Reversible dietary effect on intestinal stem cells
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE186811 | GEO | 2023/04/12
REPOSITORIES: GEO
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Project description:Bl6 mice were fed with New Western diet 1 (NWD1) or Americal Instititue of Nutrition 76A (AIN76A or AIN) diet from weaning for 3 months. Single intestinal epithelial cells were FACS isolated by the Epcam+, CD45- , and subject to scACTAseq assay.
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Project description:To investigate the effect of wetern-style diet on Paneth cells, we performed bulk RNAseq on sorted Paneth cells from mice fed for 3 months with western-style diet (NWD1) and control diet (AIN76A)
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Project description:Bmi1tm1(cre/ERT2)Mrc/J (a.k.a. Bmi1creERT2 mice), B6.Cg-Gt(ROSA)26Sortm14(CAT-tdTomato)Hze/J (a.k.a. Rosa26tom mice) were crossed. The mice were fed with New Western diet 1 (NWD1) or Americal Instititue of Nutrition 76A (AIN76A or AIN) diet from weaning for 3 months. Tamoxinfen was injected to induce Bmi1 cell dedifferentiation, featuring the expression of tomato red fluoresence in the Bmi1 locus. Single intestinal epithelial cells were FACS isolated by the Epcam+, CD45- and Tomato (red fluorescence)+, and subject to scRNAseq assay.
2023-04-12 | GSE188338 | GEO
Project description:Dietary n-3 polyunsaturated fatty acids can reduce inflammation via a range of mechanisms. This study tested the effect of dietary eicosapentaenoic acid (EPA) on intestinal inflammation using interleukin-10 gene-deficient (Il10-/-) mice. Methods: At 35 days of age, 12 weaned Il10-/- and 12 C57 mice were randomly assigned to one of two modified AIN-76A diets, supplemented with 3.7% purified ethyl esters of either EPA (n-3) or oleic acid (OA, control). To identify genes relevant to colon inflammation, transcription profiling (microarrays and qRT-PCR) and bioinformatic analyses were used. Results: In this study, dietary EPA reversed the decrease in colon fatty acid β-oxidation gene expression observed in OA-fed Il10-/- compared to C57 mice. Il10-/- mice fed the OA diet showed decreased expression of antioxidant enzyme genes, as well as those involved in detoxification of xenobiotics, compared to C57 mice on the same diet. In contrast, dietary EPA increased the expression of these genes in Il10-/- mice. Conclusions: These data indicate that dietary EPA induced endogenous lipid oxidation which might have a potential anti-inflammatory effect on colon tissue. This is supported by the activation of the Ppara gene that regulates the expression of pro-inflammatory and immunomodulatory genes and proteins. Experiment Overall Design: The diet abbreviations EPA, OA, AA and CO used in the sample records Experiment Overall Design: refer to the following : Experiment Overall Design: CO : AIN-76A (control) Experiment Overall Design: OA : AIN-76A (fat-free) + 1% corn oil + 3.7% oleic acid Experiment Overall Design: EPA : AIN-76A (fat-free) + 1% corn oil + 3.7% eicosapentaenoic acid Experiment Overall Design: AA : AIN-76A (fat-free) + 1% corn oil + 3.7% arachidonic acid Experiment Overall Design: Corn oil was supplemented with purified linoleic and alpha-linolenic acid to meet the nutritional requirements of mice for these essential fatty acids. Diets fed for 6 weeks.
