scholarly journals A high-fat diet: an unexpected role in preventing the metastatic seeding of colorectal cancer

2020 ◽  
Vol 5 (1) ◽  
Author(s):  
Min Long ◽  
Wenjing Wang ◽  
Qiu Sun
Keyword(s):  
Colorectal Cancer ◽  
High Fat Diet ◽  
High Fat

scholarly journals Toll-like receptor 4 is a master regulator for colorectal cancer growth under high-fat diet by programming cancer metabolism

2021 ◽  
Vol 12 (8) ◽  
Author(s):  
Xianjing Hu ◽  
Sarwat Fatima ◽  
Minting Chen ◽  
Keyang Xu ◽  
Chunhua Huang ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Palmitic Acid ◽  
High Fat Diet ◽  
Cancer Metabolism ◽  
Cancer Growth ◽  
Dependent Manner ◽  
Tlr4 Expression ◽  
High Fat ◽  
Master Regulator ◽  
Tumor Tissues

AbstractAlthough high-fat diet (HFD) has been implicated in the development of colorectal cancer (CRC), the critical signaling molecule that mediates the cancer growth is not well-defined. Identifying the master regulator that controls CRC growth under HFD can facilitate the development of effective therapeutics for the cancer treatment. In this study, the global lipidomics and RNA sequencing data show that, in the tumor tissues of CRC-bearing mouse models, HFD not only increases tumor weight, but also the palmitic acid level and TLR4 expression, which are reduced when HFD is replaced by control diet. These concomitant changes suggest the roles of palmitic acid and TLR4 in CRC growth. Subsequent studies show that palmitic acid regulates TLR4 expression in PU.1-dependent manner. Knockdown of PU.1 or mutations of PU.1-binding site on TLR4 promoter abolish the palmitic acid-increased TLR4 expression. The role of palmitic acid/PU.1/TLR4 axis in CRC growth is further examined in cell model and animal models that are fed either HFD or palmitic acid-rich diet. More importantly, iTRAQ proteomics data show that knockdown of TLR4 changes the metabolic enzyme profiles in the tumor tissues, which completely abolish the HFD-enhanced ATP production and cancer growth. Our data clearly demonstrate that TLR4 is a master regulator for CRC growth under HFD by programming cancer metabolism.

Polysaccharide from Rosa roxburghii Tratt fruit attenuates high-fat diet-induced intestinal barrier dysfunction and inflammation in mice by modulating gut microbiota

2022 ◽  
Author(s):  
Lei Wang ◽  
Pan Zhang ◽  
Chao Li ◽  
Fei Xu ◽  
Jie Chen
Keyword(s):  
Colorectal Cancer ◽  
High Fat Diet ◽  
Inflammatory Diseases ◽  
Intestinal Barrier ◽  
High Fat ◽  
Barrier Dysfunction ◽  
Effective Agent ◽  
Colonic Inflammation ◽  
Rosa Roxburghii Tratt ◽  
Rosa Roxburghii

Obesity-induced colonic inflammation-stimulated colitis is one of the main causes of colorectal cancer. Dietary polysaccharides are considered an effective agent for relieving obesity-induced inflammatory diseases such as diabetes and colitis....

Shinan Sea Salt Intake Ameliorates Colorectal Cancer in AOM/DSS with High Fat Diet-Induced C57BL/6N Mice

2021 ◽  
Vol 24 (4) ◽  
pp. 431-435
Author(s):  
Eui-Seong Park ◽  
Ting Yu ◽  
Hey-Jin Lee ◽  
Yang-Iee Lim ◽  
Seung-Min Lee ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
High Fat Diet ◽  
Salt Intake ◽  
Sea Salt ◽  
High Fat

scholarly journals High-fat diet and colorectal cancer: myths and facts

2018 ◽  
Vol 14 (6) ◽  
pp. 493-495 ◽  
Author(s):  
Sheelarani Karunanithi ◽  
Liraz Levi
Keyword(s):  
Colorectal Cancer ◽  
High Fat Diet ◽  
High Fat

scholarly journals Effects of high‐fat diet‐induced adipokines and cytokines on colorectal cancer development

FEBS Open Bio ◽  
2019 ◽  
Vol 9 (12) ◽  
pp. 2117-2125 ◽  
Author(s):  
Jian Zhang ◽  
Shikui Guo ◽  
Jinyuan Li ◽  
Weimin Bao ◽  
Peng Zhang ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
High Fat Diet ◽  
Cancer Development ◽  
High Fat

scholarly journals The High-Fat Diet Based on Extra-Virgin Olive Oil Causes Dysbiosis Linked to Colorectal Cancer Prevention

Nutrients ◽  
2020 ◽  
Vol 12 (6) ◽  
pp. 1705
Author(s):  
Carmen Rodríguez-García ◽  
Cristina Sánchez-Quesada ◽  
Ignacio Algarra ◽  
José J. Gaforio
Keyword(s):  
Colorectal Cancer ◽  
Gut Microbiota ◽  
Olive Oil ◽  
High Fat Diet ◽  
Virgin Olive Oil ◽  
Extra Virgin Olive Oil ◽  
High Fat ◽  
Inflammatory Microenvironment ◽  
Increased Risk ◽  
Colorectal Cancer Prevention

