Ontology highlight
ABSTRACT:
PROVIDER: PRJNA592027 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR10572015.fastq.gz | Fastqsanger.gz | |||
| SRR10572016.fastq.gz | Fastqsanger.gz | |||
| SRR10572017.fastq.gz | Fastqsanger.gz | |||
| SRR10572018.fastq.gz | Fastqsanger.gz | |||
| SRR10572019.fastq.gz | Fastqsanger.gz |
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Project description:The effect of krill powder, a mixed source of protein and n-3 PUFAs from Antarctic Krill (Euphausia superba), on hepatic gene expression was analyzed in CBA/J mice. Mice were fed a low-fat control diet or a 3% (w/w) krill powder low-fat diet for three months. Gene expression profiling on liver samples revealed that the krill powder supplemented diet modulated a large number of pathways compared to the control diet, and we focused on the genes involved in metabolic processes. Pathways involved β-oxidation, glucose metabolism, and amino acid catabolism were downregulated. In contrast, genes involved in the mitochondrial electron transport chain were upregulated. Thus, a krill powder supplemented diet had potent and specific effects on energy metabolism and oxidative phosphorylation at the gene level. This indicates that krill powder supplementation could be an approach to prevent age-related decline in mitochondrial respiratory chain function and weight loss.
2021-11-25 | GSE46049 | GEO
Project description:We used Affymetrix microarrays to investigate gene expression changes in the liver of wild-type C57BL-6 mice exposed to a high-fat diet that might have been caused by the oral consumption of the probiotic B. pseudocatenulatum CECT 7765. The aim of this work was to determine whether the daily intake (by oral gavage) of the probiotic (P) B. pseudocatenulatum for seven weeks exerted any modulatory effects, at the level of gene expression, in the liver of C57BL-6 male mice exposed to a high-fat diet (HFD). Male mice were randomly assigned to four experimental groups (n= 5 animals per group) as follows: (1) control group, fed a standard diet (SD); (2) obese group, fed a high-fat diet (HFD); (3) a group that received the SD and a daily dose of the probiotic (1M-CM-^W109 CFU B. pseudocatenulatum CECT 7765) (SD+P); and (d) an obese group that was fed the HFD and a daily dose of the probiotic (1M-CM-^W109 CFU B. pseudocatenulatum CECT 7765) (HFD+P). At the end of the experimental procedure total RNA was extracted from the liver to compare differential gene expression between the groups. Liver differential gene expression after 7 weeks of supplementation between: 1) the HFD group and the SD group (effects of the high-fat diet); 2) the HFD+P and the HFD (effects of the probiotic on the consumption of a high-fat diet) and 3) the SD+P group and the SD (direct effects of the probiotic on the liver of animals consuming a normal diet).
2012-11-20 | E-GEOD-40638 | biostudies-arrayexpress
Project description:Background: Post-menopausal obesity is an established risk factor for breast cancer. Consumption of diets high in fat is known to be highly correlated with obesity. In this, we sought to evaluate the interaction(s) between high fat diet, weight gain and mammary carcinogenesis using an obese-resistant and obese-prone rat model with direct correlates to human disease. Methods: Female obese-prone (OP) and obese-resistant (OR) weanling rats were placed on either a low fat (10% kcal) or a high fat (39% kcal) n-6 polyunsaturated (PUFA) safflower diet for 30 days. At post natal day (PND) 50, global gene expression profiling was performed on microdissected mammary epithlelium from one cohort of rats and another cohort of rats were given a single oral gavage of either 7,12-dimethylbenz[a]anthracene (DMBA at 14 mg/kg) or vehicle. Rats were then maintained on the diets and body weights, food consumption and development of mammary lesions were monitored weekly. Results: The DMBA-treated OR rats on the 39% safflower diet had significantly greater incidence of ductal carcinoma-in-situ (DCIS) lesions and significantly greater DCIS multiplicity than DMBA-treated OR rats on the 10% safflower diet. These differences were not seen in the OP strain. Gene expression analysis of mammary ductal epithelium from OR rats on the high fat diet showed significant upregulation of proliferation-related genes compared to those consuming the low fat safflower diet. Again, these differences were not seen in the OP strain. Conclusion: Our findings indicate that consumption of high fat safflower diet enhances mammary carcinogenesis in an OR rat strain through increased proliferation of mammary epithelium at the time of exposure, but not in the OP rat strain. Thus, the diet-induced increase in sensitivity was strain-specific and independent of weight gain or obesity level. Female obese-prone (OP) and obese-resistant (OR) weanling rats were placed on either a low fat (10% kcal) or a high fat (39% kcal) n-6 polyunsaturated (PUFA) safflower diet for 30 days. At post natal day (PND) 50, global gene expression profiling was performed on microdissected mammary epithlelium from one cohort of rats and another cohort of rats were given a single oral gavage of either 7,12-dimethylbenz[a]anthracene (DMBA at 14 mg/kg) or vehicle. Rats were then maintained on the diets and body weights, food consumption and development of mammary lesions were monitored weekly.