2008-10-21 | E-GEOD-12028 | biostudies-arrayexpress
Project description:SCOPE: We investigated whether a novel dietary intervention consisting of an every-other-week calorie-restricted diet could prevent nonalcoholic fatty liver disease (NAFLD) development induced by a medium-fat (MF) diet. METHODS AND RESULTS: Nine-week-old male C57BL/6J mice received either a (i) control (C), (ii) 30E% calorie restricted (CR), (iii) MF (25E% fat), or (iv) intermittent (INT) diet, a diet alternating weekly between 40E% CR and an ad libitum MF diet until sacrifice at the age of 12 months. The metabolic, morphological, and molecular features of NAFLD were examined. The INT diet resulted in healthy metabolic and morphological features as displayed by the continuous CR diet: glucose tolerant, low hepatic triglyceride content, low plasma alanine aminotransferase. In contrast, the C- and MF-exposed mice with high body weight developed signs of NAFLD. However, the gene expression profiles of INT-exposed mice differed to those of CR-exposed mice and showed to be more similar with those of C- and MF-exposed mice with a comparable body weight. CONCLUSIONS: Our study reveals that the INT diet maintains metabolic health and reverses the adverse effects of the MF diet, thus effectively prevents the development of NAFLD in 12-month-old male C57BL/6J mice. Male C57Bl/6J mice were divided to 4 dietary intervention groups: Control (AIN-93W), 30% calorie restriction (CR; AIN-93W-CR), medium fat (MF; AIN-93W-MF; 25% energy from fat) and intermittent diet (INT; weekly alternating diet between AIN-93W-MF ad lib and 40% CR of AIN-93W). We performed various measurements on metabolic parameters and gene expression analysis on the liver. This entry represents the microarray data of the liver gene expression of each mouse.
2015-10-26 | E-GEOD-61233 | biostudies-arrayexpress
Project description:Resveratrol delays age-related deterioration and mimics transcriptional aspects of dietary restriction without extending lifespan A small molecule that safely mimics the ability of dietary restriction (DR) to delay age-related diseases in laboratory animals is greatly sought after. We and others have shown that resveratrol mimics effects of DR in lower organisms. In mice, we find that resveratrol induces gene expression patterns in multiple tissues that parallel those induced by DR and every-other-day feeding. Moreover, resveratrol-fed elderly mice shows a marked reduction in signs of aging including reduced albuminuria, decreased inflammation and apoptosis in the vascular endothelium, increased aortic elasticity, greater motor coordination, reduced cataract formation, and preserved bone mineral density. However, mice fed a standard diet did not live longer when treated with resveratrol beginning at mid-life. Our findings indicate that resveratrol treatment has a range of beneficial effects in mice but does not increase the longevity of ad libitum-fed animals when started mid-life. Male C57BL/6NIA mice at 11 months of age were maintained on a standard purified mouse diet (AIN-93G) for one month prior to the start of the experiment. Beginning at one year of age, SD and EOD groups were fed a standard AIN-93G diet or AIN-93G plus 0.01% or 0.04% resveratrol for the duration of the study. Three separate groups were placed on an HC diet (AIN-93G modified by the addition of hydrogenated coconut oil to provide 60% of calories from fat) or HC + 0.01% or 0.04% resveratrol 6 weeks later and remained on those diets throughout the study. SD and HC mice were fed ad libitum. EOD mice were fed ad libitum on alternate days then moved to a separate cage without food for 24 h. Food intake and body weight were measured on a weekly basis for the duration of the study.
2008-08-04 | E-GEOD-11845 | biostudies-arrayexpress
Project description:Persimmon (Diospyros kaki L. f.) is a most popular fruit in Asian countries but its peels are totally wasted despite of containing a plenty of antioxidants such as carotenoids and polyphenols. We prepared a fat-soluble extract from a persimmon peel (PP) fraction and fed type 2 diabetic Goto-Kakizaki (GK) rats with a PP extract-containing AIN-93G diet (PP diet) for 12 weeks. Compared with the control AIN-93G diet, the feeding of the PP diet reduced the plasma glutamic-pyruvate transaminase activity significantly, with accumulation of M-NM-2-cryptoxanthin in the liver. A DNA microarray analysis revealed that the PP diet altered the hepatic gene expression profiles. In particular, insulin signaling pathway-related genes were significantly enriched in differentially expressed gene sets. Moreover, Western blotting analysis actually showed the promotion of IRM-NM-2 tyrosine phosphorylation. All these data suggest that the PP extract administration to the GK rats improves their insulin resistance. Male GK rats (90M-bM-^@M-^S107 g), aged 5 weeks, were purchased from Japan SLC Co. (Hamamatsu, Japan). The rats were maintained in a room at 22 M-BM-1 1M-BM-0C under a 12-h light-dark cycle (lights on at 0800) and administered a commercial diet (AIN-93G, Research Diets, Inc., New Brunswick, NJ, USA) for a week. The rats were allowed free access to diet and water. After one week, they were divided into two groups with similar average body weights. The control group rats (n = 4) were fed on the commercial diet, and the PP group rats (n = 4) on the same diet containing the PP extract. After the 12-week-feeding the liver was excised and analyzed the effect of PP extract administration on hepatic gene expression.
