scholarly journals Research Evidence on High-Fat Diet-Induced Prostate Cancer Development and Progression

2019 ◽  
Vol 8 (5) ◽  
pp. 597 ◽  
Author(s):  
Shintaro Narita ◽  
Taketoshi Nara ◽  
Hiromi Sato ◽  
Atsushi Koizumi ◽  
Mingguo Huang ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Dietary Fat ◽  
High Fat Diet ◽  
Cancer Development ◽  
Preclinical Studies ◽  
Preclinical Models ◽  
High Fat ◽  
Prostate Cancer Development ◽  
Underlying Mechanisms ◽  
The Impact

Although recent evidence has suggested that a high-fat diet (HFD) plays an important role in prostate carcinogenesis, the underlying mechanisms have largely remained unknown. This review thus summarizes previous preclinical studies that have used prostate cancer cells and animal models to assess the impact of dietary fat on prostate cancer development and progression. Large variations in the previous studies were found during the selection of preclinical models and types of dietary intervention. Subcutaneous human prostate cancer cell xenografts, such as LNCaP, LAPC-4, and PC-3 and genetic engineered mouse models, such as TRAMP and Pten knockout, were frequently used. The dietary interventions had not been standardized, and distinct variations in the phenotype were observed in different studies using distinct HFD components. The use of different dietary components in the research models is reported to influence the effect of diet-induced metabolic disorders. The proposed underlying mechanisms for HFD-induced prostate cancer were divided into (1) growth factor signaling, (2) lipid metabolism, (3) inflammation, (4) hormonal modulation, and others. A number of preclinical studies proposed that dietary fat and/or obesity enhanced prostate cancer development and progression. However, the relationship still remains controversial, and care should be taken when interpreting the results in a human context. Future studies using more sophisticated preclinical models are imperative in order to explore deeper understanding regarding the impact of dietary fat on the development and progression of prostate cancer.

scholarly journals Per- and Polyfluoroalkyl Substance Exposure Combined with High-Fat Diet Supports Prostate Cancer Progression

Nutrients ◽  
2021 ◽  
Vol 13 (11) ◽  
pp. 3902
Author(s):  
Ozan Berk Imir ◽  
Alanna Zoe Kaminsky ◽  
Qian-Ying Zuo ◽  
Yu-Jeh Liu ◽  
Ratnakar Singh ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cancer Progression ◽  
High Fat Diet ◽  
Flame Retardants ◽  
Epidemiological Studies ◽  
Cancer Development ◽  
Prostate Cancer Progression ◽  
High Fat ◽  
The Impact

Per- and polyfluoroalkyl substances (PFAS) are synthetic chemicals utilized in various industrial settings and include products such as flame retardants, artificial film-forming foams, cosmetics, and non-stick cookware, among others. Epidemiological studies suggest a link between increased blood PFAS levels and prostate cancer incidence, but the mechanism through which PFAS impact cancer development is unclear. To investigate the link between PFAS and prostate cancer, we evaluated the impact of metabolic alterations resulting from a high-fat diet combined with PFAS exposure on prostate tumor progression. We evaluated in vivo prostate cancer xenograft models exposed to perfluorooctane sulfonate (PFOS), a type of PFAS compound, and different diets to study the effects of PFAS on prostate cancer progression and metabolic activity. Metabolomics and transcriptomics were used to understand the metabolic landscape shifts upon PFAS exposure. We evaluated metabolic changes in benign or tumor cells that lead to epigenomic reprogramming and altered signaling, which ultimately increase tumorigenic risk and tumor aggressiveness. Our studies are the first in the field to provide new and clinically relevant insights regarding novel metabolic and epigenetic states as well as to support the future development of effective preventative and therapeutic strategies for PFAS-induced prostate cancers. Our findings enhance understanding of how PFAS synergize with high-fat diets to contribute to prostate cancer development and establish an important basis to mitigate PFAS exposure.

Will metformin postpone high-fat diet promotion of TRAMP mouse prostate cancer development and progression?

