Project description:Some studies have shown that acute intake of high-phenol virgin olive oil reduces pro-inflammatory, pro-oxidant and pro-thrombotic states, but nowadays still remains unclear if those effects attributed to its phenolic fraction could be exerted at transcriptional level in vivo. Two virgin olive oil-based breakfasts with high (398 ppm) and low (70 ppm) content of phenolic compounds were administered to twenty patients (9 men and 11 women) with metabolic syndrome following a double-blinded random crossover design. Prior to the first breakfast intervention, participants followed a 6-week washout period in which they were instructed to not take vitamins, soy supplements, or any drug. To eliminate the potential effect that might exist in their usual dietary habits, all subjects followed a low-fat, carbohydrate rich (CHO) diet during this period and untill the end of the study. In the 24 h before each breakfast intervention, participants were instructed to avoid consuming phenol-rich foods such as fruit or juices, wine, grape juice, chocolate, coffee, tea, olive oil, or soya, and to refrain from intense physical exercise during that period. After a 12 h fasting and following a randomized sequential crossover design with one-week washout period, participants reported to the hospital and received two fat meals consisting of 60 g of white bread, 40 mL of VOO (CANOLIVA®, Antonio Cano e Hijos™, Córdoba, Spain) with high (398 ppm) or low (70 ppm) content in phenolic compounds, and 60,000 IU of vitamin A per m2 of body surface. Olive oil with low content in phenolic compounds was obtained as a result of extraction by physical procedures of most of the phenolic compounds in the high-phenol olive oil, so that both oils kept a similar composition of the remaining macro- and micronutrients. Throughout the 4-h duration of the study, the subjects performed no physical activity, nor did they consume anything but water. Gene expression was performed on peripheral blood mononuclear cells (PBMCs) at postprandial period (4 hours after breakfast) by microarray analysis and verified by qRT-PCR. Two sets of dye-swaped experiments were performed making a total of four technical replicates per subject. Each of the hybridizations compared total RNA from PBMCs obtained 4h after the intake of virgin olive oil with high phenolic content vs. total RNA from PBMCs obtained 4h after low-phenol virgin olive oil consumption.

Project description:PURPOSE: Previous mouse studies using corn oil (ω-6) as the dietary fat source suggest that decreasing dietary fat content can slow prostate cancer (PCa) growth. However, other studies, in which the diet was composed around saturated fat, showed no difference in outcomes between high-fat and low-fat diets. The relative effects of other fats, such as fish oil and olive oil, also remain unexplored. To our knowledge, no trial has yet compared the effect of various fats on prostate cancer progression. Therefore, we sought to systematically study the effect of fish oil, olive oil, corn oil, and saturated fat on prostate cancer progression. METHODS: A total of 96 male SCID mice were injected with LAPC-4 human PCa cells. Two weeks following injection, mice were singly-housed and randomized to either a fish oil, olive oil, corn oil, or saturated fat based diet. Animals were euthanized when tumors reached 1,000 mm3. Serum was collected at sacrifice and assayed for PSA, insulin, IGF-1, IGFBP-3, and PGE-2 levels. Tumors were also assayed for PGE-2, and COX-2 levels, and gene array analysis was performed. RESULTS: Mice weights and tumor volumes were equivalent across groups at randomization. Overall, fish-oil consumption was associated with improved survival, relative to all other dietary groups (Log-rank, all p<0.05). We did not detect any significant difference in serum PSA, insulin, IGF-1, IGFBP-3, and PGE-2 levels. Glucose at the time of sacrifice was statistically different between groups, with the fish-oil fed mice having the highest levels of serum glucose (Kruskal-Wallis, p=0.03). CONCLUSIONS: In this prostate cancer xenograft model, we found that consuming a diet in which fish-oil was the only fat source slowed tumor growth in improved survival, compared to mice consuming diets composed of olive oil, corn oil, or saturated fat sources. These results suggest that type of dietary fat consumed may be as important as amount of dietary fat consumed in the setting of prostate cancer.

Project description:PURPOSE: Previous mouse studies using corn oil (Ï?-6) as the dietary fat source suggest that decreasing dietary fat content can slow prostate cancer (PCa) growth. However, other studies, in which the diet was composed around saturated fat, showed no difference in outcomes between high-fat and low-fat diets. The relative effects of other fats, such as fish oil and olive oil, also remain unexplored. To our knowledge, no trial has yet compared the effect of various fats on prostate cancer progression. Therefore, we sought to systematically study the effect of fish oil, olive oil, corn oil, and saturated fat on prostate cancer progression. METHODS: A total of 96 male SCID mice were injected with LAPC-4 human PCa cells. Two weeks following injection, mice were singly-housed and randomized to either a fish oil, olive oil, corn oil, or saturated fat based diet. Animals were euthanized when tumors reached 1,000 mm3. Serum was collected at sacrifice and assayed for PSA, insulin, IGF-1, IGFBP-3, and PGE-2 levels. Tumors were also assayed for PGE-2, and COX-2 levels, and gene array analysis was performed. RESULTS: Mice weights and tumor volumes were equivalent across groups at randomization. Overall, fish-oil consumption was associated with improved survival, relative to all other dietary groups (Log-rank, all p<0.05). We did not detect any significant difference in serum PSA, insulin, IGF-1, IGFBP-3, and PGE-2 levels. Glucose at the time of sacrifice was statistically different between groups, with the fish-oil fed mice having the highest levels of serum glucose (Kruskal-Wallis, p=0.03). CONCLUSIONS: In this prostate cancer xenograft model, we found that consuming a diet in which fish-oil was the only fat source slowed tumor growth in improved survival, compared to mice consuming diets composed of olive oil, corn oil, or saturated fat sources. These results suggest that type of dietary fat consumed may be as important as amount of dietary fat consumed in the setting of prostate cancer. DESIGN: A total of 96 male SCID mice were injected with LAPC-4 human prostate cancer cells. After 2 weeks of tumor growth, the mice were randomized to one of four diets: corn oil, fish oil, olive oil, and saturated fat source diets. Animals were euthanized when tumor volumes exceeded 1000 mm^3. Sera and tissues from the median 6 surviving animals from each of the four dietary groups were analyzed.

