α-adrenergic suppression of very-low-density-lipoprotein triacylglycerol secretion by isolated rat hepatocytes

Abstract

The effect of adrenaline on triacylglycerol synthesis and secretion was examined in isolated rat hepatocytes. Cells were incubated with 0.5 mM-[1-14C]oleate, and the accumulation of triacylglycerol and [14C]triacylglycerol was measured in the incubation medium. Triacylglycerol appearing in the medium was present in a form with properties similar to very-low-density lipoproteins. Triacylglycerol, [14C]triacylglycerol and [14C]phospholipid contents of hepatocytes were also determined. Addition of 10 microM-(-)adrenaline decreased accumulation of glycerolipid in the incubation medium and also decreased cellular [14C]phospholipid content. Prazosin abolished these effects, whereas propranolol did not. The hormone did not affect cellular triacylglycerol content or rates of incorporation of [1-14C]oleate into cell triacylglycerol. The effect of adrenaline on the removal of newly secreted triacylglycerol and the secretion of synthesized glycerolipid was also examined. The catecholamine did not affect rates of removal of newly secreted triacylglycerol. Adrenaline did inhibit the secretion of pre-synthesized lipid by the cells, as assessed by the appearance of radiolabelled triacylglycerol from hepatocytes that had been preincubated with [1,2,3-3H]-glycerol. Adrenaline did not affect rates of fatty acid uptake by hepatocytes, but did stimulate oxidation of [1-14C]oleate, principally to 14CO2.

Hepatic denervation impairs the assembly and secretion of VLDL‐TAG

“…15,16 It has been shown that adrenaline suppresses the secretion of VLDL-TAG in isolated rat hepatocytes and that this effect is mediated by the a 1 adrenergic receptor. 17,18 Similar results were obtained in a model of perfused liver, in which noradrenaline decreased the secretion of TAG and apoB. 19 A previous study by our group demonstrated decreased capacity of fatty acid oxidation and the incorporation of lipid in the VLDL secreted by denervated livers.…”

“…4,25 Previous studies in our laboratory had already shown that hepatic denervation alters lipid metabolism in the organ, leading towards lower oxidation of fatty acids and decreased incorporation into VLDL. 20 It is known that catecholamines play a role in the regulation of VLDL secretion, 17,19,26 but no studies, to our knowledge, have so far examined the importance and contribution of the sympathetic innervation to the process. Our results show a lower secretion of VLDL in the denervated animals compared with controls, which was related with a lower expression of apoB in these.…”

Acute hypoxia induces hypertriglyceridemia by decreasing plasma triglyceride clearance in mice

“…It is not clear why hepatic TG secretion decreased at FiO 2 ϭ 0.10, although we exonerated transcriptional changes in MTP or apoB. Perhaps catecholamines played a role, since epinephrine has been shown to suppress VLDL secretion (9,13). Why does acute hypoxia decrease VLDL secretion while chronic IH apparently augments it (39)?…”

The role of pancreatic hormones in the regulation of lipid storage, oxidation and secretion in primary cultures of rat hepatocytes. Short- and long-term effects

“…Alternatively, glucagon, in terms of its activation of AMPdependent protein kinase, could effect apoB phosphorylation similarly to that described for acetyl-CoA carboxylase [49] and HMG-CoA reductase [50]. Glucagon may also act via'changes in intracellular Ca21 concentration [51] and, in this respect, it has previously been shown that a-adrenergic stimulation of hepatocytes, which results in a redistribution of intracellular Ca2+, also inhibits VLDL triacylglycerol secretion [52]. Although the shorter-term effects (i.e.…”