HFD and genetic lipid overflow models do not disrupt growth and developmental timing.

(A) Hemolymph abundances of myristic (C14:0), myristoleic (C14:1), and oleic (C18:1) acids in STD and HFD larvae. Abundance (ion counts per mg) was measured by GC–MS and normalised to larval wet weights. (B–D) Graphs compare STD and HFD animals, indicating that they have similar larval weight (mg), nephrocyte volume (μm³), and developmental timing (% pupariation versus hours after larval hatching). Note that nephrocyte size is significantly different (p < 0.0005) between STD and HFD animals. (E–G) Graphs compare STD animals expressing ATGL in the fat body (Lpp>ATGL) with controls (Lpp-GAL4). indicating that they have similar larval weight (mg), nephrocyte volume (μm³), and developmental timing (% pupariation versus hours after larval hatching). Note that nephrocyte size is significantly different (p < 0.0005) between control and ATGL expressing animals. See S1 Data for details of p-values and the type of statistical model used for all graphs in this study. S2 Data provides the source data used for all graphs and statistical analyses. ATGL, adipose triglyceride lipase; GC–MS, gas chromatography–mass spectrometry; HFD, high-fat diet; STD, standard diet.

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