Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.1.1.34 (lipoprotein lipase)
7,025 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The role of genetic and environmental factors in the regulation of plasma high density lipoprotein (HDL) was estimated in 17 monozygotic (MZ) and 18 dizygotic (DZ) male twins randomly selected from the Finnish Twin Cohort Study. In addition to HDL cholesterol, we determined the HDL subfractions, HDL2 and HDL3, and the major HDL apoproteins (apo) A-I and A-II. The activities of lipoprotein lipase (LPL) and hepatic lipase (HL) were also assayed from postheparin plasma to get information on their possible contribution to the heritability of HDL. Evidence for the genetic component in the regulation of plasma HDL received support from the heritability estimate of 0.34. The different heritability estimates of HDL2 and HDL3 (h2 of 0.56 and less than 0, respectively) support the idea that the HDL subfraction distribution might be important in the genetic regulation of plasma HDL level. This also received support from the heritability of apo A-I (h2 = 0.66), mainly varying in HDL2, and the lack of it in apo A-II, found mainly in HDL3. These conclusions were strengthened by standardizing the data with relative ponderosity. Postheparin plasma HL activity had a high pairwise correlation coefficient in the MZ twins (r = 0.80, p less than 0.001), whereas LPL displayed no within-pair correlation. Neither of the lipolytic enzymes, LPL or HL, showed any correlation in the DZ twins. Therefore, it is suggested that part of the genetic regulation of the HDL and its subfraction distribution might be mediated through the activity of HL.
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PMID:Inheritance of high density lipoprotein and lipoprotein lipase and hepatic lipase activity. 311 55

In order to investigate the in vivo function of hepatic lipase, cats were injected with anti-cat hepatic lipase antibodies which produced a complete and specific inhibition of heparin-releasable hepatic lipase. The cat was chosen as an animal model because it displays, like man, a relative deficiency of lipoprotein lipase compared to hepatic lipase and because the possession of two subfractions of high density lipoproteins, HDL2 and HDL3. In fasted cats no changes were observed in plasma triglycerides or phospholipids. In fed animals triglycerides increased considerably, indicating that hepatic lipase may have a function in the postprandial phase. In fat-loaded cats (6 g of fat/kg) triglycerides in the d less than 1.019 g/ml fraction increased from 4 h after the blockade due to accumulation of lipoproteins with pre-beta-mobility containing the apoproteins, apo B-100, apo E and apo A-I. Apo B-48 did not accumulate consistently. Phospholipids in the HDL2-fraction and those in the HDL3-fraction of the fat-loaded cats tended to increase and decrease from 6 and 9 h after the blockade, respectively. The absolute change in HDL2 phospholipids approximated that of HDL3-phospholipids. Overall, the density of HDL particles decreased, apparently secondary to the accumulation of apo A-I in the d less than 1.019 g/ml fraction. Our findings suggest that hepatic lipase is involved in the hydrolysis of a special class of apo A-I containing triglyceride-rich lipoproteins synthesised in the postprandial phase.
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PMID:Studies on the function of hepatic lipase in the cat after immunological blockade of the enzyme in vivo. 312 48

With the advent of nocturnal intragastric feeding which protects against acute metabolic complications and promotes growth, patients with glycogen storage disease type I are attracting less attention. However, several biochemical alterations persist and suggest that the long-term risk of atherosclerotic heart disease remains high. Persisting hypertriglyceridemia and hypercholesterolemia were found in seven glycogen storage disease type I subjects, six of them following 5-6 yr of nocturnal intragastric feeding. When compared to ten age-matched controls, the patients showed significantly (P less than 0.001) higher low density lipoprotein cholesterol (LDL-C) (247.7 +/- 46.8 vs. 115.3 +/- 5.0 mg/dl) and lower high density lipoprotein cholesterol (HDL-C) (26.4 +/- 3.4 vs. 55.8 +/- 2.9 mg/dl). Triglyceride (TG) enrichment with cholesteryl ester depletion characterized the lipoprotein classes. The diameters of very low density lipoproteins (VLDL) and LDL were larger, while that of HDL was smaller and consistent with the predominance of the HDL3 subclass and a lower apoA-I/apoA-II ratio. The raised levels of TG appeared attributable not only to the well-described lipogenesis, but also to impaired catabolism of fat, as evidenced by the significantly (P less than 0.001) decreased activity of both peripheral lipoprotein lipase (3.17 +/- 0.43 vs. 14.15 +/- 0.50 mumol FFA.ml-1.hr-1) and hepatic lipase (1.88 +/- 0.30 vs. 4.83 +/- 0.90). This may well explain the high concentration of intermediate density lipoprotein (IDL) and the impaired conversion of HDL3 to HDL2. Low apoC-II/apoC-III1 could be related to defective lipoprotein lipase activity. These data suggest that glycogen storage disease type I patients on nocturnal intragastric feeding remain at risk for atherosclerosis and its complications.
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PMID:Circulating lipids and lipoproteins in glycogen storage disease type I with nocturnal intragastric feeding. 313 Apr 54

