The present investigation was directed to study the effect of in vitro or ex vivo NO donors, sodium nitroprusside and molsidomine, using isolated sliced adipose tissue or in the form of immobilized and perfused adipocytes on the basal and isoprenaline-stimulated lipolysis. The results demonstrated that 1) in vitro application of sodium nitroprusside to perfused adipocytes or molsidomine to sliced adipose tissues affects isoprenaline-induced lipolysis in two ways, an increase in lipolysis at low isoprenaline concentrations (which means the sensitization of adipose tissues to adrenergic effect by NO) and decreased adrenergic agonist-stimulated lipolysis at higher concentration of isoprenaline (a decrease in the maximum lipolytic effect of isoprenaline), 2) low concentrations of molsidomine alone induced lipolysis from adipose tissue which attained more than 60 % of that by isoprenaline (pD2 value for molsidomine = 11.2, while pD2 for isoprenaline = 8.17) while sodium nitroprusside did not affect the basal lipolysis significantly, 3) in vivo administration of molsidomine for 2 days reduced the maximum lipolytic effect of isoprenaline and (only non-significantly) increased the sensitivity to low doses of isoprenaline. In conclusion the present data demonstrate that NO plays an important role in adrenergic lipolysis in adipose tissues and further investigations are needed to unravel the exact role of NO in lipolysis., D. Lincová, D. Mišeková, E. Kmoníčková, N. Canová, H. Farghali., and Obsahuje bibliografii
In the present study the hypothesis that there is a feedback between juvenile hormone and adipokinetic hormones (AKHs) was investigated by topical application of the juvenoid methoprene on 9-day-old adult males of the firebug Pyrrhocoris apterus. This juvenoid (2 µg) induced a significant reduction of haemolymph lipids 24 h after treatment; however, it did not significantly reduce the ability of Pyrap-AKH (10 pmol/bug) to mobilize fat body lipids 6-72 h after the methoprene application. The same methoprene treatment elicited a significant increase of AKH content in the CNS (central nervous system: brain + corpora cardiaca + corpora allata) of experimental males 24 and 48 h after the juvenoid application. A significant decrease in the AKH level in the haemolymph was recorded at the same times and under the same experimental conditions. Similar results were observed when production of the AKHs from the CNS of topically treated males was measured under in vitro conditions. It is suggested that methoprene may reduce AKH release from the CNS resulting in an increase in the AKH content of the CNS due to accumulation rather than stimulation of AKH synthesis. Possible consequences of this phenomenon on the physiology of P. apterus are discussed.