Both somatostatin and the caudal neuropeptide, urotensin II, stimulate lipid mobilization from coho salmon liver incubated in vitro.

The direct effects of somatostatin-14 (SRIF; synthetic ovine) and the fish caudal neuropeptide, urotensin II (UII; synthetic Gillichthys), on fatty acid (FA) release and on lipolytic enzyme (triacylglycerol lipase) activity were determined on coho salmon liver slices incubated in vitro. FA release was continuously measured by pH-stat titration. Additionally, gas chromatographic analysis of the incubation medium was performed to determine the type and relative composition of medium fatty acid constituents. SRIF and UII both stimulated FA release in a dose-dependent manner; the two peptides appeared to stimulate FA release in an equimolar manner. Maximal response was obtained at 1 X 10(-5) M; ED50 was approximately 2 X 10(-7) M. SRIF-stimulated FA release did not result in differential secretion of any particular FA type. Tissue triacylglycerol lipase activity was significantly enhanced by addition of UII or SRIF (2 X 10(-6) M). Dibutyryl cAMP and IBMX both stimulated FA release and lipase activity; dbcAMP stimulated FA release in dose-dependent manner. These results indicate that SRIF and UII directly enhance lipid mobilization from salmon liver slices and suggest that SRIF- and UII-stimulated lipid mobilization from salmon liver slices is mediated through cAMP.