Triglyceride lipase, hepatic

Selected entries from Methods in Enzymology [vol, page(s)] Detergent-resistant phospholipase Ai from Escherichia coll membranes, 197, 309 phospholipase Ai activity of guinea pig pancreatic lipase, 197, 316 purification of rat kidney lysosomal phospholipase Ai, 197, 325 purification and substrate specificity of rat hepatic lipase, 197, 331 human postheparin plasma lipoprotein lipase and hepatic triglyceride lipase, 197, 339 phospholipase activity of milk lipoprotein lipase, 197, 345. 

Baginsky ML, Brown WV (1979) A newmethodfor the measurement of lipoprotein lipase in postheparin plasma using sodium dodecyl sulfate for the inactivation of hepatic triglyceride lipase. J Lipid Res 20 548-556... 

Yamagishi S, Abe T, Sawada T. Human recombinant interferon alpha-2a (r IFN alpha-2a) therapy suppresses hepatic triglyceride lipase, leading to severe hypertriglyceridemia in a diabetic patient. Am J Gastroenterol 1994 89(12) 2280. 

LCAT), which catalyzes the synthesis of cholesterol esters (F14, S46, S59) apoA-II, which activates hepatic triglyceride lipase (J2) and apoC-II, which activates lipoprotein lipase, responsible for the hydrolysis of triglycerides in chylomicrons and VLDL (H20, L5). Their mode of action is considered in Section 4 when the individual apolipoproteins are discussed. 

Purified apoA-II was shown by Jahn et al. (J2) to increase hepatic triglyceride lipase activity by threefold in vitro. Human plasma also activates hepatic triglyceride lipase activity, and it is a reasonable assumption that this activation is due to apoA-II. The physiological importance of this effect is not yet clear. 

The size of the VLDL particle in plasma diminishes and its density increases as triglyceride is hydrolyzed by endothelial lipoprotein lipase, and the particles are thus converted to intermediate-density lipoproteins (IDL) (B32, S35). The IDL detach from the endothelium, and some are taken up by hepatic B-100, E receptors. The remaining particles in the circulation are further depleted of some cholesteryl ester (by an unknown mechanism), and most of the remaining triglyceride (probably by hepatic triglyceride lipase, in the liver sinusoids) (D5). Hie resulting LDL particles are largely composed of cholesteryl ester as the core lipid and apoB-100 as the apolipoprotein. 

In functional lipoprotein lipase deficiency there appears to be a normal removal rate for VLDL from the plasma (B31, F19, N7), and an unimpaired rate for the conversion of VLDL apoB to LDL apoB (N7). It may be that VLDL is hydrolyzed by hepatic triglyceride lipase (unaffected in lipoprotein lipase deficiency) (N7). Hepatic triglyceride lipase does not require apoC-II as a cofactor (E2). 

As hepatic triglyceride lipase is released into the circulation by heparin, it might be thought that postheparin plasma hepatic triglyceride lipase activity... 

M46. Murase, T., and Hakura, H., Accumulation of intermediate density lipoprotein in plasma after intravenous administration of hepatic triglyceride lipase antibody in rats. Atherosclerosis 38, 293-300 (1981). 

R6. Reardon, M. F.,. Sakai, H., and Steiner, G., Roles of lipoprotein lipase and hepatic triglyceride lipase in the catabolism in vivo of triglyceride-rich lipoproteins. Arteriosclerosis 2, 396-402 (1982). 

Heparin-releasable hepatic triglyceride lipase deficiency... 

Heparin Growth factors, coagulation faaors, lipoproteins, DNA polymerase, DNA ligase, RNA polymerases, restriction endonucleases, polynucleotide kinase, lipoprotein lipase, hepatic triglyceride lipase, reverse transcriptase, hyaluronidase, neurauninidase, trypsin, pepsin, fumarase, lectin from chicken liver and embryonic chicken muscle, platelet-secreted antiheparin proteins, platelet-endoglycosidase... 

