Evaluation of the roles of lipoprotein lipase and hepatic lipase in lipoprotein metabolism: <i>in vivo</i> and <i>in vitro</i> studies in man

Nicoll, A.; Lewis, Barry

doi:10.1111/j.1365-2362.1980.tb02090.x

Cited by 108 publications

(36 citation statements)

References 46 publications

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“…Although LPL can convert VLDL to LDL in vitro (40), this degradative process may be heavily shared with HTGL in vivo. Such a parallel role for HTGL is consistent with the continued metabolism of VLDL and the production of some LDL by human subjects with primary lipoprotein lipase deficiency (41)(42)(43).…”

Section: Inhibition Of Hepatic Triglyceride Lipasementioning

confidence: 57%

Lipoprotein Metabolism during Acute Inhibition of Hepatic Triglyceride Lipase in the Cynomolgus Monkey

Goldberg¹,

Le²,

Paterniti³

et al. 1982

J. Clin. Invest.

250

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A B S T R A C T The role of the enzyme hepatic triglyceride lipase was investigated in a primate model, the cynomolgus monkey. Antisera produced against human postheparin hepatic lipase fully inhibited cynomolgus monkey posttheparin plasma hepatic triglyceride lipase activity. Lipoprotein lipase activity was not inhibited by this antisera. Hepatic triglyceride lipase activity in liver biopsies was decreased by 65-90% after intravenous infusion of this antisera into the cynomolgus monkey. After a 3-h infusion of the antisera, analytic ultracentrifugation revealed an increase in mass of very low density lipoproteins (Sf 20-400). Very low density lipoprotein triglyceride isolated by isopycnic ultracentrifugation increased by 60-300%. Analytic ultracentrifugation revealed an increase in mass of lipoproteins with flotation greater than Sf 9 (n = 4). The total mass of intermediate density lipoproteins approximately doubled during the 3 h of in vivo enzyme inhibition. While more rapidly floating low density lipoproteins (Sf 9-12) increased, the total mass of low density lipoproteins decreased after infusion of the antibodies. The changes in high density lipoproteins did not differ from those in control experiments.In order to determine whether the increases of plasma concentrations of very low density lipoproteins were due to an increase in the rate of synthesis or a decrease in the rate of clearance of these particles, the metabolism of radiolabeled homologous very low density lipoproteins was studied during intravenous infusion of immunoglobulin G prepared from the antisera against hepatic triglyceride lipase (n = 3) or preimmune goat sera (n = 3). Studies performed in the

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Section: Inhibition Of Hepatic Triglyceride Lipasementioning

confidence: 57%

Lipoprotein Metabolism during Acute Inhibition of Hepatic Triglyceride Lipase in the Cynomolgus Monkey

Goldberg¹,

Le²,

Paterniti³

et al. 1982

J. Clin. Invest.

250

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“…This could result in the removal of excess triglycerides and/or phospholipids and be a requirement for receptor-mediated catabolism. A role for the HTGL in VLDL remnant metabolism has recently been suggested (48)(49)(50)(51)(52). This enzyme, evidently, may also be involved in chylomicron remnant metabolism.…”

Section: Discussionmentioning

confidence: 99%

Different patterns of postprandial lipoprotein metabolism in normal, type IIa, type III, and type IV hyperlipoproteinemic individuals. Effects of treatment with cholestyramine and gemfibrozil.

Weintraub¹,

Eisenberg²,

Breslow³

1987

J. Clin. Invest.

268

141

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To study exogenous fat metabolism, we used the vitamin A-fat loading test, which specifically labels intestinally derived lipoproteins with retinyl palmitate (RP). Postprandial RP concentrations were followed in total plasma, and chylomicron (Sf > 1,000) and honchylomicron (Sf < 1,000) fractions. In normal subjects postprandial lipoproteins were present for more than 14 h, and chylomicron levels correlated inversely with lipoprotein lipase activity and fasting high density lipoprotein (HDL) cholesterol levels and nonchylomicron levels correlated inversely with hepatic triglyceride lipase activity. The main abnormality in type IV patients was a 5.6-fold increase in the chylomicron fraction, whereas in type III patients it was a 6.4-fold increase in nonchylomicrons. Type Ha patients had abnormally low chylomicron fractions. In type IV patients gemfibrozil decreased, whereas in type Ha patients cholestyramine increased the chylomicron fraction 66 and 88%, respectively.This study demonstrates an unexpectedly large magnitude and long duration of postprandial lipemia in normal subjects and patients. These particles are potentially atherogenic, and their role in human atherosclerosis warrants further study.

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“…While VLDL lipids are hydrolyzed more effectively by LpL than HL, IDL, and LDL lipids are significantly better substrates for HL than LpL (94). HL has a higher affinity for LDL than LpL and has the capability to act as a phospholipase as well, hence removing both core and surface components from the particle (90,95). Buoyant, triglyceride-rich LDL particles accumulate in patients with HL deficiency (96,97) after acute inhibition of HL activity in the cynomolgus monkey (82) and in hepatic knockout mice (98).…”

Section: Role Of Plasma Lipase Activities In Production Of Ldl From Tmentioning

confidence: 99%

Metabolic origins and clinical significance of LDL heterogeneity

Berneis

Krauss

2002

Journal of Lipid Research

775

633

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LDLs in humans comprise multiple distinct subspecies that differ in their metabolic behavior and pathologic roles. Metabolic turnover studies suggest that this heterogeneity results from multiple pathways, including catabolism of different VLDL and IDL precursors, metabolic remodeling, and direct production. A common lipoprotein profile designated atherogenic lipoprotein phenotype is characterized by a predominance of small dense LDL particles. Multiple features of this phenotype, including increased levels of triglyceride rich lipoprotein remnants and IDLs, reduced levels of HDL and an association with insulin resistance, contribute to increased risk for coronary heart disease compared with individuals with a predominance of larger LDL. Increased atherogenic potential of small dense LDL is suggested by greater propensity for transport into the subendothelial space, increased binding to arterial proteoglycans, and susceptibility to oxidative modification. Large LDL particles also can be associated with increased coronary disease risk, particularly in the setting of normal or low triglyceride levels. Like small LDL, large LDL exhibits reduced LDL receptor affinity compared with intermediate sized LDL. Future delineation of the determinants of heterogeneity of LDL and other apoB-containing lipoproteins may contribute to improved identification and management of patients at high risk for atherosclerotic disease. -Berneis, K. K., and R. M. Krauss. Metabolic origins and clinical significance of LDL heterogeneity.

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Evaluation of the roles of lipoprotein lipase and hepatic lipase in lipoprotein metabolism: in vivo and in vitro studies in man

Cited by 108 publications

References 46 publications

Lipoprotein Metabolism during Acute Inhibition of Hepatic Triglyceride Lipase in the Cynomolgus Monkey

Lipoprotein Metabolism during Acute Inhibition of Hepatic Triglyceride Lipase in the Cynomolgus Monkey

Different patterns of postprandial lipoprotein metabolism in normal, type IIa, type III, and type IV hyperlipoproteinemic individuals. Effects of treatment with cholestyramine and gemfibrozil.

Metabolic origins and clinical significance of LDL heterogeneity

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