scholarly journals 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

2015 ◽  
Vol 2015 ◽  
pp. 1-21 ◽  
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.

scholarly journals The Intrauterine and Nursing Period Is a Window of Susceptibility for Development of Obesity and Intestinal Tumorigenesis by a High Fat Diet inMin/+Mice as Adults

2015 ◽  
Vol 2015 ◽  
pp. 1-25
Author(s):  
Ha Thi Ngo ◽  
Ragna Bogen Hetland ◽  
Inger-Lise Steffensen
Keyword(s):  
High Fat Diet ◽  
Tumor Development ◽  
Adult Life ◽  
Tolerance Test ◽  
In Utero ◽  
Negative Control ◽  
Wild Type ◽  
Intestinal Tumorigenesis ◽  
Intestinal Neoplasia ◽  
Small Intestinal

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.

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

2012 ◽  
Vol 46 (3) ◽  
pp. 207-214 ◽  
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.

scholarly journals Primary Small Intestinal Sarcomatoid Carcinoma: Report of a Rare Case and Literature Review

2021 ◽  
pp. 538-544
Author(s):  
Nozomi Karakuchi ◽  
Senichiro Yanagawa ◽  
Kei Kushitani ◽  
Shinya Kodama ◽  
Yukio Takeshima ◽  
...  
Keyword(s):  
Lymph Node ◽  
Lymph Node Metastasis ◽  
Early Stage ◽  
Vena Cava ◽  
Sarcomatoid Carcinoma ◽  
Additional Treatment ◽  
Intestinal Tumors ◽  
Gastrointestinal Malignancies ◽  
Node Metastasis ◽  
Small Intestinal

Sarcomatoid carcinoma (SC) is a rare malignant tumor with properties of both epithelial and mesenchymal carcinomas. SC has been reported in various organs, but the number of reports for each type is small. Small intestinal tumors make up about 3–6% of gastrointestinal malignancies. Discovering them in the early stage is rare and difficult, with anemia and/or abdominal pain as the major symptoms of small intestinal tumors. Primary small intestinal SC (SISC) is rare among small intestinal tumors, and currently very few cases have been reported in the literature. Previous studies have reported that neither chemotherapy nor radiotherapy improves the overall survival rate of patients with SISC, and the prognosis is extremely poor. Currently, surgical resection remains the only optimal therapeutic approach for SISC. Here, we present the case of a 90-year-old woman who had acute peritonitis due to perforation of a small intestinal tumor. She underwent emergency exploratory laparotomy and partial resection of the small intestine, including the tumor. The tumor was pathologically identified as a primary SISC with mesenteric lymph node metastasis. Subsequently, she had recurrence in the intra-abdominal area and lymph node metastasis anterior to the inferior vena cava and died 15 months after surgery without any additional treatment.

Su1211 The Utility of Small Intestine Capsule Endoscopy and Balloon-Assisted Enteroscopy in the Diagnosis of Small Intestinal Tumors

2017 ◽  
Vol 85 (5) ◽  
pp. AB316
Author(s):  
Ryoichi Sawada ◽  
Ryosuke Miyazaki ◽  
Ayako Ishii ◽  
Yusuke Nagata ◽  
Makio Ogawa ◽  
...  
Keyword(s):  
Small Intestine ◽  
Capsule Endoscopy ◽  
Intestinal Tumors ◽  
Small Intestinal

Estrogen receptor β deficiency enhances small intestinal tumorigenesis inApcMin/+mice

2008 ◽  
Vol 123 (2) ◽  
pp. 303-311 ◽  
Author(s):  
Véronique Giroux ◽  
Frédéric Lemay ◽  
Gérald Bernatchez ◽  
Yolaine Robitaille ◽  
Julie C. Carrier
Keyword(s):  
Estrogen Receptor ◽  
Estrogen Receptor Β ◽  
Intestinal Tumorigenesis ◽  
Small Intestinal

scholarly journals NO-Donating NSAIDs, PPARδ, and Cancer: Does PPARδContribute to Colon Carcinogenesis?

