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NUTRITIONAL OPTIMISATION WITH SPECIFIC NUTRIENTS IN COLORECTAL CANCER PATIENTS RECEIVING CHEMOTHERAPY; A CASE CONTROL STUDY, RANDOMIZED CONTROLLED TRIAL

ABSTRACT: Intervention 1: Fish oil /intervention. 1200mg (providing omega-3 420 mg EPA and 280 mg DHA) 5 times daily for 8 weeks after starting chemotherapy. Intervention 2: Probiotics/ intervention. 3 gr Granule contains the following probiotic strains: L.acidophilus, L. lactis, L. casei subsp, L. longum, L. bifidum, L. infantis twice a day for 4 weeks after starting chemotherapy. Intervention 3: Sunflower oil /control 1200mg 5 times daily for 8 weeks after starting chemotherapy. Intervention 4: Lactose / control 3 gr Granule contains: Lactose, Maltodextrin, Citric Acid, Ascorbic Acid, Skim Milk Powder, and Sugar twice a day for 4 weeks after starting chemotherapy.;Treatment - Drugs;Treatment - Drugs;Placebo;Placebo;Fish oil /intervention. 1200mg (providing omega-3 420 mg EPA and 280 mg DHA) 5 times daily for 8 weeks after starting chemotherapy;Probiotics/ intervention. 3 gr Granule contains the following probiotic strains: L.acidophilus, L. lactis, L. casei subsp, L. longum, L. bifidum, L. infantis twice a day for 4 weeks after starting chemotherapy;Sunflower oil /control 1200mg 5 times daily for 8 weeks after starting chemotherapy;Lactose / control 3 gr Granule contains: Lactose, Maltodextrin, Citric Acid, Ascorbic Acid, Skim Milk Powder, and Sugar twice a day for 4 weeks after starting chemotherapy Primary outcome(s): Quality of life. Timepoint: Before starting chemotherapy and supplementationa nd after completion of supplementation and chemotherapy. Method of measurement: EORTC QLQ C-30. Study Design: Randomization: Randomized, Blinding: Double blinded, Placebo: Used, Assignment: Parallel, Purpose: Prevention.

DISEASE(S): Malignant Neoplasm Of Rectum,Malignant Neoplasm Of Rectosigmoid Junction,Condition 1: Colorectal Cancer. Condition 2: Rectosigmoid Cancer. Condition 3: Rectal Cancer,Malignant Neoplasm Of Colon

PROVIDER: 2476898 | ecrin-mdr-crc |

REPOSITORIES: ECRIN MDR

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Project description:Fish oil supplementation has been shown to alter gene expression of mononuclear cells both in vitro and in vivo. However, little is known about the total transcriptomic profile in healthy subjects after intake of fish oil compared to a control group. The objective was to examine the gene expression profile in peripheral blood mononuclear cells (PBMCs) in healthy subjects after intake of fish oil for seven weeks using whole-genome transcriptomic analysis. In a double-blinded randomized controlled study, healthy subjects received capsules containing either 8 g/d of fish oil (1.6 g/d EPA+DHA) (n=17) or 8 g/d of high oleic sunflower oil (n=19) for seven weeks. The results provide important information on how fish oil may modulate basic cellular processes involved in normal cell function and lymphocyte activation such as ER stress, cell cycle and apoptosis. The subjects were taking 16 capsules/d containing 8 g/d of either fish oil (FO) or high oleic sunflower oil (HOSO) for seven weeks. Subjects in the FO group received capsules containing 0.7 g/d EPA + 0.9 g/d DHA from cod liver oil (Gadidae sp., TINE EPADHA Oil 1200) provided by TINE SA (Oslo, Norway) and subjects in HOSO group received high oleic sunflower oil purchased from AarhusKarlshamn AB (Malmӧ, Sweden). Prior to the baseline visit (visit 2, wk 0), the subjects conducted a four-week washout period, where foods containing marine n-3 fatty acids were excluded from the diet. The first three weeks of the intervention period the subjects conducted a fully-controlled isocaloric diet, provided with all food and beverages at Akershus University College, Norway. During the last four weeks of the intervention the subjects returned to their habitual diet. Use of fish, fish products, marine n-3 enriched food or dietary supplements was not allowed during the entire study period of 11 weeks. The study was registered at www.clinicaltrial.gov (IDno. NCT01034423). The subjects met for four visits and blood samples for the transcriptome analyses were collected at wk 0, 3 and 7. After blood collection, PBMCs were isolated by using the BD Vacutainer Cell Preparation tubes according to the manufacturer's instructions (Becton, Dickinson and Company, NJ 07417, USA). Pellets were frozen and stored at -80o C for further RNA isolation.

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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NUTRITIONAL OPTIMISATION WITH SPECIFIC NUTRIENTS IN COLORECTAL CANCER PATIENTS RECEIVING CHEMOTHERAPY; A CASE CONTROL STUDY, RANDOMIZED CONTROLLED TRIAL

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