Serum lipid and lipoprotein levels, apolipoproteins A-I and B, and lipolytic enzyme activities were studied in 14 young male cyclists and in 21 age-matched sedentary controls. While there were no significant differences in serum cholesterol between the two groups, the cyclists showed a significant decrease in serum triglycerides (P less than 0.05) and LDL cholesterol (P less than 0.05) and had significantly higher levels of HDL cholesterol (P less than 0.01) and HDL2 cholesterol (P less than 0.001). Significantly lower serum cholesterol/HDL cholesterol (P less than 0.001) and LDL cholesterol/HDL cholesterol (P less than 0.001) ratios and a significantly higher HDL2 cholesterol/HDL3 cholesterol ratio (P less than 0.001) were observed in the athletes. Serum apolipoprotein B was lower and the Apo B/Apo A-I ratio significantly reduced in the athletes. No significant differences emerged between the two groups in plasma post-heparin lipoprotein lipase activity (LPL) and in hepatic triglyceride lipase activity (HTGL), and there were no correlations between HDL cholesterol and lipolytic enzyme activities. In conclusion, this cross-sectional study may indicate that an aerobic training program such as cycling is associated with an advantageous lipoprotein pattern; some factors other than lipolytic activity may contribute to increase the HDL cholesterol levels in physical training.
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PMID:Heparin-released plasma lipase activities, lipoprotein and apoprotein levels in young adult cyclists and sedentary men. 314 6

Lipids are transported in the blood in four major classes of lipoproteins. The triacylglycerol-rich lipoproteins are chylomicrons and very-low-density lipoproteins (VLDL) which are produced by the small intestine and liver, respectively. These lipoproteins mainly carry fatty acids to adipose tissue and muscle where the triacylglycerol is hydrolysed by lipoprotein lipase. The resulting particles that remain in the blood are chylomicron remnants and low-density lipoprotein (LDL), respectively. The remnant is taken up by the liver via endocytosis which is mediated by a specific receptor for apolipoprotein E (apoE). LDL, which are rich in cholesterol, can also be taken up by the liver or extrahepatic tissues by a receptor-mediated endocytosis that specifically recognises apoB or apoE. 'Nascent' high-density lipoprotein (HDL) particles are secreted by the liver and intestine and then undergo modification to become HDL3 and then HDL2 as they acquire cholesterol ester. They facilitate the reverse transport of cholesterol back to the liver. Little is known of the hormonal regulation of lipoprotein uptake by the liver. Recently, we have shown that insulin and tri-iodothyronine (T3) increase the specific binding of LDL to cultured hepatocytes whereas dexamethasone (a synthetic glucocorticoid) has the opposite effect. The changes in binding produced by insulin and dexamethasone are paralleled by alterations in the rate of degradation of apoB. These findings may in part explain the hypercholesterolaemia and increased risk of premature atherosclerosis that can be associated with poorly controlled diabetes or hypothyroidism.
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PMID:The biochemistry of lipoproteins. 314 85

The effect of high dose medroxyprogesterone acetate (MPA) on serum lipids, on adipose tissue lipoprotein lipase (LPL) and serum lecithin cholesterol acyltransferase activities were studied in 15 postmenopausal patients with endometrial cancer. After 2 weeks of MPA treatment total cholesterol decreased by 14% (P less than 0.001) and HDL cholesterol by 33% (P less than 0.01) from the respective pretreatment values; correspondingly the ratio of HDL to total cholesterol decreased (P less than 0.05). The decrease of HDL2 cholesterol was 35% (P less than 0.01) and that of HDL3 cholesterol 15% (P less than 0.01). The levels of serum triglycerides decreased significantly (P less than 0.05) during the treatment period. Serum LCAT activity was significantly lower (P less than 0.05) after treatment than before, but adipose tissue LPL activity was not altered. The mean serum testosterone level decreased significantly (P less than 0.001) from the pretreatment values. Significant positive correlations were present between LPL activity and MPA concentrations and between LPL activity and testosterone concentrations after the drug treatment.
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PMID:Effects of high dose progestin on serum lipids and lipid metabolizing enzymes in patients with endometrial cancer. 315 2

