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Expression data from germ-free and conventional mice fed lard or fish oil for 11 weeks

ABSTRACT: Dietary lipids and gut microbiota may both influence adipose tissue physiology. By feeding conventional and germ-free mice high fat diets with different lipid compositon we aimed to investigate how dietary lipids and the gut microbiota interact to influence inflammation and metabolism in epididymal adipiose tissue (EWAT)

ORGANISM(S): Mus musculus

PROVIDER: GSE70922 | GEO | 2015/07/14

SECONDARY ACCESSION(S): PRJNA289927

REPOSITORIES: GEO

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Expression data from germ-free and conventional mice fed lard or fish oil for 11 weeks

Project description:Dietary lipids and gut microbiota may both influence adipose tissue physiology. By feeding conventional and germ-free mice high fat diets with different lipid compositon we aimed to investigate how dietary lipids and the gut microbiota interact to influence inflammation and metabolism in epididymal adipiose tissue (EWAT) Wild-type C57Bl/6 male mice 11 weeks of age were fed isocaloric diets (45% kcal fat) with either menhaden fish oil (Research Diets, D05122102) or lard (Research Diets, D10011202) for 11 weeks. Epididymal WAT samples were harvested at the end of the experiment and analyzed by microarray.

2015-07-14 | E-GEOD-70922 | biostudies-arrayexpress

Expression data in liver from germ-free and conventional mice fed lard or fish oil for 11 weeks

2016-02-29 | GSE73195 | GEO

Expression data in liver from germ-free and conventional mice fed lard or fish oil for 11 weeks

Project description:Dietary lipids and gut microbiota may both influence adipose tissue physiology. By feeding conventional and germ-free mice high fat diets with different lipid compositon we aimed to investigate how dietary lipids and the gut microbiota interact to influence inflammation and metabolism in the liver Wild-type C57Bl/6 male mice 11 weeks of age were fed isocaloric diets (45% kcal fat) with either menhaden fish oil (Research Diets, D05122102) or lard (Research Diets, D10011202) for 11 weeks. Liver samples were harvested at the end of the experiment and analyzed by microarray.

2016-02-29 | E-GEOD-73195 | biostudies-arrayexpress

The interplay between dietary fatty acids and gut microbiota influences host metabolism and hepatic steatosis

Project description:Dietary lipids can affect metabolic health through gut microbiota-mediated mechanisms, but the influence of lipid-microbiota interaction on liver steatosis is unknown. We investigated the effect of dietary lipid composition on human microbiota in an observational study and combined diet experiments with microbiota transplants to study lipid-microbiota interactions and liver status in mice. In humans, low intake of saturated fatty acids (SFA) was associated with increased microbial diversity independent of fiber intake. In mice, cecum levels of SFA correlated negatively with microbial diversity and were associated with a shift in butyrate and propionate producers. Mice fed poorly absorbed SFA had improved metabolism and liver status. These features were transmitted by microbial transfer. Diets enriched in n-6- and/or n-3-polyunsaturated fatty acids were protective against steatosis but had minor influence on the microbiota. In summary, we find that unabsorbed SFA correlate with microbiota features that may be targeted to decrease liver steatosis.

2023-08-03 | GSE222060 | GEO

Rat colon LC-MSMS - Intake of Fish Oil Specifically Modulates Colonic Muc2 Expression in Middle-Aged Rats by Suppressing the Glycosylation Process

Project description:Dietary fats have been shown to affect gut microbiota composition and aging gene transcription of middle-aged rats at a normal dose, but little is known about such an effect on gut barrier. In colon, the main component of mucus layer is Muc2, produced by the goblet cells. This study investigated the changes in Muc2 expression, goblet cells proliferation, TLRs and inflammatory cytokines in the colon of middle-aged rats. Proteome technology was applied to explore the possible molecular mechanisms. The results indicated that intake of fish oil at a normal dose downregulated colonic Muc2 expression, and this negative effect of fish oil probably involved the suppression of mucin glycosylation process.

2018-01-02 | PXD007229 | Pride

Fiber and Fish Oil Supplements for the Prevention of Colorectal Cancer

Project description:This trial studies how fiber and fish oil supplements affect the metabolism and activities of colon cells in healthy individuals. Diet is an important risk factor for colorectal cancer, and several dietary components important in colorectal cancer prevention are modified by gut microbial metabolism. Giving fiber and fish oil supplements may inhibit the growth of gut cells and ultimately reduce risk of colorectal cancer.

| 2325667 | ecrin-mdr-crc

Long-term dietary replacement of fish meal and fish oil in diets for rainbow trout: effects on intestinal and hepatic gene expression

Project description:In the context of replacing fish meal and fish oil in feeds for aquaculture, rainbow trout alevins received from first-feeding onwards, one of the three experimental diets: V (100% plant-based), C (mix of FM-FO & plant ingredients) or M (100% FM-FO based). The long term effects of such dietary replacement on the intestinal (mid gut) and hepatic transcriptome were studied in juveniles after a 7-month feeding trial at 7°C.