The present study aims to examine the effects of three different high-fat diet (HFD) on mice gut microbiota in order to analyse whether they create the microenvironmental conditions that either promote or prevent colorectal cancer (CRC). We evaluated colonic mucosa-associated microbiota in CD1 mice fed with HFD, based on 60% kcal from fat-containing coconut, sunflower or extra-virgin olive oil as the only source of fat. The main findings were as follows: (a) All HFD produced a decrease in the richness and diversity of the intestinal microbiota that was independent of mouse weight, (b) HFD switched Lactobacillus to Lactococcus. In general, the results showed that both sunflower- and coconut-HFD generated a pro-inflammatory intestinal microenvironment. In brief, coconut-HFD decreased Akkermansia and increased Staphylococcus, Prevotella and Bacteroides spp. abundance. Sunflower-HFD reduced Akkermansia and Bifidobacterium, while enhancing Sphingomonas and Neisseria spp. abundance. In contrast, EVOO-HFD produced an anti-inflammatory microenvironment characterised by a decreased Enterococcus, Staphylococcus, Neisseria and Pseudomonas spp. abundance. At the same time, it increased the Firmicutes/Bacteroidetes ratio and maintained the Akkermansia population. To conclude, EVOO-HFD produced changes in the gut microbiota that are associated with the prevention of CRC, while coconut and sunflower-HFD caused changes associated with an increased risk of CRC.

scholarly journals Irinotecan-Induced Steatohepatitis: Current Insights

2021 ◽  
Vol 11 ◽  
Author(s):  
Jun Han ◽  
Jing Zhang ◽  
Chengliang Zhang
Keyword(s):  
Colorectal Cancer ◽  
Body Mass Index ◽  
High Fat Diet ◽  
Current Knowledge ◽  
High Body Mass Index ◽  
Research Progress ◽  
High Fat ◽  
Colorectal Cancer Liver Metastasis ◽  
Therapeutic Drugs ◽  
Lobular Inflammation

The hepatotoxicity of irinotecan is drawing wide concern nowadays due to the widespread use of this chemotherapeutic against various solid tumors, particularly metastatic colorectal cancer. Irinotecan-induced hepatotoxicity mainly manifests as transaminase increase and steatosis with or without transaminase increase, and is accompanied by vacuolization, and lobular inflammation. Irinotecan-induced steatohepatitis (IIS) increases the risk of morbidity and mortality in patients with colorectal cancer liver metastasis (CRCLM). The major risks and predisposing factors for IIS include high body mass index (BMI) or obesity, diabetes, and high-fat diet. Mitochondrial dysfunction and autophagy impairment may be involved in the pathogenesis of IIS. However, there is currently no effective preventive or therapeutic treatment for this condition. Thus, the precise mechanisms underlying the pathogenesis of IIS should be deciphered for the development of therapeutic drugs. This review summarizes the current knowledge and research progress on IIS.

scholarly journals Effects of high-fat diet and intestinal aryl hydrocarbon receptor deletion on colon carcinogenesis

2020 ◽  
Vol 318 (3) ◽  
pp. G451-G463 ◽  
Author(s):  
Erika L. Garcia-Villatoro ◽  
Jennifer A. A. DeLuca ◽  
Evelyn S. Callaway ◽  
Kimberly F. Allred ◽  
Laurie A. Davidson ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Colon Cancer ◽  
Epithelial Cells ◽  
Aryl Hydrocarbon Receptor ◽  
Knockout Mice ◽  
High Fat Diet ◽  
Intestinal Epithelial Cells ◽  
Intestinal Epithelial ◽  
High Fat ◽  
Aryl Hydrocarbon

Consumption of a high-fat diet has been associated with an increased risk of developing colorectal cancer (CRC). However, the effects of the interaction between dietary fat content and the aryl hydrocarbon receptor (AhR) on colorectal carcinogenesis remain unclear. Mainly known for its role in xenobiotic metabolism, AhR has been identified as an important regulator for maintaining intestinal epithelial homeostasis. Although previous research using whole body AhR knockout mice has revealed an increased incidence of colon and cecal tumors, the unique role of AhR activity in intestinal epithelial cells (IECs) and modifying effects of fat content in the diet at different stages of sporadic CRC development are yet to be elucidated. In the present study, we have examined the effects of a high-fat diet on IEC-specific AhR knockout mice in a model of sporadic CRC. Although loss of AhR activity in IECs significantly induced the development of premalignant lesions, in a separate experiment, no significant changes in colon mass incidence were observed. Moreover, consumption of a high-fat diet promoted cell proliferation in crypts at the premalignant colon cancer lesion stage and colon mass multiplicity as well as β-catenin expression and nuclear localization in actively proliferating cells in colon masses. Our data demonstrate the modifying effects of high-fat diet and AhR deletion in IECs on tumor initiation and progression. NEW & NOTEWORTHY Through the use of an intestinal-specific aryl hydrocarbon receptor (AhR) knockout mouse model, this study demonstrates that the expression of AhR in intestinal epithelial cells is required to reduce the formation of premalignant colon cancer lesions. Furthermore, consumption of a high-fat diet and the loss of AhR in intestinal epithelial cells influences the development of colorectal cancer at various stages.

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