Project description:This SuperSeries is composed of the following subset Series: GSE30905: Microarray analysis on livers, spleens and hearts of mice given distilled water fed with either a normal diet or an atherogenic diet GSE30907: Microarray analysis on livers, spleens and hearts of mice fed an atherogenic diet and supplemented with either oil palm phenolics (OPP) or distilled water Refer to individual Series
Project description:OPP (1500 ppm gallic acid equivalent (GAE)) was supplemented to BALB/c mice given an atherogenic diet for six weeks to observe for possible anti-atherogenic effects. The control group received distilled water instead of OPP. Livers, spleens and hearts were harvested six weeks after the feeding regimen for gene expression studies. Results from the separate microarray data analysis carried out on the different organs show that OPP attenuated the effects of the atherogenic diet in the organs. Total RNA obtained from livers, spleens and hearts of BALB/c mice given OPP (six weeks after administration of an atherogenic diet) were compared to controls given distilled water (liver: three replicates in the treatment group versus four replicates in the control group; spleen and heart: three replicates in the treatment group versus three replicates in the control group for both organs)
Project description:Palmitic acid (C16:0) is the most abundant saturated fatty acid in animals serving as a substrate in lipid synthesis and β-oxidation, and in the modification of proteins called palmitoylation. The influence of dietary palmitic acid on protein palmitoylation in the context of metabolic processes remains largely unknown. In this study we performed high-throughput proteomic analyses of the liver membrane fraction in the mouse to examine the influence of a palm oil-rich diet on the level and S-palmitoylation of proteins. For this purpose, mice were fed for 4 or 12 weeks a diet containing 19.1% of palm oil in addition to 4% soybean oil (45% kcal from fat) while 4% soybean oil (10% kcal from fat) was the only fat source in the control diet. Liver functioning and pro-inflammatory responses of the liver and peritoneal macrophages as well as the input of protein S-palmitoylation to these aspects were assessed in parallel. We found that the diet rich in palm oil induced transient accumulation of C16:0 and C18:1 fatty acids in murine liver leading to changes of the level and S-palmitoylation of numerous proteins involved in liver metabolism and selected innate immune responses. The relatively mild negative impact of such diet on liver functioning can be attributed to a lower bioavailability of palm oil-derived C16:0 vs. that of C18:1 and the efficiency of mechanisms preventing liver injury, including dynamic protein S-palmitoylation.
Project description:BALB/c mice were given an atherogenic diet and compared to those given a normal diet to observe for gene expression changes caused by the atherogenic diet. Both groups of mice received distilled water as drinks ad libitum. Livers, spleens and hearts were harvested six weeks after the feeding regimen for gene expression studies. Results from the separate microarray data analysis carried out on the different organs show that the atherogenic diet caused oxidative stress and inflammation in the organs. Total RNA obtained from livers, spleens and hearts of BALB/c mice given an atherogenic diet (six weeks after the feeding regimen) was compared to those from organs of mice given normal diet (liver: four replicates in the treatment group versus four replicates in the control group; spleen and heart: three replicates in the treatment group versus four replicates in the control group for both organs)
Project description:The beneficial effects of dietary long-chain (LC) n-3 polyunsaturated fatty acids (PUFA) in the prevention and/or treatment of some metabolic disorders result largely from their capacity to regulate the transcription level of many genes involved in metabolic and physiological homeostasis, especially in the liver. In this respect, they are known to bind and activate the Peroxisome Proliferator-Activated Receptor alpha (PPARalpha). The precursor of LC-PUFA, a-linoleic acid (ALA, C18:3 n-3) share some beneficial metabolic effects with its LC derivatives, however its role in gene regulation is poorly documented. Here, we analysed the hepatic transcriptome of mice fed for 5 weeks diets rich in either saturated FA from palm oil (PALM group) or ALA from linseed oil (LIN group). This modification of dietary fatty acid composition in a context of a high fat diet had a subtle but significant effect on the hepatic transcriptome. We identified mainly a group of genes that were upregulated in the LIN vs the PALM group and that include several well-known PPARalpha target genes involved in lipid and xenobiotic metabolism. Liver gene expression was measured in male C57BL/6J mice fed during 5 weeks a high fat diet (51% energy from fat) containing palm oil, rich in saturated fatty acids (n=10) or linseed oil, rich in 18:3 n-3 (n=8)
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
Project description:Microarray analysis on livers, spleens and hearts of mice fed an atherogenic diet and supplemented with either oil palm phenolics (OPP) or distilled water
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.
Project description:H3K4me3 profiling of OSCC secondary (2ary) recipient primary tumors (PTs) following in vivo exposure to control (CTRL) or palm oil-enriched (PALM) diet in primary recipient mice