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.

scholarly journals Proinflammatory Cytokines in Prostate Cancer Development and Progression Promoted by High-Fat Diet

2015 ◽  
Vol 2015 ◽  
pp. 1-7 ◽  
Author(s):  
Hua Xu ◽  
Meng-bo Hu ◽  
Pei-de Bai ◽  
Wen-hui Zhu ◽  
Sheng-hua Liu ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Mortality Rate ◽  
Proinflammatory Cytokines ◽  
High Fat Diet ◽  
Formation Rate ◽  
Diet Group ◽  
Normal Diet ◽  
Tumor Formation ◽  
High Fat ◽  
Tramp Mice

Background. We aimed to examine whether proinflammatory cytokines participated in prostate cancer (PCa) development and progression promoted by high-fat diet (HFD).Methods. TRAMP (transgenic adenocarcinoma mouse prostate) mice were randomly divided into two groups: normal diet group and HFD group. Mortality rate and tumor formation rate were examined. TRAMP mice were sacrificed and sampled on the 20th, 24th, and 28th week, respectively. Levels of proinflammatory cytokines, including IL-1α, IL-1β, IL-6, and TNF-α, were tested by FlowCytomix. Prostate tissue of TRAMP mice was used for histology study.Results. A total of 13 deaths of TRAMP mice were observed, among which 3 (8.33%) were from the normal diet group and 10 (27.78%) from the HFD group. The mortality rate of TRAMP mice from HFD group was significantly higher than that of normal diet group (P=0.032). Tumor formation rate at 20th week of age of HFD group was significantly higher than that of normal diet group (P=0.045). Proinflammatory cytokines levels, including IL-1α, IL-1β, IL-6, and TNF-α, were significantly higher in HFD TRAMP mice.Conclusions. HFD could promote TRAMP mouse PCa development and progression with elevated proinflammatory cytokines levels. Proinflammatory cytokines could contribute to PCa development and progression promoted by HFD.

scholarly journals Differential Effects of Maternal High Fat Diet During Pregnancy and Lactation on Taste Preferences in Rats

Nutrients ◽  
2020 ◽  
Vol 12 (11) ◽  
pp. 3553
Author(s):  
Gabor C. Mezei ◽  
Serdar H. Ural ◽  
Andras Hajnal
Keyword(s):  
High Fat Diet ◽  
Metabolic Disorders ◽  
Taste Preference ◽  
Normal Diet ◽  
Taste Preferences ◽  
Adult Offspring ◽  
High Fat ◽  
Preference Testing ◽  
Pregnancy And Lactation ◽  
The Impact

Maternal intake of high fat diet (HFD) increases risk for obesity and metabolic disorders in offspring. Developmental programming of taste preference is a potential mechanism by which this occurs. Whether maternal HFD during pregnancy, lactation, or both, imposes greater risks for altered taste preferences in adult offspring remains a question, and in turn, was investigated in the present study. Four groups of offspring were generated based on maternal HFD access: (1) HFD during pregnancy and lactation (HFD); (2) HFD during pregnancy (HFD-pregnancy); (3) HFD during lactation (HFD-lactation); and (4) normal diet (ND) during pregnancy and lactation (ND). Adult offspring 70 days of age underwent sensory and motivational taste preference testing with various concentrations of sucrose and Intralipid solutions using brief-access automated gustometers (Davis-rigs) and 24 h two-bottle choice tests, respectively. To control for post-gestational diet effects, offspring in all experimental groups were weaned on ND, and did not differ in body weight or glucose tolerance at the time of testing. Offspring exposed to maternal HFD showed increased sensory taste responses for 0.3, 0.6, 1.2 M sucrose solutions in HFD and 0.6 M in HFD-pregnancy groups, compared to animals exposed to ND. Similar effects were noted for lower concentrations of Intralipid in HFD (0.05, 0.10%) and HFD-pregnancy (0.05, 0.10, 0.5%) groups. The HFD-lactation group showed an opposite, diminished responsiveness for sucrose at the highest concentrations (0.9, 1.2, 1.5 M), but not for Intralipid, compared to ND animals. Extended-access two-bottle tests did not reveal major difference across the groups. Our study shows that maternal HFD during pregnancy and lactation has markedly different effects on preferences for palatable sweet and fatty solutions in adult offspring and suggests that such developmental programing may primarily affect gustatory mechanisms. Future studies are warranted for determining the impact of taste changes on development of obesity and metabolic disorders in a “real” food environment with food choices available, as well as to identify specific underlying mechanisms.

