Background Neonicotinoids, including imidacloprid (IM), cause harm to Apis mellifera in a number of ways, among others by impairing body maintenance, resistance and immunity. Energy resources are important to preventing this, as we hypothesized, not only in the hemolymph but particularly in the fat body, the insufficiently investigated, as yet, equivalent of the mammalian liver and pancreas. Both suppression and hormesis (diaphasic stressor response) of energy supply was reported in the energy-dependent traits of bees exposed to sublethal doses of imidacloprid. Therefore, our goal was to answer which of these two phenomena occurs in the hemolymph/fat body and at what doses of imidacloprid. Methods concentrations/activities of respiratory/citric cycle compounds (acetyl-CoA, IDH-2, AKG, succinate, fumarate, NADH2, COX, UQRC, and ATP) were compared in the hemolymph and fat bodies of nurse workerbees sampled from honeybee colonies fed with diets containing 200 ppb (IM-200), 5 ppb (IM-5; sublethal), and 0 ppb of IM in a field experiment. Results the assayed compounds had higher values in the fat body than in the hemolymph, whereas their variability was higher in the hemolymph. The pattern of response to IM was the same in both tissues, but markedly differed between IM-200 and IM-5. The concentrations of the strongly correlated NADH2, ATP and acetyl-CoA decreased both in IM-200 and IM-5, whereas the levels of the other compounds decreased in IM-200 but increased in IM-5. Conclusions and significance decreased ATP and acetyl-CoA levels both in IM-5 and IM-200 show that the pesticide impairs the hemolymph and fat-body energy metabolism in spite of hormesis in six of the nine respiratory and citric cycle compounds even in low, residual doses. This finding better explains how residual doses of neonicotinoids may disturb the fat body functions, and therefore suppress the apian resistance, which expands our knowledge about honeybee colony losses.