PPAR Research ◽  
2008 ◽  
Vol 2008 ◽  
pp. 1-11 ◽  
Author(s):  
Gerardo G. Mackenzie ◽  
Shaheen Rasheed ◽  
William Wertheim ◽  
Basil Rigas
Keyword(s):  
Cancer Biology ◽  
Antitumor Effect ◽  
Colon Carcinogenesis ◽  
Wild Type ◽  
Antineoplastic Effect ◽  
Intestinal Neoplasia ◽  
Chemopreventive Effect ◽  
The Relationship ◽  
Epithelial Cell Death

The chemopreventive NO-donating NSAIDs (NO-NSAIDs; NSAIDs with an NO-releasing moiety) modulate PPARδand offer the opportunity to revisit the controversial role of PPARδin carcinogenesis (several papers report that PPARδeither promotes or inhibits cancer). This review summarizes the pharmacology of NO-NSAIDs, PPARδcancer biology, and the relationship between the two. In particular, a study of the chemopreventive effect of two isomers of NO-aspirin on intestinal neoplasia inMinmice showed that, compared to wild-type controls, PPARδis overexpressed in the intestinal mucosa ofMinmice; PPARδresponds tom- andp-NO-ASA proportionally to their antitumor effect (p->m-). This effect is accompanied by the induction of epithelial cell death, which correlates with the antineoplastic effect of NO-aspirin; and NO-aspirin's effect on PPARδis specific (no changes in PPARαor PPARγ). Although these data support the notion that PPARδpromotes intestinal carcinogenesis and its inhibition could be therapeutically useful, more work is needed before a firm conclusion is reached.

LDL receptor but not apolipoprotein E deficiency increases diet-induced obesity and diabetes in mice

2002 ◽  
Vol 282 (1) ◽  
pp. E207-E214 ◽  
Author(s):  
Sandra A. Schreyer ◽  
Cynthia Vick ◽  
Theodore C. Lystig ◽  
Paul Mystkowski ◽  
Renée C. LeBoeuf
Keyword(s):  
Apolipoprotein E ◽  
Low Density Lipoprotein ◽  
Ldl Receptor ◽  
Density Lipoprotein ◽  
Wild Type ◽  
Glucose Levels ◽  
Diet Induced Obesity ◽  
Obesity And Diabetes ◽  
Glucose And Lipid Homeostasis

The aim of this study was to determine whether phenotypes associated with type 2 diabetes are altered in dyslipidemic obese mice. C57BL/6 wild-type, low-density lipoprotein (LDL) receptor-deficient (LDLR−/−), and apolipoprotein E-deficient (apoE−/−) mice were fed a high-fat, high-carbohydrate diet (diabetogenic diet), and the development of obesity, diabetes, and hypertriglyceridemia was examined. Wild-type mice became obese and developed hyperglycemia, but not hypertriglyceridemia, in response to this diet. LDLR−/− mice fed the diabetogenic diet became more obese than wild-type mice and developed severe hypertriglyceridemia and hyperleptinemia. Surprisingly, glucose levels were only modestly higher and insulin levels and insulin-to-glucose ratios were not strikingly different from those of wild-type mice. In contrast, diabetogenic diet-fed apoE−/− mice were resistant to changes in glucose and lipid homeostasis despite becoming obese. These data suggest that modifications in lipoprotein profiles associated with loss of the LDL receptor or apoE function have profound and unique consequences on susceptibility to diet-induced obesity and type 2 diabetic phenotypes.

scholarly journals Hypolignification: A Decisive Factor in the Development of Hyperhydricity

Plants ◽  
2021 ◽  
Vol 10 (12) ◽  
pp. 2625
Author(s):  
Nurashikin Kemat ◽  
Richard G. F. Visser ◽  
Frans A. Krens
Keyword(s):  
Cell Wall ◽  
Lignin Content ◽  
Coumaric Acid ◽  
Wild Type ◽  
Higher Plant ◽  
Gene Coding ◽  
Phenylpropanoid Biosynthesis ◽  
Total Lignin ◽  
Total Lignin Content

One of the characteristics of hyperhydric plants is the reduction of cell wall lignification (hypolignification), but how this is related to the observed abnormalities of hyperhydricity (HH), is still unclear. Lignin is hydrophobic, and we speculate that a reduction in lignin levels leads to more capillary action of the cell wall and consequently to more water in the apoplast. p-coumaric acid is the hydroxyl derivative of cinnamic acid and a precursor for lignin and flavonoids in higher plant. In the present study, we examined the role of lignin in the development of HH in Arabidopsis thaliana by checking the wild-types (Ler and Col-0) and mutants affected in phenylpropanoid biosynthesis, in the gene coding for cinnamate 4-hydroxylase, C4H (ref3-1 and ref3-3). Exogenously applied p-coumaric acid decreased the symptoms of HH in both wild-type and less-lignin mutants. Moreover, the results revealed that exogenously applied p-coumaric acid inhibited root growth and increased the total lignin content in both wild-type and less-lignin mutants. These effects appeared to diminish the symptoms of HH and suggest an important role for lignin in HH.

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