Olive oil phenols and miRNA in the aging mouse brain
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
SUBMITTER: Cristina Luceri
PROVIDER: E-MTAB-1549 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
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Project description:The aim of this study was to evaluate whether the dietary treatment with olive oil phenols modifies the profile of microRNA and gene expression in different areas of the aging mouse brain and to correlate these changes with the cognitive and motor changes observed in the same aging animals. C57Bl/6J mice were fed from middle age to senescence with extra-virgin olive oil (10% wt/wt dry diet) rich in polyphenols (H-EVOO group, total polyphenol dose/day, 6mg/kg) or with the same extra-virgin olive oil deprived of phenolic compounds (L-EVOO group). By whole gene expression analysis we identified 53 genes differentially expressed in the cortex of H-EVOO mice compared to L-EVOO mice and no genes differentially expressed in the cerebellum. Gene Set Expression analysis (GSEA) found 6 gene sets significantly modulated by the dietary treatments in cortex, like the agrin-related postsynaptic differentiation gene set, involved in cholinergic synaptic differentiation and maintenance, exerting effects on axonal and dendritic growth. miRNA profiling found only 6 miRNA differentially modulated after 12 months of feeding and 63 after six months. Among them we noted miRNAs previously associated to neurodegenerative disorders such as mir101, 8.5 time more expressed in the cortex of L-EVOO fed mice compared to the H-EVOO group and no expressed in young mice. We extended our analysis on cortex harvested from transgenic TgCRND8 mice, a model of Alzheimer's disease, observing an overall down-regulation of miRNAs compared to mice of the same age. On the contrary, the H-EVOO fed mice cortex showed expression profiles similar to those of young mice, results supporting our previous data demonstrating that extra virgin olive oil rich in polyphenols may improve some age-related dysfunctions.
2013-09-10 | E-MTAB-1530 | biostudies-arrayexpress
Project description:HLA-B27 transgenic rats, experimental model of chronic colitis, fed with a diet in which the lipid component was provided by corn oil (CO group), extra-virgin olive oil rich in phenols, 718.8 mg of total phenols/kg of olive oil (EVOO group) or the same extra-virgin olive oil, deprived of phenolic compounds but retaining other minor components such as a-tocopherol (ROO group).
2018-11-26 | E-MTAB-6218 | biostudies-arrayexpress
Project description:Since the liver is the central organ of metabolism, changes in diet have a great impact on this organ and overall on health with aging. It is well known that dietary fat source strongly influences many parameters of the hepatic mitochondria. These changes includes modification of lipid composition of mitochondrial membrane, affecting the mtETC functions, oxidative stress and mtDNA alterations. We used microarrays to detail the changes in gene expression provides by feeding lifelong on different dietary fat sources, and identified distinct classes of up and down-regulated genes during aging under different dietary conditions. Rats were fed lifelong on a normolipidic diet (4% w/w) with virgin olive, sunflower or fish oil as dietary fat source. At 6 and 24 months, animals were killed and liver were removed for RNA extraction and hybridization on Affymetrix microarrays. We sought to obtain changes in gene expression due to both aging and dietary conditions. There were 6 experimental groups (virgin olive oil at 6 months, sunflower oil at 6 months, fish oil at 6 months, virgin olive oil at 24 months, sunflower oil at 24 months and fish oil at 24 months. 3 animals were studied of each experimental group, so a total of 18 samples were analyzed.
2014-03-26 | E-GEOD-56166 | biostudies-arrayexpress
Project description:Microarray gene expression profiling of aorta genes of APOE-deficient mice receiving atherosclerosis treatment with the ACE inhibitor captopril. Hypercholesterolemic APOE-deficient mice were used as a standard model of atherosclerosis to study gene expression changes during atherosclerosis treatment with the ACE inhibitor captopril. Microarray analysis was performed of whole aortas isolated from captopril-treated APOE-deficient mice relative to untreated APOE-deficient mice with overt atherosclerosis, and nontransgenic control mice. Microarray gene expression profiling revealed that captopril-mediated atherosclerosis prevention involved inhibition of aorta-infiltrating immune cells such as pro-atherogenic T lymphocytes and macrophages. Experiment Overall Design: Microarray gene expression profiling was performed of whole aortas isolated from APOE-deficient mice with atherosclerosis relative to captopril-treated APOE-deficient mice, and nontransgenic control mice. Three study groups were analyzed, i.e. 8-months-old untreated APOE-deficient mice with overt atherosclerosis, age-matched APOE-deficient mice treated for 7 months with the angiotensin-converting enzyme (ACE) inhibitor, captopril (20 mg/kg in drinking water), and nontransgenic control C57BL/6J mice. Two biological replicates were made of each group, and total RNA of three aortas was pooled for one gene chip.
2009-12-14 | E-GEOD-19286 | biostudies-arrayexpress
Project description:Background and Aims: Inflammasome-mediated caspase-1 activity regulates the maturation and release of the pro-inflammatory cytokines interleukin (IL)-1M-CM-^_ and IL-18. Recently, we showed that caspase-1 deficiency strongly reduces high fat diet-induced adiposity although the mechanism is still unclear. We now aimed to elucidate the mechanism by which caspase-1 deficiency reduces modulates resistance to high fat diet-feeding fat accumulation in adipose tissue by focusing on the role of caspase-1 in the regulation of triglyceride (TG)-rich lipoprotein metabolism. Methods: Caspase-1 deficient and wild-type mice (both C57Bl/6 background) were used to determine postprandial TG kinetics, intestinal TG absorption, VLDL-TG production as well as TG clearance, all of which strongly contribute to the supply of TG for storage in adipose tissue. Micro-array and qPCR analysis were used to unravel intestinal and hepatic metabolic pathways involved. Results: Caspase-1 deficiency reduced the postprandial response to an oral lipid load, while tissue specific clearance of TG-rich lipoproteins was not changed. Indeed, an oral olive oil gavage containing [3H]TG revealed that caspase-1 deficiency significantly decreased intestinal chylomicron-TG production and reduced the uptake of [3H]TG-derived FA by liver, muscle, and adipose tissue. Similarly, caspase-1 deficiency reduced the hepatic VLDL-TG production without reducing VLDL-apoB production, despite an elevated hepatic TG content. Pathway analysis revealed that caspase-1 deficiency reduces intestinal and hepatic expression of genes involved in lipogenesis. Conclusions: Absence of caspase-1 reduces assembly and secretion of TG-rich lipoproteins, thereby reducing the availability of TG-derived FA for uptake by peripheral organs including adipose tissue. We anticipate that caspase-1 represents a novel link between innate immunity and lipid metabolism. Keywords: Expression profiling by array Wild-type (WT) and Casp1-null mice were maintained at lab chow. Animals, aged between 14 and 16 weeks (n=3 per genotype), were killed and liver and intestinal segments were removed. Livers were isolated from mice that were fasted over night, whereas intesines were removed from mice 2 hrs after they received an oral lipid load.Total RNA was isolated and subjected to gene expression profiling.
2013-09-15 | E-GEOD-32515 | biostudies-arrayexpress
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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