E-MTAB-8332
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ABSTRACT:
PROVIDER: E-MTAB-8332 | ExpressionAtlas | 2019-10-04
REPOSITORIES: ExpressionAtlas
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Project description:RNA-seq of full thickness small intestine from wild type mice that were either exposed or not with western diet for 8 weeks
| PRJEB34408 | ENA
Project description:The peroxisome proliferator-activated receptor alpha (PPARα) is a fatty acid-activated transcription factor that governs a variety of biological processes. Little is known about the role of PPARα in the small intestine. Since this organ is frequently exposed to high levels of PPARα ligands via the diet, we set out to characterize the function of PPARα in small intestine using functional genomics experiments and bioinformatics tools. PPARα was expressed at high levels in both human and murine small intestine. Detailed analyses showed that PPARα was expressed highest in villus cells of proximal jejunum. Microarray analyses of total tissue samples revealed, that in addition to genes involved in fatty acid and triacylglycerol metabolism, transcription factors and enzymes connected to sterol and bile acid metabolism, including FXR and SREBP1, were specifically induced. In contrast, genes involved in cell cycle and differentiation, apoptosis, and host defense were repressed by PPARα activation. Additional analyses showed that intestinal PPARα dependent gene regulation occurred in villus cells. Functional implications of array results were corroborated by morphometric data. The repression of genes involved in proliferation and apoptosis was accompanied by a 22% increase in villus height, and a 34% increase in villus area of wild-type animals treated with WY14643. This is the first report providing a comprehensive overview of processes under control of PPARα in the small intestine. We show that PPARα is an important transcriptional regulator in small intestine, which may be of importance for the development of novel foods and therapies for obesity and inflammatory bowel diseases. Experiment Overall Design: Pure bred wild-type (129S1/SvImJ) and PPARα-null (129S4/SvJae) mice were treated with the synthetic PPARα ligand WY14,643 (0.1% w/w) for 5 days. The complete intestines were then removed and total RNA was isolated. Experiment Overall Design: In total 4 experimental groups were present: wild type mice fed the control diet (AIN93M), wild type mice fed the control diet supplemented with 0.1% w/w WY14,643 for 5 days, PPARα knockout mice fed the control diet, PPARα knockout mice fed the control diet supplemented with 0.1% w/wWY14,643 for 5 days. Experiment Overall Design: RNA of 3 biological replicates was hybridized to Affymetrix 430A arrays. Experiment Overall Design: Five microgram total RNA was labelled according to the ENZO-protocol, fragmented and hybridized according to Affymetrix's protocols.
2008-06-13 | E-GEOD-5475 | biostudies-arrayexpress
Project description:By regulating digestion and absorption of nutrients and providing a barrier against the external environment the intestine provides a crucial contribution to the maintenance of health. To what extent aging-related changes in the intestinal system contribute to the impaired health of the aging body is still under debate. Young (4 months) and old (21 months) male C57BL/6J mice were fed a control low-fat (10E%) or a high-fat diet (45E%) for 2 weeks. During the intervention gross energy intake and energy excretion in the feces were measured. After sacrifice the small and large intestine were isolated whereby the small intestine was divided in three equal parts. Of each of the isolated segments Swiss rolls were prepared for histological analysis and the luminal content was isolated to examine alterations in the microflora with 16S rRNA Q-PCR. Furthermore, mucosal scrapings were isolated from each segment to determine differential gene expression by microarray analysis and global DNA methylation by pyrosequencing. Digestible energy intake was similar between the two age groups on both the control and the high-fat diet implying that macronutrient metabolism is not affected in 21-month-old mice. This observation was supported by the fact that the microarray analysis on RNA from intestinal scrapings showed no marked changes in expression of genes involved in metabolic processes. Decreased expression of Cubilin was observed in the intestine of 21-month-old mice, which might contribute to aging-induced vitamin B12 deficiency. Furthermore, microarray data analysis revealed enhanced expression of a high number of genes involved in immune response and inflammation in the colon, but not in the small intestine of the 21-month-old mice. Aging-induced global hypomethylation was observed in the colon and the distal part of the small intestine, but not in the first two sections of the small intestine. In 21-month old mice the most pronounced effects of aging was observed in the colon, limited changes were observed in the small intestine. Young (4M) and old (21M) wild type C57BL/6J mice were fed a low-fat diet or high-fat diet for 2 weeks. After the diet intervention period, the animals were killed and scrapings were made of the colon. Total RNA was isolated and subjected to gene expression profiling.
2012-09-03 | E-GEOD-39973 | biostudies-arrayexpress
Project description:Fatty acid transport protein 2 (FATP2) is highly expressed in liver, small intestine, and kidney where it functions in both the uptake of exogenous long chain fatty acids (LCFAs) and in the activation to CoA thioesters of very long chain fatty acids (VLCFAs). Here we address the phenotypic impacts of deleting FATP2 followed by an unbiased RNA-seq analysis of the liver transcriptome. Wild type (C57BL/6J) and fatp2 null (fatp2-/-) mice (5 weeks old) were maintained on a standard chow diet for 6 weeks (11 weeks old). The male fatp2-/- mice had 258 differentially expressed genes (DEGs) and the female mice had a total of 91. Of significance was the finding that most of the genes with increased expression in the fatp2-/- liver are regulated by the transcription factor peroxisome proliferator-activated receptor alpha (PPARα). Taken together, FATP2 has a broad impact on the expression of key lipid metabolic genes in the liver regulated by PPARα.
