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.
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.
Project description:We have previously demonstrated that the gut microbiota can play a role in the pathogenesis of conditions associated with exposure to environmental pollutants. It is well accepted that diets high in fermentable fibers such as inulin can beneficially modulate the gut microbiota and lessen the severity of pro-inflammatory diseases. Therefore, we aimed to test the hypothesis that hyperlipidemic mice fed a diet enriched with inulin would be protected from the pro-inflammatory toxic effects of PCB 126.
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
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)
Project description:Increasing the consumption of dietary fibre has been proposed to alleviate the progression of non-communicable diseases such as obesity, type 2 diabetes and cardiovascular disease, yet the effect of dietary fibre on host physiology remains unclear. In this study, we performed a multiple diet feeding study in C57BL/6J mice to compare high fat and high fat modified with dietary fibre diets on host physiology and gut homeostasis by combining proteomic, metagenomic, metabolomic and glycomic techniques with correlation network analysis. We observed significant changes in physiology, liver proteome, gut microbiota and SCFA production in response to high fat diet. Dietary fibre modification did not reverse these changes but was associated with specific changes in the gut microbiota, liver proteome, SCFA production and colonic mucin glycosylation. Furthermore, correlation network analysis identified gut bacterial-glycan associations.
Project description:The mouse stool samples were collected from different diets fed mice and bacterial cells were harvest for metaproteomic analysis for understanding the role ofdiet on gut microbiota.
Project description:To determine whether diet-induced changes in gut microbiota modified intestinal immune cell gene expression, we analyzed the transcriptome of CD4 T lymphocytes isolated from the lamina propria of the small intestine from mice fed with different diets.
Project description:Diet plays a major role in altering the composition and function of the gut microbiota. Previously most studies have focused on the effects of fiber, fat, and different amounts of protein on the gut microbiota. In this study we investigated how different sources of protein affect the gut microbiota of mice. We fed conventional and germ-free C57BL/6J mice a series of defined diets where the source of dietary protein was the key difference, which made up twenty or forty percent of the diet. The dietary protein sources used were purified protein. The diets were fed to the same mice for one week each with a fecal sample collected at the end of each week. The diets were fed in this order: standard chow, 20% soy, 20% casein, 20% rice, 40% soy, 20% yeast, 40% casein, 20% pea, 20% egg white protein, 20% chicken bone broth, and lastly at the end of the experiment half of the mice were fed the 20% soy and half the mice the 20% casein diet again as a control. We did not collect fecal samples for the chicken bone broth diet as the diet was stopped prematurely due to diet intolerance. 12 germ-free mice (6 female, 6 male) in four cages were used. 12 mice with a conventional gut microbiota in four cages were used (6 female, 6 male). One germ-free mouse was found dead after diet 5 (20% yeast) and one conventional mouse was sacrificed after the second diet (20% casein). No sample could be collected from one of the conventional mice after the 20% egg white diet.
Project description:A number of studies have proposed that excess food intake, particularly of high fat diets arise due dysregulation of homeostatic mechanisms regulating neuroendocrine control of appetite and energy balance. Current dogma suggests high fat diets invoke hypothalamic inflammation which reduces hypothalamic sensitivity to metabolic and hormonal cues of conveying peripheral status of energy balance, such as leptin and insulin. A hypothesis for the mechanism leading to hypothalamic inflammation is based on high fat diet mediated changes in gut microbiota which are then proposed to increase circulating levels of lipopolysaccharide (LPS). This in turn activates a hypothalamic inflammatory response via the toll-like receptor (TLR4) and CD14. The aim of this study was to determine hypothalamic gene expression in response to long term feeding of a high fat diet, taking into account the importance of using a control diet with a similar composition and balanced for sucrose content.