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Metabolomics Workbench ST000661 - GNPS - CHOICE clinical weight loss study

ABSTRACT: Evaluation of plasma samples from the CHOICE clinical weight loss study in which obese post menopausal breast cancer survivors lost >15% initial body weight following either a low carbohydrate or a low fat dietary pattern. These samples will be interrogated for changes in metabolic intermediates and lipid metabolites that may be indicative of changes in prognosis for long term survival following treatment for breast cancer. Samples will be subjected to LCMS and shotgun lipidomics. In parallel, plasma and mammary gland fat pad from an obese rat model for breast cancer in which rats were subjected to a parallel level of weight loss will also be interrogated using the same procedures in an effort to inform the interpretation of the clinical data.

INSTRUMENT(S): QTOF - NEGATIVE, QTOF - POSITIVE

ORGANISM(S): Homo Sapiens/rattus Norvegicus

SUBMITTER: Maureen Kachman

PROVIDER: MSV000082728 | GNPS | Thu Aug 02 17:25:00 BST 2018

REPOSITORIES: GNPS

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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.

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Metabolomics Workbench ST000661 - GNPS - CHOICE clinical weight loss study

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