2019-11-09 | GSE140147 | GEO
Project description:We found that western diet consumption for 8 weeks resulted in decrease in the percentage of normal Paneth cell population in wild type mice, indicating that western diet could negatively affect Paneth cell function. We performed transcriptional profiling to identify molecular mechanisms associated with Paneth cell defect in wild type mice exposed to western diet. Male mice were used at 4-5 weeks of age. The whole ileum of the mice were harvested for transcriptomic analysis after completing 8 weeks of western diet treatment.
2021-12-02 | E-MTAB-8334 | biostudies-arrayexpress
Project description:We found that low protein diet consumption for 3 weeks resulted in reduction in the Paneth cells and goblet cells and villous height in wild type mice, indicating that low protein diet could negatively affect gut pathology. We performed transcriptional profiling to identify dysregulated molecular pathways in wild type mice exposed to low diet. Male mice were used at 4-5 weeks of age. The full-thickness ileum of the mice were harvested for transcriptomic analysis after completing 4 weeks of low protein diet treatment.
2023-07-02 | E-MTAB-11276 | biostudies-arrayexpress
Project description:We found that western diet consumption resulted in decrease in the percentage of normal Paneth cell population in wild type mice, indicating that western diet negatively regulates Paneth cell homeostasis. We performed transcriptional profiling to identify molecular mechanisms associated with Paneth cell defect in wild type mice exposed to western diet. Male mice were used at 4-5 weeks of age, and were fed with either standard or western diet. The whole ileum of the mice were harvested for transcriptomic analysis after completing 8 weeks of diet consumption.
2021-12-02 | E-MTAB-8332 | biostudies-arrayexpress
Project description:By regulating digestion and absorption of nutrients and providing a barrier against the external environment the intestine provides a crucial contribution to the maintenance of health. To what extent aging-related changes in the intestinal system contribute to the impaired health of the aging body is still under debate. Young (4 months) and old (21 months) male C57BL/6J mice were fed a control low-fat (10E%) or a high-fat diet (45E%) for 2 weeks. During the intervention gross energy intake and energy excretion in the feces were measured. After sacrifice the small and large intestine were isolated whereby the small intestine was divided in three equal parts. Of each of the isolated segments Swiss rolls were prepared for histological analysis and the luminal content was isolated to examine alterations in the microflora with 16S rRNA Q-PCR. Furthermore, mucosal scrapings were isolated from each segment to determine differential gene expression by microarray analysis and global DNA methylation by pyrosequencing. Digestible energy intake was similar between the two age groups on both the control and the high-fat diet implying that macronutrient metabolism is not affected in 21-month-old mice. This observation was supported by the fact that the microarray analysis on RNA from intestinal scrapings showed no marked changes in expression of genes involved in metabolic processes. Decreased expression of Cubilin was observed in the intestine of 21-month-old mice, which might contribute to aging-induced vitamin B12 deficiency. Furthermore, microarray data analysis revealed enhanced expression of a high number of genes involved in immune response and inflammation in the colon, but not in the small intestine of the 21-month-old mice. Aging-induced global hypomethylation was observed in the colon and the distal part of the small intestine, but not in the first two sections of the small intestine. In 21-month old mice the most pronounced effects of aging was observed in the colon, limited changes were observed in the small intestine. Young (4 months) and old (21 months) C57BL/6J mice were fed a low-fat (10E%) diet or high-fat (45%E) diet for 2 weeks. After the diet intervention period, the animals were killed and scrapings were made of the proximal, middle and distal part of the small intestine. Total RNA was isolated, pooled and subjected to gene expression profiling.
2012-09-03 | E-GEOD-39974 | biostudies-arrayexpress
Project description:Obesity and insulin resistance are two major risk factors underlying the metabolic syndrome. To gain more insight in the role of the small intestine in the etiology of these metabolic disorders, a microarray study was performed on small intestines (SI) of C57BL/6J mice that were fed a high fat diet mimicking the fatty acid composition of a Western-style human diet. The mice became obese and developed dietary fat-induced glucose intolerance. For gene expression profiling, the small intestines were subdivided in three equal parts along the longitudinal axis. The most pronounced effects of dietary fat were detected in part 2 of the small intestine. The biological processes that were most extensively modulated on a high fat diet were related to lipid metabolism, especially β- and Ï-fatty acid oxidation seemed to play an important role, cell cycle and inflammation/immune response. An additional secretome analysis revealed differentially expressed secreted proteins, such as Il18, Ffgf15, Mif, Igfbp3 and Angptl4, which might provoke systemic effects in peripheral organs by influencing their metabolic homeostasis. Furthermore, many of the dietary fat-modulated genes and biological processes in small intestine were previously already associated with obesity and/or insulin resistance. Together, the data of this exploratory study provided various leads for an essential role of the small intestine in development of obesity and/or insulin resistance. Experiment Overall Design: After a run-in period of 3 weeks on a low-fat diet, 9 weeks old mice were fed a high- (HF) or a low-fat (LF) purified diet for 2, 4, and 8 weeks (n=6 per diet, per time point). Body weight was recorded weekly and after 7 weeks of diet intervention an oral glucose tolerance test was performed. At the end of the experiment, mice were anaesthetized with a mixture of isofluorane (1.5%), nitrous oxide (70%) and oxygen (30%). The small intestines were excised and the 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).
2008-06-20 | E-GEOD-8582 | biostudies-arrayexpress
Project description:The aim of this project was to explore the role of Alginate oligosaccharides (AOS) on the development small intestine. The mice were treated with one dose busulfan then the mice were dosed with AOS for 5 weeks. Then the small intestine were collected. The RNA from small intestine was used for the RNA-seq analysis to search the role of AOS on small intestine development. Groups: W5A0 was from AOS 0 treatment; W5A10 was from AOS 10 treatment; W5BA0 was from busulfan and AOS 0 treatment; W5BA10 was from busulfan and AOS 10 treatment.
2020-09-30 | GSE137989 | GEO