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Results for “LIPOPROTEIN LIPASE”

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At least 19 recordsLinked to original sources
PubMed1975

Serum-stimulated lipases (lipoprotein lipases). Immunological crossreaction between the bovine and the human enzymes.

A rabbit antiserum prepared against the serum-stimulated lipase (lipoprotein lipase) from bovine milk crossreacted with serum-stimulated lipases from human milk and from human postheparin plasma, but not with bile salt-stimulated lipase from human milk or with salt-resistant lipase from human postheparin plasma. Thus, the serum-stimulated lipase in bovine milk has immunological determinants in common with the serum-stimulated lipases in human milk and in human postheparin plasma. The time-courses for the appearance of serum-stimulated lipase and salt-resistant lipase activities in human plasma after heparin injection were different. The two activities were separated by heparin-Sepharose chromatography. After treatment of postheparin plasma with the antiserum only the salt-resistant lipase activity could be eluted from the column. Thus, these two enzyme activities in postheparin plasma reside in two different enzyme molecules.

Animals↗
PubMed1976

Clearing factor lipase (lipoprotein lipase) activator. A method for the measurement of the net activating ability of human sera.

The hydrolysis of an emulsified triglyceride substrate by clearing factor lipase (lipoprotein lipase) normally requires the presence of particular activating polypeptide species. These are present in serum, together with other inhibitory species, as part of the serum lipoproteins. The paper describes a method whereby the net activating ability of individual human sera may be measured routinely. In a normal population, this activating ability is shown to be correlated positively with the fasting serum triglyceride concentration. As the fasting triglyceride concentration increases, there is a rise in the proportion of the total activating ability that is associated with the very low density lipoproteins. A dietary fat load does not raise the total activating ability but does increase the proportion of the total that is associated with the serum lipoproteins of lowest density.

Animals↗
PubMed1970

Effect of fasting on the clearing factor lipase (lipoprotein lipase) activity of fresh and defatted preparations of rat heart muscle.

The clearing factor lipase (lipoprotein lipase) activities of homogenates of fresh tissue and of acetone-ether powders have been compared in hearts from fed and starved rats. The activity of the enzyme measured in homogenates of acetone-ether powders is generally higher than that in homogenates of the fresh tissue. Activation is due to an effect of the acetone-ether treatment on enzyme which is associated with the tissue residue in fresh tissue homogenates. A similar activation occurs when the tissue residue is treated with deoxycholate. When rats are fasted, a marked increase in the clearing factor lipase activity of the heart occurs. Peak activities are reached after 10-24 hr, and thereafter the activity falls slowly. This pattern of activity is observed in homogenates of fresh tissue and of acetone-ether powders. The activity of clearing factor lipase in diaphragm muscle also increases in rats starved for 8 or 24 hr. The importance of the change in muscle clearing factor lipase activity on fasting in relation to triglyceride fatty acid utilization by this tissue is emphasized.

Acetone↗
PubMed1984

Treatment of hyperthyroidism: effects on hepatic lipase, lipoprotein lipase, LCAT and plasma lipoproteins.

The activities of hepatic lipase and of lipoprotein lipase, the elimination rate of exogenous triglyceride and the cholesterol esterification rate were determined and related to plasma lipoprotein concentrations in 16 patients before and after treatment for hyperthyroidism. The activity of hepatic lipase was significantly higher (65%) before than after treatment, while the activity of lipoprotein lipase and the elimination rate of exogenous triglyceride remained unchanged. The endogenous cholesterol esterifying ability decreased after treatment, whereas no change occurred in the fractional cholesterol esterification rate measured with normal plasma as substrate. The concentrations of LDL-cholesterol and HDL-cholesterol increased significantly after treatment. The decrease in hepatic lipase activities was correlated to the decrease in S-T3 concentrations (r = 0.77, P less than 0.001) and to the increase in HDL-cholesterol concentrations (r = 0.51, P less than 0.05). The activities of lipoprotein lipase were positively correlated to the concentrations of HDL-cholesterol both before (r = 0.54, P less than 0.05) and after (r = 0.59, P less than 0.05) treatment. These results support the view that hepatic lipase and lipoprotein lipase are both important determinants of plasma HDL concentrations and suggest that an increased hepatic lipase activity contributes to the lower HDL levels in hyperthyroid patients.

Adolescent↗
PubMed1993

Lipoprotein lipases, lipoprotein density gradient profile and LDL receptor activity in miniature pigs fed fish oil and corn oil.

