-76A (caloric intake reduced 30%); 2) NWD (fed ad libitum) vs. NWD (caloric intake reduced 30%); and 3) AIN-76A (fed ad libitum) vs. NWD (paired-fed with NWD providing equal caloric intakes to AIN-76A). Intestinal tumor incidences were 78-100% with intergroup variation P > 0.05; however, tumor multiplicity responded differently to dietary treatment: 1) Tumor multiplicity was unchanged after AIN-76A (caloric intake reduced 30% vs. mice fed AIN-76A ad libitum); 2) tumor multiplicity was unchanged after NWD (caloric intake reduced 30% vs. NWD ad libitum); and 3) tumor multiplicity increased 130% after NWD was paired-fed with the same caloric intake as mice fed AIN-76A ad libitum (P < 0.05). Body weights showed no association with tumor development. Findings indicated modified nutrients in NWD were mainly responsible for increased tumors in mice fed NWD vs. AIN-76A in this preclinical mouse model for human FAP.

AB - Increased caloric intake has been associated with increased risk for cancer of the large intestine. We studied caloric intake effect on tumor formation in Apc1638 N/+ mice, a preclinical model for human familial adenomatous polyposis. Mice were fed a controlled AIN-76A diet or a new Western-style diet (NWD). Intestinal tumor development was evaluated after 6 mo of feeding 1) AIN-76A diet (fed ad libitum) vs. AIN-76A (caloric intake reduced 30%); 2) NWD (fed ad libitum) vs. NWD (caloric intake reduced 30%); and 3) AIN-76A (fed ad libitum) vs. NWD (paired-fed with NWD providing equal caloric intakes to AIN-76A). Intestinal tumor incidences were 78-100% with intergroup variation P > 0.05; however, tumor multiplicity responded differently to dietary treatment: 1) Tumor multiplicity was unchanged after AIN-76A (caloric intake reduced 30% vs. mice fed AIN-76A ad libitum); 2) tumor multiplicity was unchanged after NWD (caloric intake reduced 30% vs. NWD ad libitum); and 3) tumor multiplicity increased 130% after NWD was paired-fed with the same caloric intake as mice fed AIN-76A ad libitum (P < 0.05). Body weights showed no association with tumor development. Findings indicated modified nutrients in NWD were mainly responsible for increased tumors in mice fed NWD vs. AIN-76A in this preclinical mouse model for human FAP.

UR - http://www.scopus.com/inward/record.url?scp=84859757533&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84859757533&partnerID=8YFLogxK

U2 - 10.1080/01635581.2012.660672

DO - 10.1080/01635581.2012.660672

M3 - Article

VL - 64

SP - 401

EP - 408

JO - Nutrition and Cancer

JF - Nutrition and Cancer

SN - 0163-5581

IS - 3

ER -