Evidence for the participation of arachidonic acid metabolites in trehalose efflux from the hormone activated fat body of the cockroach (Periplaneta americana)

The hypertrehalosemic hormones, HTH-I and HTH-II, activate trehalose synthe sis and increase the rate of sugar efflux from Periplaneta americana fat bo dy in vitro. These processes are unaffected by the diacylglycerol, 1-oleyl- 2-acetyl-sn-glycerol. an activator of protein kinase C. Similarly, H-7 and spingosine, inhibitors of protein kinase C, are also inactive against treha lose efflux. The possibility that diacylglycerol lipase might generate an a ctive fatty acid species was ruled out because of the failure of the inhibi tor RHC-80267 to inhibit trehalose efflux. Activation of trehalose efflux f rom the intact fat body by HTH-I was strongly inhibited in a concentration dependent manner by the cyclooxygenase inhibitors indomethacin and diclofen ac, but not by acetylsalicylic acid. Nordihydroguaiaretic acid: a lipoxygen ase inhibitor, also blocked HTH-I activated trehalose efflux in a concentra tion dependent fashion. The phospholipase A(2) inhibitors mepacrine and 4'- bromophenacyl bromide were also effective in decreasing the efflux of treha lose from HTH-I challenged fat body. The data suggest possible roles for ar achidonic acid metabolites in the regulation of trehalose synthesis and in the efflux of the sugar from the fat body. (C) 1998 Elsevier Science Ltd. A ll rights reserved.