The effects of fish oil and corn oil on plasma lipoprotein concentrations, the lipolytic enzymes, lipoprotein lipase and hepatic triacylglycerol lipase, the density distribution of the plasma lipoproteins and LDL receptor activity were studied. These experiments were designed, in part, to define the mechanism(s) responsible for the increased conversion of plasma VLDL apolipoprotein B to LDL and a decreased LDL apolipoprotein B fractional catabolic rate described in previous apolipoprotein B kinetic studies. Miniature pigs were fed diets for 3 to 6 weeks containing supplements of corn oil or fish oil as Maxepa. Triacylglycerol and cholesterol in plasma and VLDL were significantly reduced by the fish oil diet. LDL and HDL cholesterol were not significantly changed. The fish oil diet significantly reduced post-heparin plasma lipoprotein lipase and hepatic triacylglycerol lipase activities, which may be an adaptive response to the low concentration of substrates (triacylglycerol-rich lipoproteins) for these enzymes. No differences were observed in the density of VLDL, LDL or HDL as determined by density gradient ultracentrifugation with the fish oil diet. No major changes in percent lipid composition of VLDL, LDL and HDL were observed. No differences were found with respect to LDL uptake by J774 macrophages. Receptor mediated clearance of LDL in vivo, as assessed by measuring the difference in fractional catabolic rate of native vs. methylated LDL decreased significantly by 17% (P < 0.032). We conclude that the increased conversion of VLDL apolipoprotein B to LDL in miniature pigs fed fish oil is not related to an increase in lipolytic enzymes or density distribution of VLDL, but may be due in part to a decrease in LDL receptor activity.

Animals↗
PubMed2002

Contribution of hepatic lipase, lipoprotein lipase, and cholesteryl ester transfer protein to LDL and HDL heterogeneity in healthy women.

Hepatic lipase (HL) and cholesteryl ester transfer protein (CETP) have been independently associated with low density lipoprotein (LDL) and high density lipoprotein (HDL) size in different cohorts. These studies have been conducted mainly in men and in subjects with dyslipidemia. Ours is a comprehensive study of the proposed biochemical determinants (lipoprotein lipase, HL, CETP, and triglycerides) and genetic determinants (HL gene [LIPC] and Taq1B) of small dense LDL (sdLDL) and HDL subspecies in a large cohort of 120 normolipidemic, nondiabetic, premenopausal women. HL (P<0.001) and lipoprotein lipase activities (P=0.006) were independently associated with LDL buoyancy, whereas CETP (P=0.76) and triglycerides (P=0.06) were not. The women with more sdLDL had higher HL activity (P=0.007), lower HDL2 cholesterol (P<0.001), and lower frequency of the HL (LIPC) T allele (P=0.034) than did the women with buoyant LDL. The LIPC variant was associated with HL activity (P<0.001), HDL2 cholesterol (P=0.034), and LDL buoyancy (P=0.03), whereas the Taq1B polymorphism in the CETP gene was associated with CETP mass (P=0.002) and HDL3 cholesterol (P=0.039). These results suggest that HL activity and HL gene promoter polymorphism play a significant role in determining LDL and HDL heterogeneity in healthy women without hypertriglyceridemia. Thus, HL is an important determinant of sdLDL and HDL2 cholesterol in normal physiological states as well as in the pathogenesis of various disease processes.

Adult↗
PubMed1990

Effect of dietary palm oil on lipoprotein lipases: lipoprotein levels and tissue lipids in rat.

The aims of our study were to investigate the effect of dietary palm oil on the levels of lipoprotein lipase, hepatic lipase, fat distribution (in the aorta and liver), and total cholesterol, HDL, LDL, and triacylglycerol levels in young rats (70 g body wt) over a period of 10 weeks. Palm oil-fed rats showed higher growth rate and lower triacylglycerol levels than the control group. Hepatic lipase activity was correlated to the liver fat distribution (correlation coefficient, r = +0.682) as seen by histopathological sections and was similar for both the palm oil and the control diets. Palm oil-fed rats exhibited a significantly higher HDL cholesterol to total plasma cholesterol ratio when compared to animals fed the control diet. The triacylglycerol levels correlated inversely to the HDL cholesterol levels (r = -0.536) while the lipoprotein lipase (LPL) activity correlated directly to the LDL level (r = +0.617) for both groups of animals. The fatty acid profiles of adipose and liver tissues and plasma revealed that saturated fatty acids--palmitic and stearic--were preferentially incorporated in liver and adipose tissues and less in the plasma. This accounts for lack of deposition in the arterial wall and for the antithrombotic tendency of palm oil. Thus, our present findings suggest that dietary palm oil may not contribute to the risk for coronary heart disease.

Animals↗
PubMed1996

Effect of estrogen replacement therapy on hepatic triglyceride lipase, lipoprotein lipase and lipids including apolipoprotein E in climacteric and elderly women.

