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Lipidomics pilot project for mice exposure to bisphenol A and high fat diets

ABSTRACT: Wild type (a/a) agouti mouse dams were randomized to one of three diets (control, Mediterranean, western) two weeks prior to pairing with an agouti (Avy/a) sire. Diet exposure continued through pregnancy and lactation. All pups were weaned onto the control diet and then followed for metabolic phenotyping measures to 10 months of age. Comprehensive phenotyping (body composition, CLAMS, blood draw) was completed at 2, 4, and 8 months, with an OGTT at 8 months. Weekly weights were also recorded. The study examines whether prenatal dietary exposure to high fat diets (HFD) and bisphenol a (BPA, those groups will not be tested in this pilot) impacts metabolic programming in offspring as measured by hepatic steatosis, serum hormone levels, and epigenetic changes in hepatic lipid metabolism genes. Shotgun lipidomics will add insight into the potentially changing lipid composition of membranes in offspring following different prenatal diet exposures as a means of assessing risk of steatosis and metabolic changes.

ORGANISM(S): Mouse Mus Musculus

TISSUE(S): Blood

DISEASE(S): Fatty Liver Disease

SUBMITTER: Maureen Kachman

PROVIDER: ST000779 | MetabolomicsWorkbench | Mon Jun 05 00:00:00 BST 2017

REPOSITORIES: MetabolomicsWorkbench

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Exposure to high fat diets and bisphenol

Project description:Wild type (a/a) agouti mouse dams were randomized to one of three diets (control, mediterranean, western) two weeks prior to pairing with an agouti (Avy/a) sire. Diet exposure continued through pregnancy and lactation. All pups were weaned onto the control diet and then followed for metabolic phenotyping measures to 10 months of age. Comprehensive phenotyping (body composition, CLAMS, blood draw) was completed at 2, 4, and 8 months, with an OGTT at 8 months. Weekly weights were also recorded. The study examines whether prenatal dietary exposure to high fat diets (HFD) and bisphenol a (BPA, those groups will not be tested in this pilot) impacts metabolic programming in offspring as measured by hepatic steatosis, serum hormone levels, and epigenetic changes in hepatic lipid metabolism genes.

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