Regulation of fat body mitochondrial respiration in Periplaneta americana by a novel factor from the corpus cardiacum

Abstract

Respiration of fat body ( Periplaneta americana) mitochondria is increased by pretreatment of the tissue with corpus cardiacum (CC) extract. The magnitude of the increase depends on the type of substrate supplied for oxidation. With 5 m M pyruvate the respiration increased 22%, decreasing to 0 with 1 m M pyruvate. In contrast, 50 μ M and 0.2 m M palmitic acid supported an increase in CC-stimulated respiration of 14 and 44%, respectively. Unlike crude CC extract, the synthetic hyperglycemic peptides CCI and CCII failed to alter the respiratory activity of fat body mitochondria. In common with the action of CC extract pretreatment of the fat body in vitro with 10 −5, M cyclic AMP, 10 −5, M 8-bromo-cyclic AMP, or 10 −5, M forskolin increased mitochondrial respiration approximately 30%. Octopamine (10 −4, M) elicited a response similar to that obtained with CC extract. Neither 10 −5, M cyclic AMP nor 10 −5, M 8-bromo-cyclic AMP stimulated respiration when applied directly to the mitochondria. These results suggest that the factor in CC extract manifests its effect intracellularly through the activation of a cyclic AMP-dependent protein kinase. This interpretation is also based on the finding that diamide, an inhibitor of protein kinase, inhibits CC-dependent and cyclic AMP-dependent mitochondrial respiration. The physiological role of the CC factor responsible is not known.