scholarly journals The Role of Exercise in Reducing Hyperlipidemia-Induced Neuronal Damage in Apolipoprotein E-Deficient Mice

2021 ◽  
Vol 2021 ◽  
pp. 1-9
Author(s):  
Yumeng Bai ◽  
Yali Feng ◽  
Bo Jiang ◽  
Yan Yang ◽  
Zuowei Pei ◽  
...  
Keyword(s):  
Exercise Training ◽  
Apolipoprotein E ◽  
Real Time ◽  
Real Time Pcr ◽  
High Fat Diet ◽  
Neuronal Injury ◽  
Serum Levels ◽  
Normal Diet ◽  
High Fat ◽  
Expression Levels

Hyperlipidemia causes nervous system-related diseases. Exercise training has developed into an established evidence-based treatment strategy that is beneficial for neuronal injury. This study investigated the effect of exercise on hyperlipidemia-induced neuronal injury in apolipoprotein E-deficient (ApoE-/-) mice. Male ApoE-/- mice (age: 8 weeks) were randomly divided into four groups as follows: mice fed a normal diet (ND), normal diet+swimming training (ND+S), high-fat diet (HD), and high-fat diet+swimming (HD+S). Exercise training consisted of swimming for 40 min/day, 5 days/week for 12 weeks. After 12 weeks, we measured serum levels of total cholesterol (TC), triglyceride (TG), and low-density lipoprotein cholesterol (LDL-c). We also evaluated glial fibrillary acidic protein (GFAP) expression levels using immunohistochemistry, real-time PCR, and immunoblotting. In addition, NLR family pyrin domain-containing 3 (NLRP3), interleukin- (IL-) 18, caspase-1, Bax, Bcl-2, and phosphorylated extracellular signal-regulated kinase (p-ERK) expression levels were measured using immunoblotting. Serum levels of TG, TC, and LDL-c were lower in ApoE-/- HD+S mice than in ApoE-/- HD mice. Immunohistochemistry, real-time PCR, and immunoblotting showed increased levels of GFAP in the ApoE-/- HD group. Immunoblotting revealed increased levels of NLRP3, IL-18, caspase-1, Bax, Bcl-2, and p-ERK in the ApoE-/- HD group; however, they were significantly suppressed in the ApoE-/- HD+S group. Therefore, exercise has protective effects against neuronal injury caused by hyperlipidemia.

scholarly journals Kiwifruit Supplementation Increases the Activity of the Paraoxonase Enzyme and decreases Oxidized Low-Density Lipoprotein in High-Fat Diet Fed Hamsters

2020 ◽  
Vol 8 (2) ◽  
pp. 58-63
Author(s):  
Narjes Rezaei ◽  
Zahra Zaherijamil ◽  
Shirin Moradkhani ◽  
Massoud Saidijam ◽  
Iraj khodadadi ◽  
...  
Keyword(s):  
High Fat Diet ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Normal Diet ◽  
Paraoxonase 1 ◽  
Low Density ◽  
Oxidized Low Density Lipoprotein ◽  
High Fat ◽  
Beneficial Effects ◽  
The Impact

Background: It is shown that kiwifruit elevates serum high-density lipoprotein cholesterol (HDL-C) levels and exhibits beneficial effects on human health due to its antioxidant potential. Objectives: This study aimed to investigate the impact of kiwifruit on the activity of the paraoxonase 1 (PON1) enzyme, as a main antioxidant enzyme in HDL functionality, in a high-fat diet (HFD). Methods: To this end, 42 male Syrian hamsters were divided into 6 groups including hamsters receiving a normal diet (the control normal group), a regular diet supplemented with kiwifruit at two concentrations (i.e., 1.86 g/kg and 3.73 g/kg), a HFD comprised of 15% butterfat + 0.05% cholesterol (the control high-fat group), and a HFD supplemented with kiwifruit at two concentrations (i.e., 1.86 and 3.73 g/kg) for 8 weeks. Results: The results showed that supplementation of kiwifruit to the HFD increased the levels of HDL-C and remarkably reduced the concentrations of oxidized low-density lipoprotein (ox-LDL) and malondialdehyde (MDA) compared with the control-HF group. In addition, the paraoxonase activity of PON1 significantly increased in HFD supplemented with kiwifruit (1.86 g/kg), and finally, arylesterase (ARE) activity increased in all treated groups when compared with untreated groups. Conclusion: Our findings suggested that kiwifruit can improve the lipid profile and prevent oxidative stress-induced by lipid peroxidation in hamsters receiving HFD, thus increasing the ARE and paraoxonase activities of PON1.

