Whole head tissue of mated female w1118 Drosophila melanogaster exposed to 20% w/v coconut oil in solid medium high fat diet
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ABSTRACT: Obesity predisposes humans and other mammals to a range of life-threatening comorbidities, including type 2 diabetes and cardiovascular disease. Obesity and its associated dietary habits also aggravate neural pathologies, such as Alzheimer’s disease, but this class of comorbidity is less understood. When Drosophila melanogaster (flies) are exposed to high fat diet (HFD) by supplementing a standard cornmeal-sucrose-yeast medium with coconut oil, they adopt an obese phenotype of decreased lifespan, increased triglyceride storage, and hindered climbing ability. The latter development is an indicator of neurological decline in flies. Our objective was to establish the obesity-like phenotype in Drosophila and identify a correlation, if any, between obesity and neurological decline in flies through behavioral and expression microarray. We found that mated female w1118 flies exposed to HFD maintained an obese phenotype throughout adult life with onset at seven days, evidenced by increased triglyceride stores, diminished life span, and impeded climbing ability. Analysis of gene expression of the fly head via microarray and qRT-PCR validation revealed functionally relevant genes with significant fold changes. These genes had functions including in memory, metabolism, olfaction, mitosis, cell signaling, and motor function. An Aversive Phototaxis Suppression assay indicated short term memory impairment as a result of HFD. Meanwhile, there was a decline but no significant difference in odor-seeking ability with HFD. Overall, our results point to the suitability of Drosophila melanogaster to investigate connections between diet-induced obesity and nervous or neurobehavioral pathology, and to the existence of such a dynamic in an evolutionarily broad range of organisms.
ORGANISM(S): Drosophila melanogaster
PROVIDER: GSE117834 | GEO | 2018/07/30
REPOSITORIES: GEO
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