Expression data from Jejunums of C57BL/6J mice
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE21042 | GEO | 2011/03/20
SECONDARY ACCESSION(S): PRJNA126421
REPOSITORIES: GEO
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Project description:Many diseases in digestive system have been improved related to the uptake of high-carbohydrate diet. The underlying mechanism might be related the changes of genes expression in digestive system. We used microarrays to detail the global programme of gene expression during this process. Jejunums from mice fed with high-glucose diet or control were selected for RNA extraction and hybridization on Affymetrix microarrays. We sought to obtain populations of genes related to lipid metabolism in order to increase the temporal resolution of expression profiles. To that end, we analyzed the expressions of genes related to lipid metabolism according to clustering analysis and references.
2011-03-20 | E-GEOD-21042 | biostudies-arrayexpress
Project description:Microarrays experiment was performed to detail the global programme of gene expression in liver of WT male mice in response to fasting (for 24h) or challenged with high glucose or high fructose compared to mice fed ad libitum.
2017-10-13 | GSE92502 | GEO
Project description:The pathogenesis of obesity-related metabolic diseases has been linked to the inflammation of white adipose tissue (WAT), but the molecular interconnections are still not fully understood. MiR-146a controls inflammatory processes by suppressing pro-inflammatory signaling pathways. The aim of this study was to characterize the role of miR-146a in obesity and insulin sensitivityresistance . MiR-146a-/- mice were subjected to a high fat diet followed by metabolic tests and WAT transcriptomics. Gain- and loss-of-function studies were performed using human Simpson-Golabi-Behmel syndrome (SGBS) adipocytes. Compared to controls, miR-146a-/- mice gained significantly more body weight on a high fat diet with increased fat mass and adipocyte hypertrophy. This was accompanied by exacerbated liver steatosis, insulin resistance, and glucose intolerance. Likewise, adipocytes transfected with an inhibitor of miR-146a displayed a decrease in insulin-stimulated glucose uptake, while transfecting miR-146a mimics caused the opposite effect. Natriuretic peptide receptor 3 (NPR3) was identified as a direct target gene of miR-146a in adipocytes and CRISPR/Cas9-mediated knockout of NPR3 increased insulin-stimulated glucose uptake and enhanced de-novo lipogenesis. In summary, miR-146a regulates systemic and adipocyte insulin sensitivity via downregulation of NPR3.
2020-10-12 | GSE151268 | GEO
Project description:Following 20wk of either chow or high fat feeding, tissues were collected from C57BL/6J mice. Gene expression in four tissues that have been associated with obesity-related metabolic complications: white adipose tissue (WAT), skeletal muscle, the liver, and the heart were examined. Data suggest that some tissues may be attempting to reduce the metabolic perturbations that occur in the early stages of obesity. Also, many identified genes were associated with a variety of disorders, thereby serving as potential links between obesity and related health risks. After 3 wk of weaning, male C57BL/6J littermates were randomly separated into control (n=6) and treatment (n=6) groups for each tissue. After an acclimatization period of 1wk, animals were given free access to a chow diet (23% protein, 21% fat, and 55% carbohydrate) or a high fat (HF) diet (15% protein, 59% fat, and 26% carbohydrate) for 20wk. Following the feeding period, animals were fasted for 6h, anesthetized with pentobarbital, and weighed. Blood glucose was assessed in anesthetized mice. Non-esterified fatty acids and immunoreactive insulin was assayed with a double antibody method. Samples of WAT, the liver, gastrocnemius muscle and heart were obtained, frozen with liquid nitrogen, and stored at -80oC until subsequent use. Tissue samples were homogenized at short intervals of time and total RNA was isolated using cold TRIzol (Invitrogen, Ontario, Canada) to prevent RNA degradation. Cdna was prepared to perform the microarrays. For every treatment sample and its corresponding control, two microarrays were performed in a dye-swap normalization experiment. Mouse M7K microarray chip from the Southern Alberta Microarray Facility (University of Calgary, Calgary, AB) were used (GEO Accession: Platform GPL3965).