2014 ◽  
Vol 46 (12) ◽  
pp. 2327-2334 ◽  
Author(s):  
Hua Xu ◽  
Meng-bo Hu ◽  
Pei-de Bai ◽  
Wen-hui Zhu ◽  
Qiang Ding ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
High Fat Diet ◽  
Cancer Development ◽  
High Fat ◽  
Tramp Mouse ◽  
Mouse Prostate ◽  
Prostate Cancer Development

scholarly journals Both p110α and p110β isoforms of PI3K can modulate the impact of loss-of-function of the PTEN tumour suppressor

2012 ◽  
Vol 442 (1) ◽  
pp. 151-159 ◽  
Author(s):  
Inma M. Berenjeno ◽  
Julie Guillermet-Guibert ◽  
Wayne Pearce ◽  
Alexander Gray ◽  
Stewart Fleming ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cell Lines ◽  
Tumour Suppressor ◽  
Negative Regulator ◽  
Cancer Development ◽  
Pten Loss ◽  
Mouse Tissues ◽  
Primary Mouse ◽  
Prostate Cancer Development ◽  
The Impact

The PI3K (phosphoinositide 3-kinase) pathway is commonly activated in cancer as a consequence of inactivation of the tumour suppressor PTEN (phosphatase and tensin homologue deleted on chromosome 10), a major negative regulator of PI3K signalling. In line with this important role of PTEN, mice that are heterozygous for a PTEN-null allele (PTEN+/− mice) spontaneously develop a variety of tumours in multiple organs. PTEN is a phosphatase with selectivity for PtdIns(3,4,5)P3, which is produced by the class I isoforms of PI3K (p110α, p110β, p110γ and p110δ). Previous studies indicated that PTEN-deficient cancer cell lines mainly depend on p110β, and that p110β, but not p110α, controls mouse prostate cancer development driven by PTEN loss. In the present study, we investigated whether the ubiquitously expressed p110α can also functionally interact with PTEN in cancer. Using genetic mouse models that mimic systemic administration of p110α- or p110β-selective inhibitors, we confirm that inactivation of p110β, but not p110α, inhibits prostate cancer development in PTEN+/− mice, but also find that p110α inactivation protects from glomerulonephritis, pheochromocytoma and thyroid cancer induced by PTEN loss. This indicates that p110α can modulate the impact of PTEN loss in disease and tumourigenesis. In primary and immortalized mouse fibroblast cell lines, both p110α and p110β controlled steady-state PtdIns(3,4,5)P3 levels and Akt signalling induced by heterozygous PTEN loss. In contrast, no correlation was found in primary mouse tissues between PtdIns(3,4,5)P3 levels, PI3K/PTEN genotype and cancer development. Taken together, our results from the present study show that inactivation of either p110α or p110β can counteract the impact of PTEN inactivation. The potential implications of these findings for PI3K-targeted therapy of cancer are discussed.

scholarly journals It’s the fiber, not the fat: Significant effects of dietary challenge on the gut microbiome

2019 ◽  
Author(s):  
Kathleen E. Morrison ◽  
Eldin Jašarević ◽  
Christopher D. Howard ◽  
Tracy L. Bale
Keyword(s):  
Body Weight ◽  
Gut Microbiota ◽  
Dietary Fat ◽  
Gut Microbiome ◽  
High Fat Diet ◽  
Body Weight Gain ◽  
Chow Diet ◽  
Soluble Fiber ◽  
High Fat ◽  
The Impact

AbstractBackgroundDietary effects on the gut microbiome has been shown to play a key role in the pathophysiology of behavioral dysregulation, inflammatory disorders, metabolic syndrome, and obesity. Often overlooked is that experimental diets vary significantly in the proportion and source of dietary fiber. Commonly, treatment comparisons are made between animals that are fed refined diets that lack soluble fiber and animals fed vivarium-provided chow diet that contain a rich source of soluble fiber. Despite the well-established role of soluble fiber on metabolism, immunity, and behavior via the gut microbiome, the extent to which measured outcomes may be driven by differences in dietary fiber is unclear. Further, the significant impact of sex and age in response to dietary challenge is likely important and should also be considered.ResultsWe compared the impact of transitioning young and aged male and female mice from a chow diet to a refined low soluble fiber diet on body weight and gut microbiota. Then, to determine the contribution of dietary fat, we examined the impact of transitioning a subset of animals from refined low fat to refined high fat diet. Serial tracking of body weights revealed that consumption of low fat or high fat refined diet increased body weight in young and aged adult male mice. Young adult females showed resistance to body weight gain, while high fat diet-fed aged females had significant body weight gain. Transition from a chow diet to low soluble fiber refined diet accounted for most of the variance in community structure and composition across all groups. This dietary transition was characterized by a loss of taxa within the phylum Bacteroidetes and a concurrent bloom of Clostridia and Proteobacteria in a sex- and age-specific manner. Most notably, no changes to gut microbiota community structure and composition were observed between mice consuming either low- or high-fat diet, suggesting that transition to the refined diet that lacks soluble fiber is the primary driver of gut microbiota alterations, with limited additional impact of dietary fat on gut microbiota.ConclusionCollectively, our results show that the choice of control diet has a significant impact on outcomes and interpretation related to body weight and gut microbiota. These data also have broad implications for rodent studies that draw comparisons between refined high fat diets and chow diets to examine dietary fat effects on metabolic, immune, behavioral, and neurobiological outcomes.

