Regulation of hepatic triacylglycerol synthesis and lipoprotein metabolism by glucocorticoids.

The excessive synthesis and storage of triacylglycerol (triglyceride) has a number of clinical implications. It is obviously the main symptom of obesity where excess lipid is stored in adipose tissue. Abnormal accumulations of triacylglycerols can also be manifested as a fatty liver, e.g. as a'result of the ingestion or inhalation of toxic compounds and damage to the liver. These conditions are often associated with an increase in the rate of triacylglycerol synthesis in the liver and are aggravated if the ability to secrete the triacylglycerol in very-low-density lipoproteins (VLDL) is impaired. If the increased synthesis of triacylglycerol results in a greater secretion of VLDL, then this implies that the flux of cholesterol into low-density lipoprotein (LDL) should also be increased. This is because cholesterol is secreted as part of the VLDL particle to facilitate the transport of triacylglycerol. When the triacylglycerol is removed from the VLDL by the action of lipoprotein lipase (EC 3.1.1.34), the cholesterol appears in the circulation in lowdensity lipoproteins. It therefore seems important to understand how the body controls triacylglycerol metabolism and to identify the mechanisms by which the synthesis of triacylglycerols in the liver becomes raised. At present this knowledge is incomplete, but it has become evident from animal work that the availability of glucocorticoids is an important factor 11, 21. Although the control of glucocorticoid metabolism in experimental animals is probably different from that in man, nevertheless their effects on metabolism are likely to be