2011-03-17 | E-GEOD-21417 | biostudies-arrayexpress
Project description:Nutritional and genetic risk factors for intestinal tumors are additive on mouse tumor phenotypes, demonstrating that diet and genetic factors impact risk by distinct combinatorial mechanisms. We analyzed expression profiles of small intestine crypts and villi from mice with nutritional and genetic risk factors. The results advanced our understanding of the mechanistic roles played by major risk factors in the pathogenesis of intestinal tumors. Small intestine crypts and villi from mice with nutritional (Ain76A, NWD1, and NWD2) and genetic risk factors (WT, Apc1638N/+ and p21-/-) were collected for RNA extraction and analysis using the Affymetrix 3' IVT expression microarray. Three or four replicates per tissue/risk factor.
2011-05-31 | E-GEOD-29538 | biostudies-arrayexpress
Project description:The ketone body β-hydroxybutyrate (BHB) is produced during dietary restriction, fasting, and exercise. A ketogenic diet (KD) results in long-term production of BHB outside of these contexts. We sought to determine a protein-matched, non-obese ketogenic diet (KD) would affect the longevity and healthspan of C57BL/6 male mice. We find that feeding KD every-other-week to prevent obesity (cyclic KD) reduces mid-life mortality but does not affect maximum lifespan. Similar feeding of a non-ketogenic high-fat/low-carbohydrate (HF) diet may have an intermediate effect on mortality. Cyclic KD improves memory performance in old age, while modestly improving composite measures of healthspan. RNAseq gene expression analysis identifies down-regulation of insulin, TOR, and fatty acid synthesis pathways as possible longevity mechanisms common to KD and HF. However, up-regulation of fasting-related PPARα target genes is unique to KD, consistent across tissues, and preserved in old age, suggesting a mechanism for an incremental benefit from KD. In all, we show that a non-obese ketogenic diet improves survival, memory, and healthspan into old age. These gene expression studies were carried out on 12 month-old male C56BL/6 mice from the NIA Aged Rodent Colony, habituated to AIN-93M control diet and then either maintained on this diet or switched for one week to a 75% kcal fat non-ketogenic high-fat diet or a 90% kcal fat ketogenic diet (all diets with 10% kcal from carbohydrates). Tissues were harvested in the middle of the nighttime feeding period (MN-3am).
2017-09-05 | GSE101657 | GEO
Project description:Dietary n-3 polyunsaturated fatty acids can reduce inflammation via a range of mechanisms. This study tested the effect of dietary eicosapentaenoic acid (EPA) on intestinal inflammation using interleukin-10 gene-deficient (Il10-/-) mice. Methods: At 35 days of age, 12 weaned Il10-/- and 12 C57 mice were randomly assigned to one of two modified AIN-76A diets, supplemented with 3.7% purified ethyl esters of either EPA (n-3) or oleic acid (OA, control). To identify genes relevant to colon inflammation, transcription profiling (microarrays and qRT-PCR) and bioinformatic analyses were used. Results: In this study, dietary EPA reversed the decrease in colon fatty acid β-oxidation gene expression observed in OA-fed Il10-/- compared to C57 mice. Il10-/- mice fed the OA diet showed decreased expression of antioxidant enzyme genes, as well as those involved in detoxification of xenobiotics, compared to C57 mice on the same diet. In contrast, dietary EPA increased the expression of these genes in Il10-/- mice. Conclusions: These data indicate that dietary EPA induced endogenous lipid oxidation which might have a potential anti-inflammatory effect on colon tissue. This is supported by the activation of the Ppara gene that regulates the expression of pro-inflammatory and immunomodulatory genes and proteins.
2008-07-10 | GSE12028 | GEO