In the absence of drugs, oxygen consumption in control and pdgy^BG02662 mutant larvae is significantly reduced compared to controls. Subsequent addition of etomoxir, a specific inhibitor of Carnitine palmitoyltransferase I, required for the transport of fatty acids into mitochondria where beta-oxidation takes place, causes this difference in oxygen consumption to be abrogated (300υM etomoxir).

pdgy^BG02662 mutants are viable, fertile, and normally patterned.

pdgy^BG02662 mutant larvae and adults have significantly elevated triglyceride and cholesteryl ester levels compared to controls.

The increased adiposity of pdgy^BG02662 mutants is consistent with the reduced levels of fatty acid oxidation observed in these mutants.

Upon complete food withdrawal, pdgy^BG02662 mutants survive significantly longer compared to controls.

pdgy^BG02662 mutants do not show any reduction in triglyceride levels in the first 6 hours of starvation (while control flies do). Only as of 8 hours of starvation do pdgy^BG02662 mutant start depleting their triglyceride stores, completely depleting them by 36 hours of fasting. In contrast to wild-type, levels of free C14:0 and C16:0 remain aberrantly high in starving pdgy^BG02662 mutants. Defects are only apparent in a subset of free fatty acids, suggesting that the metabolism of all fatty acids may not be affected equally by loss of pdgy. pdgy^BG02662 mutants display an altered profile in the catabolism of lipid species.

pdgy^BG02662 mutants are mildly, but significantly, reduced in size compared to controls and are long-lived.

pdgy^BG02662 mutants exhibit reduced glycogen stores and increased circulating sugars, suggesting elevated mobilization of carbohydrates.