Lipid metabolism and cellular energy homeostasis are tightly coupled processes that are essential for organismal health. Disruptions in these pathways are strongly associated with metabolic dysfunction and proteostatic stress. In previous work, RNA interference (RNAi) knockdown of lbp-5, a lipid-binding protein implicated in β-oxidation in the protein aggregation-accumulating EAK103 strain of Caenorhabditis elegans, produced multiple phenotypes, including increased lipid droplet accumulation, altered mitochondrial morphology, and reduced locomotor activity as measured by a thrashing assay. 

The present study extends this work by transitioning to the N2 wild-type background to reduce strain-specific effects and further investigate the relationship between lbp-5, lipid storage, and cellular energetics. To directly quantify energy balance, intracellular ATP levels were measured using luciferase-based reporter strains PE255 and GA2001, enabling real-time assessment of metabolic consequences following lbp-5 knockdown. We show that the knockdown of lbp-5 disrupts ATP production, consistent with impaired β-oxidation and mitochondrial function.