2010-09-25 | E-GEOD-21150 | biostudies-arrayexpress
Project description:High sugar consumption, as well as high-fat diet, is a known cause of obesity and metabolic syndrome. However, the synergistic effect of high-sugar and high-fat consumption rarely has been evaluated, especially in terms of transcriptional regulation. Therefore, we focused on the effect of high sugar consumption on hepatic transcriptional networks in normal and high fat-fed mice. C57BL/6J mice were divided into four groups and were provided either 23%(w/v) sugar solution or plain water with either high-fat or normal-fat diet for 10 weeks. As a result, high sugar consumption significantly altered lipid metabolism-related genes in normal fat-fed mice; however, in high fat-fed mice, high sugar consumption altered inflammation-responsive genes rather than lipid metabolism. After all, these modulations eventually increased lipid accumulation in the liver and caused systemic metabolic disturbances. These observations for the first time suggested that high sugar consumption along with high-fat diet could lead to the development of severe metabolic syndrome via altering hepatic transcriptional networks.
2017-01-01 | GSE70477 | GEO
Project description:Okra (Abelmoschus esculentus (L.) Moench) serves as a botanical resource extensively utilized in ethnomedicine. Prior investigations revealed that okra polysaccharide (OP) ameliorated hepatocellular lipotoxicity in vitro context. Nonetheless, the curative efficacy and the precise molecular mechanisms implicated in metabolic-associated fatty liver disease (MAFLD) warrant further elucidation. To address this gap, two murine models of MAFLD, namely obese Ob/Ob mice and high fat/cholesterol/fructose (HFCF) fed mice, were employed. The therapeutic implications of OP supplementation were assessed through quantification of lipid specific biomarkers and hepatic histopathological examination. Complementary transcriptomic, phosphoproteomic, and in vitro analyses were conducted to decipher the molecular underpinnings. In the Ob/Ob mouse model, OP substantively mitigated both circulating and hepatic lipid concentrations, concurrently ameliorating hepatic steatosis. In the context of HFCF-induced MAFLD, OP not only attenuated hepatic lipidic sequestration but also abrogated concomitant inflammation and fibrosis. Subsequent RNA-sequencing analyses on hepatic tissues derived from HFCF-diet mice delineated that OP modulated MAFLD-associated transcriptional signatures. A synergistic assessment of transcriptomics and phosphoproteomics disclosed a salient effect of OP on the Peroxisome Proliferator-Activated Receptor (PPAR) pathway, particularly manifested by the upregulation of PPAR-γ signaling. In murine hepatocytes, OP counteracted steatosis and inflammation via the activation of PPAR-γ signaling. The effects induced by OP were nullified upon administration of the PPAR-γ-specific antagonist GW9662. Collectively, our empirical evidence furnishes the inaugural demonstration that OP mitigates MAFLD pathology through the activation of PPAR-γ signaling, thereby presenting a novel therapeutic avenue for MAFLD intervention.
