The microscopic nematode, Caenorhabiditis elegans, is an ideal model in studying post-illness fatigue and sleep that aids in the processes of repair following injury illness, referred to as sickness-induced sleep (SIS). SIS can be induced by several environmental factors, such as infection, heat, or UV radiation exposure, resulting in decreased movement and feeding (quiescence). By using the biosensor Hylight that detects Fructose 1,6-biphosphate (FBP) in KIN-29 C.elegans mutants, we are able to observe the effects of SIS on metabolic processes like glycolysis, especially in C.elegans lacking the Salt-Inducible Kinase homolog. Using WorMotel imaging after exposure to UV radiation, we show that wild-type C.elegans exhibit quiescence in response to UV stress, and find that mutations in certain strains of C.elegans inhibit quiescence in response to stress. By using compound microscope fluorescent imaging after exposure to UV radiation, we determine that wild-type worms exhibit increases in FBP ratios following exposure to UV stress, indicating that the rate of glycolysis increases in SIS. KIN-29 mutant worms exhibit similar increases in FBP ratios to wild-type worms following exposure to UV stress, and show no significant differences in baseline FBP ratios compared to wild-type worms. Our findings indicate that while KIN-29 affects ATP levels in C.elegans, KIN-29 does not regulate the increased rate of glycolysis in SIS. These results clarify that glycolysis in relation to FBP, involving exposure to UV stress, is unaffected by the KIN-29 homolog in worms, providing insight on metabolic processes in sleep.