2018-02-14 | GSE84985 | GEO

Deciphering the combinatorial influence of diet and the microbiota on experimental colitis

Project description:Background & Aims: The complex interactions between diet and the microbiota that influence mucosal inflammation and inflammatory bowel disease are poorly understood. Experimental colitis models provide the opportunity to control and systematically perturb diet and the microbiota in parallel to quantify the contributions between multiple dietary ingredients and the microbiota on host physiology and colitis. Methods: To examine the interplay of diet and the gut microbiota on host health and colitis, we fed over 40 different diets with varied macronutrient sources and concentrations to specific pathogen free or germ free mice either in the context of healthy, unchallenged animals or dextran sodium sulfate colitis model. Results: Diet influenced physiology in both health and colitis across all models, with the concentration of protein and psyllium fiber having the most profound effects. Increasing dietary protein elevated gut microbial density and worsened DSS colitis severity. Depleting gut microbial density by using germ-free animals or antibiotics negated the effect of a high protein diet. Psyllium fiber influenced host physiology and attenuated colitis severity through microbiota-dependent and microbiota-independent mechanisms. Combinatorial perturbations to dietary protein and psyllium fiber in parallel explain most variation in gut microbial density, intestinal permeability, and DSS colitis severity, and changes in one ingredient can be offset by changes in the other. Conclusions: Our results demonstrate the importance of examining complex mixtures of nutrients to understand the role of diet in intestinal inflammation. Keywords: IBD; Diet; Microbiota; Mouse Models; Systems Biology

2017-10-30 | GSE104461 | GEO

Dietary intake of antioxidant curcumin reduces eIF2 phosphorylation and diacylglycerol and glycerolipid contents in white adipose tissue of obese mice

Project description:To elucidate the bioactive property of the dietary antioxidant curcumin, we examined tissue distribution and the gene expression- and lipidomic-profiles in epididymal white adipose tissue (eWAT) of the diet-induced obese mice. Dietary intake of curcumin (0.1% W/W) didn’t affect the eWAT weight and the plasma lipid levels but reduced the levels of lipid peroxidation marker in eWAT. Curcumin was a slightly accumulated in eWAT and altered the gene expression associated with eukaryotic translation initiation factor 2 (EIF2) signaling. Curcumin suppressed the endoplasmic reticulum (ER) stress-related eIF2 phospholyration, the accumulation of macrophages and the expression of oxidative stress-sensitive transcription factor NF-κB p65 and leptin, whereas anti-inflammatory effect wasn’t enough to reduce the TNF-α and IFN-γ levels. Lipidomic- and gene expression analysis suggests that curcumin reduced the contents of some diacylglyverols (DAGs) and DAG derived glycerophospholipids by suppressing the expressions of lipogenesis-related glycerol-3-phosphate acyltransferase 1 and lipolysis-related adipose triglyceride lipase.

2018-07-02 | GSE100388 | GEO

Microbes modulate sympathetic neurons via a gut-brain circuit

Project description:Gut-brain connections monitor the intestinal tissue and its microbial and dietary content1, regulating both intestinal physiological functions such as nutrient absorption and motility2,3, and brain–wired feeding behaviour2. It is therefore plausible that circuits exist to detect gut microbes and relay this information to central nervous system (CNS) areas that, in turn, regulate gut physiology4. We characterized the influence of the microbiota on enteric–associated neurons (EAN) by combining gnotobiotic mouse models with transcriptomics, circuit–tracing methods, and functional manipulation. We found that the gut microbiome modulates gut–extrinsic sympathetic neurons; while microbiota depletion led to increased cFos expression, colonization of germ-free mice with short-chain fatty acid–producing bacteria suppressed cFos expression in the gut sympathetic ganglia. Chemogenetic manipulations, translational profiling, and anterograde tracing identified a subset of distal intestine-projecting vagal neurons positioned to play an afferent role in microbiota–mediated modulation of gut sympathetic neurons. Retrograde polysynaptic neuronal tracing from the intestinal wall identified brainstem sensory nuclei activated during microbial depletion, as well as efferent sympathetic premotor glutamatergic neurons that regulate gastrointestinal transit. These results reveal microbiota–dependent control of gut extrinsic sympathetic activation through a gut-brain circuit.

2020-03-20 | GSE145986 | GEO

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