scholarly journals 3,3′-Diindolylmethane Dose-Dependently Prevents Advanced Prostate Cancer

2019 ◽  
Author(s):  
Yufei Li ◽  
Nathaniel W. Mahloch ◽  
Nicholas J.E. Starkey ◽  
Mónica Peña-Luna ◽  
George E. Rottinghaus ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Estrogen Receptor ◽  
High Fat Diet ◽  
Estrogen Receptor Alpha ◽  
Estrogen Receptor Beta ◽  
Control Group ◽  
High Fat ◽  
Mouse Prostate

Abstract3,3′-Diindolylmethane (DIM) is an acid-derived dimer of indole-3-carbinol, found in many cruciferous vegetables, such as broccoli, and has been shown to inhibit prostate cancer (PCa) in several in vitro and in vivo models. We demonstrated that DIM stimulated both estrogen receptor alpha (ERα) and estrogen receptor beta (ERβ) transcriptional activities and propose that ERβ plays a role in mediating DIM’s inhibition on cancer cell growth. To further study the effects of DIM on inhibiting advanced PCa development, we tested DIM in TRAMP (TRansgenic Adenocarcinoma of the Mouse Prostate) mice. The control group of mice were fed a high fat diet. Three additional groups of mice were fed the same high fat diet supplemented with 0.04%, 0.2% and 1% DIM. Incidence of advanced PCa, poorly differentiated carcinoma (PDC), in the control group was 60%. 1% DIM dramatically reduced PDC incidence to 24% (p=0.0012), while 0.2% and 0.04% DIM reduced PDC incidence to 38% (p=0.047) and 45% (p=0.14) respectively. Though DIM did affect mice weights, statistical analysis showed a clear negative association between DIM concentration and PDC incidence with p=0.004, while the association between body weight and PDC incidence was not significant (p=0.953). In conclusion, our results show that dietary DIM can inhibit the most aggressive stage of prostate cancer at concentration lower than previously demonstrated, possibly working through an estrogen receptor mediated mechanism.

Boric acid and Borax Supplementation Reduces Weight Gain in Overweight Rats and Alter L-Carnitine and IGF-I Levels

2020 ◽  
Vol 90 (3-4) ◽  
pp. 221-227 ◽  
Author(s):  
Onur Atakisi ◽  
Kezban Yildiz Dalginli ◽  
Canan Gulmez ◽  
Ruya Kaya ◽  
Ozkan Ozden ◽  
...  
Keyword(s):  
Boric Acid ◽  
High Fat Diet ◽  
Live Weight ◽  
Serum Levels ◽  
Normal Diet ◽  
High Fat ◽  
Boron Compounds ◽  
Carnitine Level ◽  
Igf I ◽  
Shock Proteins

Abstract. The aim of this study was to investigate the effects of boric acid (BA) and borax (BX) on live weight and obesity associated molecules including leptin, L-carnitine, insulin-like growth factor 1 (IGF-I), and heat shock proteins 70 (HSP70) in rats fed with high-fat diet. A total of 60 rats were equally allocated as ND (normal diet), HF (high-fat diet), HF+BA, HF+BX, ND+BX, ND+BA. Body weight increases in HF+BA (85 g) and HF+BX (86 g) were significantly lower (p<0.05) compared to HF group (126 g). Boron treatment decreased serum L-carnitine level in high-fat diet (HF+BA 11.12 mg/L, HF+BX 10.51 mg/L, p<0.05) compared to HF group (15.57 mg/L), while no change was observed in groups ND+BA (7.55 mg/L) and ND+BX (7.57 mg/L) compared to group ND (8.29 mg/L). Neither BA nor BX supplementation in ND and HF groups altered the serum levels of HSP70 and leptin. BA and BX supplementation in rats fed HF resulted in a significant reduction in live weight. Boron compounds altered L-carnitine and IGF-1 levels in rats. These results indicate that boron compounds are beneficial in the treatment of obesity as well as in the prevention of high-fat diet-induced weight increase. Alterations in serum L-carnitine and IGF-1 levels in boron treated rats also indicate possible role of boron compounds in energy metabolism in response to high fat diet.

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 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.

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