Project description:Some studies have shown that acute intake of high-phenol virgin olive oil reduces pro-inflammatory, pro-oxidant and pro-thrombotic states, but nowadays still remains unclear if those effects attributed to its phenolic fraction could be exerted at transcriptional level in vivo. Two virgin olive oil-based breakfasts with high (398 ppm) and low (70 ppm) content of phenolic compounds were administered to twenty patients (9 men and 11 women) with metabolic syndrome following a double-blinded random crossover design. Prior to the first breakfast intervention, participants followed a 6-week washout period in which they were instructed to not take vitamins, soy supplements, or any drug. To eliminate the potential effect that might exist in their usual dietary habits, all subjects followed a low-fat, carbohydrate rich (CHO) diet during this period and untill the end of the study. In the 24 h before each breakfast intervention, participants were instructed to avoid consuming phenol-rich foods such as fruit or juices, wine, grape juice, chocolate, coffee, tea, olive oil, or soya, and to refrain from intense physical exercise during that period. After a 12 h fasting and following a randomized sequential crossover design with one-week washout period, participants reported to the hospital and received two fat meals consisting of 60 g of white bread, 40 mL of VOO (CANOLIVA®, Antonio Cano e Hijos™, Córdoba, Spain) with high (398 ppm) or low (70 ppm) content in phenolic compounds, and 60,000 IU of vitamin A per m2 of body surface. Olive oil with low content in phenolic compounds was obtained as a result of extraction by physical procedures of most of the phenolic compounds in the high-phenol olive oil, so that both oils kept a similar composition of the remaining macro- and micronutrients. Throughout the 4-h duration of the study, the subjects performed no physical activity, nor did they consume anything but water. Gene expression was performed on peripheral blood mononuclear cells (PBMCs) at postprandial period (4 hours after breakfast) by microarray analysis and verified by qRT-PCR.

Project description:We studied the effect of dietary fat type, varying in polyunsaturated/saturated fatty acid ratio's (P/S) on development of metabolic syndrome. C57Bl/6J mice were fed purified high-fat diets (45E% fat) containing palm oil (HF-PO; P/S 0.4), olive oil (HF-OO; P/S 1.1) or safflower oil (HF-SO; P/S 7.8) for 8 weeks. A low-fat palm oil diet (LF-PO; 10E% fat) was used as a reference. Additionally, we analyzed diet-induced changes in gut microbiota composition and mucosal gene expression. The HF-PO diet induced a higher body weight gain and liver triglyceride content compared to the HF-OO, HF-SO or LF-PO diet. In the intestine, the HF-PO diet reduced microbial diversity and increased the Firmicutes/Bacteroidetes ratio. Although this fits a typical obesity profile, our data clearly indicate that an overflow of the HF-PO diet to the distal intestine, rather than obesity itself, is the main trigger for these gut microbiota changes. A HF-PO diet-induced elevation of lipid metabolism-related genes in the distal small intestine confirmed the overflow of palm oil to the distal intestine. Some of these lipid metabolism-related genes were previously already associated with the metabolic syndrome. In conclusion, our data indicate that saturated fat (HF-PO) has a more stimulatory effect on weight gain and hepatic lipid accumulation than unsaturated fat (HF-OO and HF-SO). The overflow of fat to the distal intestine on the HF-PO diet induced changes in gut microbiota composition and mucosal gene expression. We speculate that both are directly or indirectly contributive to the saturated fat-induced development of obesity and hepatic steatosis. Keywords: Diet intervention study Nine-week-old C57Bl/6J mice were fed a low-fat diet (LF-PO) and three different types of high-fat diet, based on palm oil (HF-PO; P/S1.0), olive oil (HF-OO; P/S4.6) and safflower oil (HF-SO; P/S10.1) for 8 weeks. Body weight was recorded weekly and after 7 weeks of diet intervention an oral glucose tolerance test was performed. After 2 weeks of diet intervention, 6 mice per high-fat diet group were anaesthetized with a mixture of isofluorane (1.5%), nitrous oxide (70%) and oxygen (30%) and the small intestines were excised. Adhering fat and pancreatic tissue were carefully removed. The small intestines were divided in three equal parts along the proximal to distal axis (SI 1, SI 2 and SI 3) and microarray analysis was performed on mucosal scrapings.

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Human in vivo nutrigenomic effect of olive oil

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