Faculty Opinions recommendation of Coagulation induced by C3aR-dependent NETosis drives protumorigenic neutrophils during small intestinal tumorigenesis.

We studied how obesogenic conditions during various life periods affected obesity and intestinal tumorigenesis in adult C57BL/6J-Min(multiple intestinal neoplasia)/+ mice. The mice were given a 10% fat diet throughout life (negative control) or a 45% fat dietin utero, during nursing, during bothin uteroand nursing, during adult life, or during their whole life-span, and terminated at 11 weeks for tumorigenesis (Min/+) or 23 weeks for obesogenic effect (wild-type). Body weight at 11 weeks was increased after a 45% fat diet during nursing, during bothin uteroand nursing, and throughout life, but had normalized at 23 weeks. In the glucose tolerance test, the early exposure to a 45% fat dietin utero, during nursing, or during bothin uteroand nursing, did not affect blood glucose, whereas a 45% fat diet given to adults or throughout life did. However, a 45% fat diet during nursing or duringin uteroand nursing increased the number of small intestinal tumors. So did exposures to a 45% fat diet in adult life or throughout life, but without increasing the tumor numbers further. The intrauterine and nursing period is a window of susceptibility for dietary fat-induced obesity and intestinal tumor development.

Download Full-text

IL-17F deficiency inhibits small intestinal tumorigenesis in ApcMin/+ mice

Biochemical and Biophysical Research Communications ◽

10.1016/j.bbrc.2011.09.016 ◽

2011 ◽

Vol 414 (1) ◽

pp. 31-36 ◽

Cited By ~ 31

Author(s):

Wook-Jin Chae ◽

Alfred L.M. Bothwell

Keyword(s):

Intestinal Tumorigenesis ◽

Small Intestinal

Download Full-text

Genetic and Diet-Induced Obesity Increased Intestinal Tumorigenesis in the Double Mutant Mouse Model Multiple Intestinal Neoplasia X Obese via Disturbed Glucose Regulation and Inflammation

Journal of Obesity ◽

10.1155/2015/343479 ◽

2015 ◽

Vol 2015 ◽

pp. 1-21 ◽

Cited By ~ 4

Author(s):

Ha Thi Ngo ◽

Ragna Bogen Hetland ◽

Unni Cecilie Nygaard ◽

Inger-Lise Steffensen

Keyword(s):

Glucose Regulation ◽

Wild Type ◽

Intestinal Tumors ◽

Intestinal Tumorigenesis ◽

Diet Induced Obesity ◽

Intestinal Neoplasia ◽

Gene Coding ◽

Induced Tumors ◽

Small Intestinal ◽

Double Mutant Mouse

We have studied how spontaneous or carcinogen-induced intestinal tumorigenesis was affected by genetic or diet-induced obesity in C57BL/6J-ApcMin/+X C57BL/6J-Lepob/+mice. Obesity was induced by theobese(ob) mutation in thelepgene coding for the hormone leptin, or by a 45% fat diet. The effects of obesity were examined on spontaneous intestinal tumors caused by themultiple intestinal neoplasia(Min) mutation in theadenomatous polyposis coli(Apc) gene and on tumors induced by the dietary carcinogen 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP). F1 ob/ob (homozygous mutated) mice had increased body weight (bw) and number of spontaneous and PhIP-induced small intestinal tumors (inApcMin/+mice), versus ob/wt (heterozygous mutated) and wt/wt mice (homozygous wild-type). A 45% fat diet exacerbated bw and spontaneous tumor numbers versus 10% fat, but not PhIP-induced tumors. Except for bw, ob/wt and wt/wt were not significantly different. The obesity caused hyperglucosemia and insulinemia in ob/ob mice. A 45% fat diet further increased glucose, but not insulin. Inflammation was seen as increased TNFαlevels in ob/ob mice. Thus the results implicate disturbed glucose regulation and inflammation as mechanisms involved in the association between obesity and intestinal tumorigenesis. Ob/ob mice had shorter lifespan than ob/wt and wt/wt mice.

Download Full-text

The impact of commercial rodent diets on the induction of tumours and flat aberrant crypt foci in the intestine of multiple intestinal neoplasia mice

Laboratory Animals ◽

10.1258/la.2012.011055 ◽

2012 ◽

Vol 46 (3) ◽

pp. 207-214 ◽

Cited By ~ 6

Author(s):

Camilla Svendsen ◽

Jan Alexander ◽

Jan Erik Paulsen ◽

Helle K Knutsen ◽

Hege Hjertholm ◽

...

Keyword(s):

Small Intestine ◽

Mouse Model ◽

Precancerous Lesions ◽

Aberrant Crypt Foci ◽

Intestinal Tumorigenesis ◽

Tumour Development ◽

Intestinal Neoplasia ◽

Small Intestinal ◽

The Impact ◽

Colonic Tumours

A large variation in spontaneous tumour development in the multiple intestinal neoplasia (Min) mouse model between laboratories has been reported. The composition of the diet might be an important factor. We examined the impact of five commercial rodent diets: the natural ingredient breeding diet Harlan Teklad 2018 (HT), the purified breeding diet AIN93G, the natural ingredient maintenance diet RM1, and the purified maintenance diets AIN93M and AIN76A, on the spontaneous intestinal tumorigenesis in the Min mouse model. The Min mice were fed one of two breeding diets during gestation and until four weeks of age, thereafter one of the three maintenance diets. Min mice bred on the breeding diet HT had significantly higher numbers and incidences of tumours in the colon, but fewer tumours in the small intestine than the breeding diet AIN93G. The maintenance diet RM1 gave a significantly higher number of small intestinal and colonic tumours and precancerous lesions called flat aberrant crypt foci (ACF) compared with the maintenance diets AIN93M and AIN76A. These findings show the importance of defining the type of diet used in experimental intestinal carcinogenesis studies, and that the diet should be taken into consideration when comparing results from different studies with Min mice.

Download Full-text