scholarly journals Maternal High-Fat Diet Promotes the Development and Progression of Prostate Cancer in Transgenic Adenocarcinoma Mouse Prostate Offspring

2018 ◽  
Vol 47 (5) ◽  
pp. 1862-1870 ◽  
Author(s):  
Tian Yang ◽  
Xiaobo Wu ◽  
Jimeng Hu ◽  
Mengbo Hu ◽  
Hua Xu ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Mortality Rate ◽  
High Fat Diet ◽  
Formation Rate ◽  
Serum Levels ◽  
Normal Diet ◽  
Tumor Formation ◽  
High Fat ◽  
Mouse Prostate ◽  
The Impact

Background/Aims: We aim to investigate the impact of maternal high fat diet (HFD) on the development and progression of prostate cancer (PCa) in transgenic adenocarcinoma mouse prostate (TRAMP) offspring. Methods: The TRAMP model was used, and divided into maternal HFD group and normal diet (ND) group in the present study. Each group contained 36 TRAMP mice. Serum levels of leptin, adiponectin, interleukin (IL) -1α, IL-1β, IL-6, tumor necrosis factor-α and monocyte chemotactic protein-1 were measured by the 20th, 24th and 28th week old through ProcartaPlex Multiplex Immunoassay. Body fat ratio was measured by MiniQMR. Tumor formation rate was measured through hematoxylin and eosin (H&E) staining, and mortality rate was measured meantime. Western blot was applied to determine the levels of Protein Kinase B (Akt) and Phosphatase and tensin homolog (PTEN). Results: The mortality rate of maternal HFD group was significantly higher than that of ND group (P = 0.046). The tumor formation rate was significantly higher in maternal HFD group than in ND group only in 20th week subgroup (P = 0.040). A significant increase of leptin was seen in maternal HFD 20th and 24th week subgroups (P = 0.001 and < 0.001, respectively) and a decrease of adiponectin was seen in maternal HFD 20th and 28th week subgroups (P =0.006 and < 0.001, respectively). Besides, an activated phos-Akt (P-Akt) and deactivated PTEN were observed in maternal HFD group. Conclusions: Maternal HFD could increase the standard serum leptin level, inhibit the expression of PTEN protein, promote P-Akt protein expression, activate the PI3K/Akt pathway, and ultimately promote the development and progression of PCa in TRAMP offspring.

The impact of hypertriglyceridemia on prostate cancer development in patients aged ≥60 years

2011 ◽  
Vol 109 (4) ◽  
pp. 515-519 ◽  
Author(s):  
Norihiro Hayashi ◽  
Masato Matsushima ◽  
Toshihiro Yamamoto ◽  
Hiroshi Sasaki ◽  
Hiroyuki Takahashi ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cancer Development ◽  
Prostate Cancer Development ◽  
The Impact

scholarly journals The Impact of Diabetes on the Risk of Prostate Cancer Development according to Body Mass Index: A 10-year Nationwide Cohort Study

2016 ◽  
Vol 7 (14) ◽  
pp. 2061-2066 ◽  
Author(s):  
Jin Bong Choi ◽  
Hyong Woo Moon ◽  
Young Hyun Park ◽  
Woong Jin Bae ◽  
Hyuk Jin Cho ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Body Mass Index ◽  
Cohort Study ◽  
Body Mass ◽  
Cancer Development ◽  
Prostate Cancer Development ◽  
The Impact
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