Endotoxin influence on lipolysis in isolated human and primate adipocytes

Abstract

The influence of E. coli endotoxin on basal and norepinephrine-stimulated lipolysis as well as on cyclic AMP accumulation was studied in human and rhesus monkey adipocytes. The effect of indomethacin on lipolysis was also investigated. Human and rhesus adipocytes exhibited qualitatively similar responses to norepinephrine (0.59–11.8 μ M). There was a positive correlation between cell volume and basal lipolysis in human, but not in rhesus, cells. A positive correlation was also noted between cell volume and the response to endotoxin and to norepinephrine in human cells. The increment in response to norepinephrine after endotoxin treatment, however, was negatively correlated to basal lipolysis. Endotoxin (0.32 μg/0.5 ml of cell suspension) increased basal free fatty acid release and significantly enhanced norepinephrine-stimulated glycerol release from rhesus adipocytes. In human fat cells, basal release of glycerol was stimulated by endotoxin at all concentrations used, whereas basal FFA release was increased at endotoxin concentrations of 0.032 and 0.320 μg/0.5 ml of cell suspension. Endotoxin significantly depressed norepinephrine-stimulated release of FFA at all endotoxin concentrations without significantly influencing concurrent glycerol release. Treatment of rhesus fat cells with endotoxin and endotoxin plus indomethacin resulted in significant increases in cAMP content. In human fat cells, endotoxin alone did not influence cAMP concentration; however, exposure to norepinephrine or to endotoxin plus indomethacin resulted in significantly increased levels of cAMP.