Hormonal control of adipose-tissue lipolysis.
Adipose-tissue triacylglycerol is the major energy store in man. The physiological importance and biochemical mechanism of the hormonal control of lipolysis in white adipose tissue is reviewed. Rates of lipolysis and fatty acid release observed when adipose tissue is incubated in vitro are compared with rates of triacylglycerol turnover in man. It appears that enhanced rates of lipolysis in vivo, for example during fasting and exercise, may be a substantial fraction of the maximum obtainable by hormone stimulation in vitro. There is considerable species variation in the hormonal sensitivity of adipose tissue. Some hormones that stimulate lipolysis in vitro may not be significant lipolytic agents at physiological concentrations in vivo. In man and rat, the most important acutely acting lipolytic and anti-lipolytic hormones are catecholamines and insulin respectively. The sympathetic nervous system may play a role at least as important as circulating catecholamines in the mobilization of stored triacylglycerol. The effects of acute lipolytic hormones are modulated in the long term by corticosteroids and thyroid hormone. Stimulation of lipolysis is believed to be mediated by the increased intracellular cyclic AMP concentration that occurs after interaction of hormones with specific receptors in the plasma membrane. The properties of membrane receptors, adenylate cyclase, cyclic AMP phosphodiesterase, cyclic AMP-dependent protein kinase and triacylglycerol lipase, as studied in rat and human adipose tissue, are discussed. Several features of the action of lipolytic hormones in vitro are difficult to account for by the hypothesis that cyclic AMP is the only "second messenger" regulating lipase activity. These include anomalous effects of hormones at high concentrations and the possible existence of feedback inhibition limiting the accumulation of cyclic AMP and the stimulation of lipolysis. The mechanism of the anti-lipolytic action of insulin is at present unknown.
D015087:2',3'-Cyclic-Nucleotide Phosphodiesterases / Q000378:metabolism; D000262:Adenylyl Cyclases / Q000378:metabolism; D000273:Adipose Tissue / Q000378:metabolism* / Q000648:ultrastructure; D000818:Animals; D002395:Catecholamines / Q000502:physiology; D000242:Cyclic AMP / Q000378:metabolism; D005230:Fatty Acids, Nonesterified / Q000378:metabolism; D005246:Feedback; D006728:Hormones / Q000502:physiology*; D006801:Humans; D007328:Insulin / Q000502:physiology; D011494:Protein Kinases / Q000378:metabolism; D051381:Rats; D011956:Receptors, Cell Surface / Q000378:metabolism; D013217:Starvation / Q000378:metabolism; D014280:Triglycerides / Q000378:metabolism*
D002395:Catecholamines; D005230:Fatty Acids, Nonesterified; D006728:Hormones; D007328:Insulin; D011956:Receptors, Cell Surface; D014280:Triglycerides; D000242:Cyclic AMP; D011494:Protein Kinases; D015087:2',3'-Cyclic-Nucleotide Phosphodiesterases; D000262:Adenylyl Cyclases