Mechanisms of Exercise-Induced Changes in Plasma Lipids Lipoprotein Lipase, Hepatic Triglyceride Lipase and Lecithin Cholesterol Acyl Transferase... 

The liver synthesizes two enzymes involved in intra-plasmic lipid metabolism hepatic triglyceride lipase (HTL) and lecithin-cholesterol-acyltransferase (LCAT). The liver is further involved in the modification of circulatory lipoproteins as the site of synthesis for cholesterol-ester transfer protein (CETP). Free fatty acids are in general potentially toxic to the liver cell. Therefore they are immobilized by being bound to the intrinsic hepatic fatty acid-binding protein (hFABP) in the cytosol. The activity of this protein is stimulated by oestrogens and inhibited by testosterone. Peripheral lipoprotein lipase (LPL), which is required for the regulation of lipid metabolism, is synthesized in the endothelial cells (mainly in the fatty tissue and musculature). 

Intolerance to intravenous lipid emulsion (IVFE), evidenced by increased serum triglyceride concentrations, is common in ARE Hypertriglyceridemia is thought to be caused by decreased catabolism of triglycerides and increased synthesis from free fatty acids (FFAs). Hepatic triglyceride lipase and peripheral lipoprotein lipase activ-... 

FIGURE 9.1 Simplified overview of lipid and lipoprotein metabolism with some key enzymes numbered (1) cholesteryl ester transfer protein (CETP), (2) hepatic triglyceride lipase, (3) lecithin cholesterol acyl transferase (LCAT), and (4) lipoprotein lipase. 

Approximately half of the VLDL remnants are not taken up by the liver but, instead, have additional core triacylglycerols removed to form IDL, a specialized class of VLDL remnants. With the removal of additional triacylglycerols from IDL through the action of hepatic triglyceride lipase within hepatic sinusoids, LDL is generated from IDL. As seen in Table 34.4, the LDL particles are rich in cholesterol and cholesterol esters. Approximately 60% of the LDL is transported back to the hver, where its apoB-100 binds to specific apoB-100 receptors in the hver cell plasma membranes, allowing particles to be endocytosed into the hepatocyte. The remaining 40% of LDL particles are carried to extrahepatic tissues such as adrenocortical... 

Plasma triacylglycerols are normally cleared by peripheral lipases (lipoprotein lipase or LPL and hepatic triglyceride lipase or HTGL). Because the activities of both LPL and HTGL are rednced in patients with hepatacellular disease, a relatively high level of plasma triacylglycerols may be found in both acute and chronic hepatitis, in patients with cirrhosis of the liver, and in patients with other diffuse hepatocellular disorders. 

C) Hepatic triglyceride lipase (HTGL) activity is increased. 

Moreover several candidate genes and their variations such as cholesterol ester transfer protein (CETP), lipoprotein lipase (LPL), hepatic triglyceride lipase (HL), LDL-receptor, ATP binding cassette transporter Al (ABCAl), and lecithin-cholesterol acyltransferase (LCAT) have been studied to demonstrate the individual s sensitivity toward developing CHD [102-108]. 

The presence of the renmants is accompanied by a decrease of the protamine-insensitive postheparin-lipolytic activity. Whether a decrease of the hepatic triglyceride lipase is responsible for the diminished renmant catabolism is not clear. It can as well be the decreased rate of hepatic uptake. I will come to this later. 

Fig, 3. Schematic representation of Apo C metabolic events. LPL, lipoprotein lipase HTGL, hepatic triglyceride lipase... 

POSTHEPARIN PLASMA LIPOPROTEIN LIPASE AND HEPATIC TRIGLYCERIDE LIPASE ACTIVITIES IN GOUT... 

Many studies have reported that gouty patients were associated frequently with hypertriglyceridemia(1). In the present study, postheparin plasma lipoprotein lipase (LPL) and hepatic triglyceride lipase (H-TGL) activities in gouty subjects were measured. 

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