Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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PolyA-enriched RNA-Seq of livers from male and female C57Bl/6J mice fed a control or high-fat diet and treated with estrogen receptor agonists

ABSTRACT: Metabolic dysfunction-associated fatty liver disease is the most prevalent liver disease and affects a quarter of the global population. Estrogens are associated to safeguard the liver from metabolic diseases. We fed male and female mice a control or high-fat diet for 13 weeks. Only male mice developed fatty livers. We injected a subset of male mice fed a high-fat diet with four different estrogen receptor (ER) agonists for the last three weeks of the high-fat diet, activating the nuclear ERalpha and ERbeta. Livers were collected and flash-frozen before RNA isolation, DNAse treatment, library preparation and sequencing on an Illumina NextSeq 500 instrument.

INSTRUMENT(S): NextSeq 500

ORGANISM(S): Mus musculus

SUBMITTER:

PROVIDER: E-MTAB-11833 | biostudies-arrayexpress |

SECONDARY ACCESSION(S): ERP138919E-MTAB-11929

REPOSITORIES: biostudies-arrayexpress

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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.

Dataset Information

PolyA-enriched RNA-Seq of livers from male and female C57Bl/6J mice fed a control or high-fat diet and treated with estrogen receptor agonists

Similar Datasets

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