Estrogen provides beneficial effects on hyperlipidemia in climacteric and elderly women. In this study of 68 women (37 to 67 years old), hepatic triglyceride lipase (HTGL), lipoprotein lipase (LpL) serum lipids and apolipoproteins were analyzed to investigate the effects of estrogen replacement therapy (ERT). After menopause, LpL, total cholesterol, low-density lipoprotein (LDL)-cholesterol, and apolipoprotein B increased. But ERT suppressed total cholesterol, LDL-cholesterol, apolipoprotein B, and especially apolipoprotein E in menopausal women. The mechanism was thought that ERT significantly suppressed HTGL, but LpL was not affected. Estrogen also increases hepatic LDL receptors and accelerates transfer of serum LDL-C (and TC). It was said that HTGL accelerates conversion of intermediate-density lipoprotein (IDL) to LDL. The suppression of HTGL by the ERT may decrease conversion of IDL to LDL and lower LDL-C (and TC). These estrogen's beneficial effects on lipids, may prevent the atherosclerosis. In addition, apolipoprotein E increases senile plaques in senile dementia-Alzheimer's type. The decrease in apolipoprotein E with ERT may be related to cognitive functions of elderly women.

Adult↗
PubMed1987

Lipoprotein lipases, lipoproteins and tissue lipids in rats fed fish oil or coconut oil.

The effect of fish oil and coconut oil on plasma lipoproteins and lipoprotein-catabolizing enzymes [lipoprotein lipase (LPL) and hepatic endothelial lipase (HL)] was studied in rats. Male rats were fed for 4 wk purified diets containing equienergetic, amounts of either coconut oil (group A), coconut oil:fish oil, 50:50 (group B) or fish oil (group C). Whole plasma triacylglycerol, cholesterol and phospholipid concentrations were appreciably lower in group C than in group A, mainly due to a fall in very low density lipoprotein (VLDL) and subgroup 2 of high density lipoprotein (HDL2), with less consistent changes in LDL and HDL3. VLDL components of group B were also considerably lower than corresponding ones in group A. LPL and HL activities were about 50% lower in groups B and C than in group A. Increased hepatic triacylglycerol and cholesterol concentrations were observed in groups B and C. It is suggested that the decrease in LPL and HL activity of fish oil-fed rats may be an adaptive response to the low concentration of the substrate (triacylglycerols) for these enzymes.

Animals↗
PubMed1998

Systemic administration of epidermal growth factor reduces fat mass in rats: effects on the hormone-sensitive-lipase, lipoprotein lipase and leptin.

We examined whether the reduction in fat mass induced by EGF treatment in mature animals was via activation of hormone-sensitive lipase (HSL) and thereby the induction of lipolysis, or through inhibition of lipoprotein lipase activity thus reducing fat uptake in adipose tissue. Sixteen male rats were treated with placebo or EGF 150 microg/kg/day for 7 days via mini-osmotic pumps. The results demonstrate that systemic EGF treatment reduces the amount of adipose tissue, most likely due to increased lipolysis as HSL activity as well as HSL mRNA were increased. The circulating levels of free fatty acids were slightly increased and leptin levels reflected the decrease in adipose tissue mass.

Adipose Tissue↗
PubMed1970

The effect of fasting on the utilization of chylomicron triglyceride fatty acids in relation to clearing factor lipase (lipoprotein lipase) releasable by heparin in the perfused rat heart.

Hearts from rats that have been starved for 10 or 24 hr oxidize (14)C-labeled chylomicron triglyceride fatty acids perfused through them at a higher rate than do hearts from rats in the fed state. Starvation for such periods increases the total clearing factor lipase activity of the heart. It is suggested that most of this increase may be accounted for by a rise in that portion of the total enzyme activity of the tissue that is released on perfusion with heparin. In rats starved for 48 hr, removal of this portion by heparin preperfusion reduces the capacity of the heart to oxidize (14)C-labeled chylomicron triglyceride fatty acids perfused subsequently by more than 80%. It is concluded that correlations between triglyceride fatty acid utilization and clearing factor lipase activity in the heart should be sought only with that portion of the total enzyme activity which is released from the intact organ by heparin.

Animals↗
PubMed1976

Effects of clofibrate treatment on plasma triglyceride concentration, plasma post-heparin clearing factor lipase (lipoprotein lipase) activity and serum clearing factor lipase activating ability in maturity-onset diabetes.

