Project description:Chronic high sugar feeding induces obesity, hyperglycemia, and insulin resistance in flies and mammals. To gain insight into the mechanisms underlying this response, we profiled gene expression in chronically high sugar fed, wandering (post-prandial) third instar wild type larvae (L3). These data were compared to control-fed larvae as well as those (mid-L3) actively feeding for twelve hours on both diets. We used microarrays to detail the response of Drosophila larvae to high sugar-induced insulin resistance.
Project description:Chronic high sugar feeding induces obesity, hyperglycemia, and insulin resistance in flies and mammals. To gain insight into the mechanisms underlying this response, we profiled gene expression in chronically high sugar fed, wandering (post-prandial) third instar wild type larvae (L3). These data were compared to control-fed larvae as well as those (mid-L3) actively feeding for twelve hours on both diets. We used microarrays to detail the response of Drosophila larvae to high sugar-induced insulin resistance. Male Canton-S third instar larvae were fed control (0.15M) or high (1M) sucrose and selected for RNA extraction and hybridization on Affymetrix microarrays. Wandering L3 were selected as those in the top half of the vial with partial blue guts to confirm that they had stopped eating the (blue) food. Mid-L3 were selected as L2, aged overnight until early L3, then transferred to fresh control or high sucrose food for 12 more hours before selection.
Project description:Chronic high sugar feeding induces obesity, hyperglycemia, and insulin resistance in flies and mammals. These phenotypes are controlled by the fat body, a liver- and adipose- like tissue in Drosophila flies. To gain insight into the mechanisms underlying the connection between diet and insulin sensitivity, we used Illumina RNA-seq to profile gene expression in fat bodies isolated from chronically high sugar fed, wandering (post-prandial) third instar wild type larvae w(L3). These data were compared to control-fed wild-type wL3 fat bodies as well as those expressing transgenic interfering RNA (i) targeting CG18362 (Mio/dChREBP) in the fat body on both diets. Female VDRC w1118, cgGAL4, UAS-Dcr2 or UAS-ChREBPi(52606), cgGAL4, UAS-Dcr2 wandering third instar larvae were fed control (0.15M) or high (0.7M) sucrose and fat bodies isolated for RNA extraction.
Project description:Chronic high sugar feeding induces obesity, hyperglycemia, and insulin resistance in flies and mammals. These phenotypes are controlled by the fat body, a liver- and adipose- like tissue in Drosophila flies. To gain insight into the mechanisms underlying the connection between diet and insulin sensitivity, we used Illumina RNA-seq to profile gene expression in fat bodies isolated from chronically high sugar fed, wandering (post-prandial) third instar wild type larvae w(L3). These data were compared to control-fed wild-type wL3 fat bodies as well as those expressing transgenic interfering RNA (i) targeting CG18362 (Mio/dChREBP) in the fat body on both diets.
Project description:To identify genes differentially expressed in the fatbody of Drosphila melanogaster bigmax mutants, a loss-of-function allele was generated by P-element mobilization. Mutant and wildtype first instar larvae were raised on two different sources of food, control and high-sugar media. When the animals reached the wandering third instar stage, animals were sacrificed and their fat bodies dissected. Total RNA was extracted, labeled fluorescently and hybridized competitively to Agilent's 4x44K Drosophila Gene Expression Microarrays. On each array, three different samples were analyzed: 1. wildtype animals raised on control food, 2. wildtype animals raised on high-sugar food and 3. bigmax mutant animals raised on high-sugar food.
Project description:Maternal obesity and diabetes is associated with increased risk of obesity and diabetes in offspring. We generated a model of maternal caloric excess in Drosophila and noted altered body composition in offspring from females fed a high-sucrose diet. To gain insight into the mechanisms underlying this response, we profiled gene expression in mid-third instar larvae (mid-L3) offspring from either control or high-sucrose fed females. All offspring were raised on control food. We used microarrays to detail the response of Drosophila larvae to maternal high calorie diet
