The amount of lipid in a fat cell (adipocyte) is determined by the rate of lipolysis as well as the rate of lipid synthesis. Both processes occur simultaneously and continuously, their relative rates determining if there is net lipid loss or accretion.
REGULATIONS OF LIPOLYSISAcute control. Hydrolysis of triacylglycerols is catalysed by hormone-sensitive lipase. The activity of this enzyme is enhanced by phosphorylation by cyclic-AMP-dependent kinase (A-kinase). Hormone-sensitive lipase, and hence lipolysis, is thus acutely stimulated by a variety of hormones (e.g. adrenaline, glucagon, adrenocorticotrophic hormone (ACTH)) and the neurohumoral transmitter, noradrenaline, which increase the adenylate cyclase-A-kinase signal transduction system. Each peptide hormone interacts with its own receptor in the plasma membrane while adrenaline and noradrenaline interact with the P-adrenergic receptor. These hormone-receptor interactions lead to dissociation and activation of the GTP-binding protein, G,, which in turn leads to activation of adenylate cyclase (also located in the plasma membrane) and the synthesis of cyclic-AMP (Fig. 1). Cyclic-AMP activates A-kinase which in turn phosphorylates and activates hormone-sensitive lipase. Signal transduction through this system is modulated by noradrenaline and adrenaline acting via a second receptor, the 1x2-adrenergic receptor, and by prostaglandins (El and E2) and adenosine, both produced within adipose tissue, and acting via their own receptors. These receptors are coupled to a second GTP-binding protein, Gi. Receptor activation leads to dissociation of Gi which inhibits adenylate cyclase (Fig. 1). Catecholamines can, thus, both stimulate and inhibit lipolysis, the net effect depending on the relative numbers of p-and cx2-adrenergic