2011-03-01 | E-GEOD-26029 | biostudies-arrayexpress
Project description:C57BL/6J (B6) and DBA/2J (D2) mice were fed a high-fat/high-cholesterol diet in order to investigate the responses to that diet over time and their underlying genetic factors. We observed distinctly diverse responses between B6 and D2 mice, including dynamic distribution of cholesterol in serum and bile, hepatic apoptosis and dynamic formation of gallstones and atherosclerosis. Hepatic microarray analysis revealed distinctly different gene expression patterns in functional pathway groups including lipid metabolism, oxidative stress, immune/inflammation response and apoptosis, which might account for the different responses.This might provide us not only new insights into gallstones formation and atherosclerosis, but also opportunities to identify candidate genes for high-fat/high-cholesterol related diseases.
2014-12-14 | GSE17810 | GEO
Project description:C57BL/6J (B6) and DBA/2J (D2) mice were fed a high-fat/high-cholesterol diet in order to investigate the responses to that diet over time and their underlying genetic factors. We observed distinctly diverse responses between B6 and D2 mice, including dynamic distribution of cholesterol in serum and bile, hepatic apoptosis and dynamic formation of gallstones and atherosclerosis. Hepatic microarray analysis revealed distinctly different gene expression patterns in functional pathway groups including lipid metabolism, oxidative stress, immune/inflammation response and apoptosis, which might account for the different responses.This might provide us not only new insights into gallstones formation and atherosclerosis, but also opportunities to identify candidate genes for high-fat/high-cholesterol related diseases. C57BL/6J (B6) and DBA/2J (D2) mice were fed a high-fat/high-cholesterol diet in 0,1,4 12,21 weeks,respectively. Liver tissues of mice from each time-point were removed for RNA extraction. Equal amounts of RNA samples from five mice of each strain at each time-point were pooled and then used to generate biotinylated cRNA targets for Affymetrix GeneChip Mouse Genome 430 2.0 Array.
2014-12-14 | E-GEOD-17810 | biostudies-arrayexpress
Project description:The classic piebald mutation in the endothelin receptor type B (Ednrb) gene was found on rolling Nagoya genetic background (PROD-s/s) mice with white coat spotting. To examine whether genetic background influenced the phenotype in the piebald mutant mice, we generated a congenic strain (B6.PROD-s/s), produced by repeated backcrosses to the C57BL/6J (B6) strain. Although B6.PROD-s/s mice showed white coat spotting, 7% of B6.PROD-s/s mice died between 2 and 5 weeks after birth due to megacolon. The PROD-s/s, s/s and Japanese fancy mouse 1 (JF1) strains, which also have piebald mutations on different genetic backgrounds with B6, showed only pigmentation defects without megacolon. In expression analyses, rectums of B6.PROD-s/s with megacolon mice showed ~5% of the level of Ednrb gene expression versus B6 mice. In histological analyses, aganglionosis was detected in the rectum of megacolon animals. The aganglionic rectum was thought to lead to severe constipation and intestinal blockage, resulting in megacolon. We also observed an abnormal intestinal flora, including a marked increase in Bacteroidaceae and Erysipelotrichaceae and a marked decrease in Lactobacillus and Clostridiales, likely inducing endotoxin production and a failure of the mucosal barrier system, leading ultimately to death. These results indicate that the genetic background plays a key role in the development of enteric ganglion neurons, controlled by the Ednrb gene, and that B6 has modifier gene (s) regarding aganglionosis.
| S-EPMC4363017 | biostudies-literature
Project description:Exposure to plant toxins or microbiota that are able to digest common food ingredients to toxic structures might be responsible for biliary atresia (BA). An isoflavonoid, biliatresone is known to effectively alter the extrahepatic bile duct (EHBD) development in BALB/c mice. Biliatresone causes a reduction of Glutathione (GSH) levels, SOX17 downregulation and is effectively countered with N-Acetyl-L-cysteine treatment in vitro. Therefore, reversing GSH-loss appears to be a promising treatment target for a translational approach. Since BALB/c mice have been described as sensitive in various models, we evaluated the toxic effect of biliatresone in robust C57BL/6J mice and confirmed its toxicity. Comparison between BALB/c and C57BL/6J mice revealed similarity in the toxic model. Affected neonates exhibited clinical symptoms of BA, such as jaundice, ascites, clay-colored stools, yellow urine and impaired weight gain. The gallbladders of jaundiced neonates were hydropic and EHBD were twisted and enlarged. Serum and histological analysis proved cholestasis. No anomalies were seen in the liver and EHBD of control animals. With our study we join a chain of evidence confirming that biliatresone is an effective agent for cross-lineage targeted alteration of the EHBD system.
