Pathological obesity can result from genetic predisposition, obesogenic diet, and circadian rhythm disruption. Obesity compromises function of muscle, which accounts for a majority of body mass. Behavioral intervention that can counteract obesity arising from genetic, diet or circadian disruption and can improve muscle function holds untapped potential to combat the obesity epidemic. Here we show that Drosophila melanogaster (fruit fly) subject to obesogenic challenges exhibits metabolic disease phenotypes in skeletal muscle; sarcomere disorganization, mitochondrial deformation, upregulation of Phospho-AKT level, aberrant intramuscular lipid infiltration, and insulin resistance. Imposing time-restricted feeding (TRF) paradigm in which flies were fed for 12 h during the day counteracts obesity-induced dysmetabolism and improves muscle performance by suppressing intramuscular fat deposits, Phospho-AKT level, mitochondrial aberrations, and markers of insulin resistance. Importantly, TRF was effective even in an irregular lighting schedule mimicking shiftwork. Hence, TRF is an effective dietary intervention for combating metabolic dysfunction arising from multiple causes.

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During the first and second resubmissions of this article, the images in question were accidentally improperly named when imported to Power Point for figure preparation which led to several duplications. The following figure panels were inadvertently and erroneously duplicated: Figure 1h panel "WT-HFD" was duplicated in Fig. 3c as panel "Fln>Sk2KD, 3 W"; Fig. 8h panel "WT TRF-LL" was duplicated in Fig. 3c as panel "Fln/+, 3 W"; Fig. 8h panel "ALF-LL WT" was duplicated in Fig. 4c as panel "Bmm/+, 3 W"; Fig. 6e panel "TRF WT-RD" was duplicated in Fig. 4c as panel "CS control, 3 W". Panel "Fln/+, 3 W" in Fig. 3c and panel "WT + bromoenol lactone" in Supplementary Fig. 3a were identical and incorrect. Furthermore, the Y-axis label in Fig. 3b was absent and should have stated "Relative NLaz Expression". This has now been added.