2024-08-21 | GSE273255 | GEO
Project description:In this study, we investigated the effects of organic vegetable juice supplementation on modulating the microbial community, and how its consumption ameliorates blood lipid profiles in diet-induced obese mice. Here, we analyzed the effect of organic vegetable juice on the microbial community and fatty acid synthesis via animal experiments using diet-induced obese mice and continuous colon simulation system. Organic vegetable juice supplement influenced intestinal bacterial composition from phylum to genus level, including decreased Proteobacteria in the ascending colon in the phylum. At the family level, Akkermansia which are associated with obesity, were significantly augmented in the transverse colon and descending colon compared to the control juice group. In addition, treatment with organic vegetable juice affected predicted lipid metabolism function genes related to lipid synthesis. Organic vegetable juice consumption did not have a significant effect on weight loss but helped reduce epididymis fat tissue and adipocytes. Additionally, blood lipid profiles, such as triglyceride, high-density lipoprotein, and glucose, were improved in the organic vegetable juice-fed group. Expression levels of genes related to lipid synthesis, including SREBP-1, PPARγ, C/EBPα, and Fas, were significantly decreased. Analysis of antioxidant markers, including 8-OHdG and MDA, in the vegetable juice group, indicated that blood lipid profiles were improved by the antioxidant effect. These results suggest that organic vegetable juice supplementation may modulate gut microbial community and reduce the potential role of hyperlipidemia in diet-obese mice.
2021-12-31 | GSE171609 | GEO
Project description:Background: Post-menopausal obesity is an established risk factor for breast cancer. Consumption of diets high in fat is known to be highly correlated with obesity. In this, we sought to evaluate the interaction(s) between high fat diet, weight gain and mammary carcinogenesis using an obese-resistant and obese-prone rat model with direct correlates to human disease. Methods: Female obese-prone (OP) and obese-resistant (OR) weanling rats were placed on either a low fat (10% kcal) or a high fat (39% kcal) n-6 polyunsaturated (PUFA) safflower diet for 30 days. At post natal day (PND) 50, global gene expression profiling was performed on microdissected mammary epithlelium from one cohort of rats and another cohort of rats were given a single oral gavage of either 7,12-dimethylbenz[a]anthracene (DMBA at 14 mg/kg) or vehicle. Rats were then maintained on the diets and body weights, food consumption and development of mammary lesions were monitored weekly. Results: The DMBA-treated OR rats on the 39% safflower diet had significantly greater incidence of ductal carcinoma-in-situ (DCIS) lesions and significantly greater DCIS multiplicity than DMBA-treated OR rats on the 10% safflower diet. These differences were not seen in the OP strain. Gene expression analysis of mammary ductal epithelium from OR rats on the high fat diet showed significant upregulation of proliferation-related genes compared to those consuming the low fat safflower diet. Again, these differences were not seen in the OP strain. Conclusion: Our findings indicate that consumption of high fat safflower diet enhances mammary carcinogenesis in an OR rat strain through increased proliferation of mammary epithelium at the time of exposure, but not in the OP rat strain. Thus, the diet-induced increase in sensitivity was strain-specific and independent of weight gain or obesity level.
2010-09-25 | GSE21150 | GEO
Project description:We have previously shown that paramylon (PM) supplementation to a high fat diet reduces the postprandial glucose rise, serum total and LDL-cholesterol, and abdominal fat accumulation in mice; however, the mechanism has not been determined. We evaluated the potential mechanism in male C57BL/6J mice fed a high-fat diet supplemented with 5% PM powder, extracted from Eu-glena gracilis, for 12 weeks. Abdominal fat weight, and serum lipids were measured; ileal and hepatic mRNA expression were assessed using DNA microarray and real-time PCR. The poten-tial mechanism of PM on modulating lipid metabolism was explored by gene ontology (GO) classification and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis. Dietary supplementation with PM resulted in decreased abdominal fat accumulation and serum LDL-cholesterol concentrations via suppression of the digestion and absorption pathway in the ileum and activation of the hepatic PPAR signaling pathway. Improvement in glucose tolerance may be the result of lipid metabolism modification because the glucose metabolism pathway was not detected by GO classification and KEGG pathway analysis. PM intake also directly enhanced immunoglobulin production.
2021-08-04 | GSE181289 | GEO