Beta-adrenergic stimulation drives CETP secretion from hamster adipose tissue through a cAMP pathway (Atherosclerosis 1998)

High levels of cholesteryl ester transfer protein (CETP) favours decreased plasma high density lipoprotein cholesterol and increased levels of cholesterol in apolipoprotein B containing lipoproteins. Adipose tissue is one of the major sources of circulating CETP. Previous studies by our group and others demonstrated that the production of CETP from hamster adipose tissue increases after fasting, a metabolic state known to affect the sympathoadrenal axis. The present study examines the influence of beta-adrenergic agonists on the secretion of CETP from hamster adipose tissue. Fifteen minutes after an intraperitoneal injection of isoproterenol (12 microg/kg), the release of CETP mass and activity from adipose tissue fragments incubated in vitro were significantly increased. This was associated with an elevation in CETP mass and activity in plasma. The effects of isoproterenol on CETP release from adipose tissue and plasma CETP levels were suppressed by propranolol, a beta-adrenoceptor inhibitor. Addition of 10(-6) M isoproterenol to adipose tissue in vitro increased the release of CETP mass and activity from adipose tissue and this was also blocked by propranolol. Isoproterenol-induced secretion of CETP activity from adipose tissue was partially inhibited by cytochalasin B, an inhibitor of actin cytoskeleton reorganization. Forskolin, a classical adenylate cyclase agonist and 8-bromo-cAMP, a functional analogue of cAMP, mimicked the effect of isoproterenol on CETP release from adipose tissue. Our results suggest that isoproterenol increases the secretion of CETP from hamster adipose tissue through a beta-adrenoceptor and a cAMP-dependent pathway. Actin cytoskeleton reorganization may be required for secretion of CETP. The findings imply that the secretion of CETP from adipose tissue is under neurosympathetic control.