The effects of clofibrate on plasma triglyceride concentration, plasma post-heparin clearing factor lipase activity and serum clearing factor lipase activating ability were studied in a group of maturity-onset diabetic patients. Significant falls in both triglyceride concentration and in activating ability occurred within 2 weeks of beginning clofibrate treatment and, when treatment was stopped after 4 weeks, these changes were reversed within a further 4 weeks. Plasma post-heparin clearing factor lipase activity, on the other hand, was significantly increased during clofibrate administration and fell again when the treatment was stopped. The possible interrelationships of these findings are discussed.

Blood Proteins↗
PubMed1987

The effects of chemically modifying serum apolipoproteins on their ability to activate lipoprotein lipase.

Lipoprotein lipase activity was measured in an acetone-dried-powder preparation from rat epididymal adipose tissue using pig serum or pig serum lipoprotein, which had been chemically modified, as activator. Modification of acidic amino acids of lipoproteins with NN-dimethyl-1,3-diamine resulted in a complete loss of ability to activate lipoprotein lipase. Modification of 34% of lipoprotein arginine groups with cyclohexanedione resulted in the loss of 75% of the activation of lipoprotein lipase; approx. 42% of the original activity was recovered after reversal of the modification. This effect was dependent on the cyclohexanedione concentration. Modification of 48% of lipoprotein lysine groups with malonaldehyde decreased the maximum activation by 20%, but three times as much lipoprotein was required to achieve this. Non-enzymic glycosylation of lipoprotein with glucose, under a variety of conditions resulting in up to 28 nmol of glucose/mg of protein, had no effect upon the ability to activate lipoprotein lipase. In contrast non-enzymic sialylation resulted in a time-dependent loss of up to 60% of ability to activate lipoprotein lipase. Reductive methylation and acetoacetylation of serum did not affect the ability to activate lipoprotein lipase. The results are compared to the effects of similar modifications to low density lipoproteins on receptor-mediated endocytosis.

Amino Acids↗
PubMed1999

Sortilin/neurotensin receptor-3 binds and mediates degradation of lipoprotein lipase.

Lipoprotein lipase and the receptor-associated protein (RAP) bind to overlapping sites on the low density lipoprotein receptor-related protein/alpha2-macroglobulin receptor (LRP). We have investigated if lipoprotein lipase interacts with the RAP binding but structurally distinct receptor sortilin/neurotensin receptor-3. We show, by chemical cross-linking and surface plasmon resonance analysis, that soluble sortilin binds lipoprotein lipase with an affinity similar to that of LRP. The binding was inhibited by heparin and RAP and by the newly discovered sortilin ligand neurotensin. In 35S-labeled 3T3-L1 adipocytes treated with the cross-linker dithiobis(succinimidyl propionate), lipoprotein lipase-containing complexes were isolated by anti-sortilin antibodies. To elucidate function in cells, sortilin-negative Chinese hamster ovary cells were transfected with full-length sortilin and shown to express about 8% of the receptors on the cell surface. These cells degraded 125I-labeled lipoprotein lipase much faster than the wild-type cells. The degradation was inhibited by unlabeled lipoprotein lipase, indicating a saturable pathway, and by RAP and heparin. Moreover, inhibition by the weak base chloroquine suggested that degradation occurs in an acidic vesicle compartment. The results demonstrate that sortilin is a multifunctional receptor that binds lipoprotein lipase and, when expressed on the cell surface, mediates its endocytosis and degradation.

Adaptor Proteins, Vesicular Transport↗
PubMed1982

Effects of threonine-poor apolipoproteins on post-heparin plasma hepatic triacylglycerol lipase and lipoprotein lipase.

Whole-irradiated rabbit pre-heparin plasma had an important inhibitory effect on hepatic triacylglycerol lipase and lipoprotein lipase activities, whereas control rabbit pre-heparin plasma slightly inhibited hepatic triacylglycerol lipase activity at a high concentration and enhanced lipoprotein lipase activity. As some apolipoproteins were known to modulate these two lipolytic enzymes, the inhibitory effects of irradiated rabbit plasma were investigated in apolipoproteins. Three apolipoproteins, with isoelectric points of about 6.58, 6.44 and 6.12, characterized by their low content in threonine (threonine-poor apolipoproteins) were produced in high concentrations in rabbit VLDL and HDL after irradiation. The effects of these apolipoproteins on control rabbit post-heparin plasma hepatic triacylglycerol lipase and extrahepatic lipoprotein lipase were studied. Threonine-poor apolipoproteins substantially inhibited the hepatic triacylglycerol lipase activity and enhanced the apolipoprotein C-II-stimulated activity of lipoprotein lipase. The amounts of these apolipoproteins in triacylglycerol-rich lipoprotein particles may determine the lipolytic activity of lipoprotein lipase and hepatic triacylglycerol lipase in triacylglycerol hydrolysis. The existence of another inhibitor of lipoprotein lipase remains to be determined.

Amino Acids↗