| S-EPMC10310722 | biostudies-literature
Project description:Defects in homocysteine and folate metabolism are associated with increased risks for neural tube and congenital heart defects, cardiovascular disease and stroke, cancers, and neurodegeneration. In many but not all cases, dietary supplementation with folate significantly reduces the severity and incidence of these conditions. Common polymorphisms modulate these metabolic pathways and disease risks, but do not fully account for the particular birth defects and adult diseases that occur in at-risk individuals. To test whether other pathways contribute to disease pathogenesis, we analyzed global and pathway-specific changes in gene expression and levels of selected metabolites after depletion and repletion of dietary folate in two genetically distinct inbred strains of mice. Compared to the C57BL/6J strain, A/J showed greater homeostatic response to folate perturbation by retaining a higher serum folate level and minimizing global gene expression changes. Remarkably, folate perturbation led to systematic strain-specific differences only in the expression profile of the cholesterol biosynthesis pathway and translated to changes in levels of serum and liver total cholesterol. By genetically increasing serum and liver total cholesterol levels in APOE deficient mice, we modestly but significantly improved folate retention during folate depletion, suggesting an interplay between homocysteine and folate metabolism and cholesterol metabolism. Absence of measurable changes in global methylation patterns or amelioration of effects with supplementation with an alternative methyl donor suggest that dietary folate perturbations do not act through large-scale or general changes in methylation. These results suggest that homeostatic responses in cholesterol metabolism contribute to the beneficial effects of dietary folate supplementation. Keywords: time course, stress response, diet, genetic, homeostasis Six-week old female C57BL/6J and B6.129P2-Apoetm1Unc/J (Piedrahita et al. 1992) mice were purchased from the Jackson Laboratory. All mice were raised on a control diet containing four ppm folic acid (Basal Diet 5755, TestDiet) for one week before the start of studies. Mice were then placed on folic acid deficient diet (58C3, TestDiet) containing 1% succinylsulfathiazole, a non-absorbable antibiotic commonly used to suppress folate production by bacteria in the intestine, for 14 days. A subset of these mice were placed back on control diet for 7 days after 14 day depletion. There were three groups of mice that underwent folic acid depletion and repletion. ApoE knockout mice on C57BL/6J background, C57BL/6J mice supplemented with 25mM choline and 50mM saccharine in drinking water, and C57BL/6J mice supplemented with 50mM saccharine. Saccharine was used to reduce the bitter taste of choline in the drinking water. We also had C57BL/6J mice on the control diet for 14 days and 21 days. These mice served as controls for treated mice from each time point during hybridization. The folate level in the control diet for this study was significantly lower than the previous study (GSE9242) due to greater loss of folic acid by irradiation of the diet. There were eight replicate mice per treatment group per folic acid perturbation protocol. An equal amount (by weight) of liver tissue from eight replicate mice was separated into two pools of four replicate tissues each. Pooled RNA from treated mice and pooled RNA from control mice for each time point were aminoallyl labeled with Cy3 and Cy5 in duplicate with reversing of dyes.
2008-08-27 | E-GEOD-9243 | biostudies-arrayexpress
Project description:The purpose of this experiment was to determine the expression traits in animals from F2 intercross of inbred strains C57BL/6J, C3H/HeJ. (N=309, 164 males and 145 females). Brain from 292 F2 female and male mice were generated by intercrossing F1 mice. Mice were fed chow diet containing 4% fat (Ralston-Purina Co., St. Louis, MO) until 8 weeks of age and then were placed on a high-fat "Western" diet containing 42% fat and 0.15%cholesterol (Teklad 88137, Harlan Teklad, Madison WI) for 12 weeks. At 20 weeks mice were sacrificed, after a 12-hour fast Brain tissues were dissected and flash frozen in LN2 and stored at -80°C.
2009-08-09 | E-GEOD-12798 | biostudies-arrayexpress