Plasma lipids, apoprotein A-I and B in serum and in lipoprotein fractions (VLDL + LDL, HDL2, and HDL3) obtained by preparative ultracentrifugation, as well as postheparin lipoprotein lipase activity (H-TGL and LPL) were evaluated in 17 subjects with primary biliary cirrhosis (stage II and III) subdivided into two groups according to the presence or absence of lipoprotein X (Lp-X). A reduction in total lipoprotein lipase activity was observed in both patient groups, compared to controls (P less than 0.01); the hepatic lipoprotein lipase was significantly reduced (P less than 0.01) only in the Lp-X-positive group. The lipid (477.8 +/- 154.3 vs 239.6 +/- 51.1; P less than 0.01) and protein (147.4 +/- 37.1 vs 83.3 +/- 19.7; P less than 0.01) masses in the VLDL + LDL fraction of the Lp-X-positive group were increased compared to controls. In the same group, the HDL2 fraction also showed an increase in lipid (186.6 +/- 80.0 vs 77.9 +/- 21.6; P less than 0.01) and protein (133.9 +/- 60.0 vs 67.9 +/- 16.5; P less than 0.01) masses; in addition, the HDL2 percent lipid composition was different in the two patient groups, showing a decrease in esterified cholesterol (20.4 +/- 3.6 vs 25.7 +/- 2.2; P less than 0.01) and an increase in phospholipids (59.2 +/- 2.9 vs 54.8 +/- 2.6; p less than 0.01) in the Lp-X-positive group.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Lipoprotein pattern and plasma lipoprotein lipase activities in patients with primary biliary cirrhosis. Relationship with increase of HDL2 fraction in Lp-X-positive and Lp-X-negative subjects. 316 90

To study the effects of rigorous insulin therapy on serum lipoproteins in patients with noninsulin-dependent diabetes not controlled with oral agents only, we measured serum lipoproteins, apoproteins, lipolytic enzymes, and glucose disposal using an insulin clamp technique before and after 4 weeks of insulin therapy. Lipoproteins were isolated by ultracentrifugation and high density lipoprotein (HDL) subfractions, by rate-zonal density gradient ultracentrifugation. The group included 11 women and eight men (age 58 +/- 1 years and RBW 125 +/- 4%). Body weight, glycosylated hemoglobin, mean diurnal glucose, plasma free insulin, and glucose uptake (M-value) were 75 vs. 76 kg; 11.9 vs. 8.9%; 234 vs. 124 mg/dl; 12 vs. 27 microU/ml; and 5.0 +/- 0.4 vs. 7.1 +/- 0.6 mg/kg/min before and after insulin therapy, respectively. After insulin therapy there was a decrease of very low density lipoprotein (VLDL) triglyceride (-60%, p less than 0.001) but an increase of HDL2 cholesterol (+21%, p less than 0.001); HDL2 phospholipids (+38%, p less than 0.001); HDL2 proteins (+23%, p less than 0.01); and HDL2 mass (127 +/- 11 vs. 158 +/- 12 mg/dl, p less than 0.001). There was a decrease of HDL3 cholesterol (-13%, p less than 0.05); HDL3 phospholipids (-16%, p less than 0.05); HDL3 proteins (-18%, p less than 0.001); and HDL3 mass (179 +/- 6 vs. 146 +/- 6, p less than 0.01). Zonal profiles showed a redistribution of particles from HDL3 to HDL2. Serum apo A-I increased (p less than 0.05), apo A-II remained constant, but apo B decreased (-29%, p less than 0.001). The most marked change during insulin therapy was a 2.3-fold increase in adipose tissue lipoprotein lipase (LPL) activity (p less than 0.001). The changes of VLDL and HDL subfractions were not explained by respective changes of the blood glucose, free insulin, or M-value. The data indicate that intensive insulin therapy induces antiatherogenic changes in serum lipids and lipoproteins and suggest that the induction of LPL by insulin is the major factor responsible for redistribution of HDL particles from HDL3 to HDL2.
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PMID:Insulin therapy induces antiatherogenic changes of serum lipoproteins in noninsulin-dependent diabetes. 327 41

Two separate studies were carried out with acipimox, a new antilipolytic agent with long-lasting activity. First, in a randomized, double-blind, cross-over study a dose of 750 mg/day of acipimox versus placebo was employed for 60 days in 11 patients with type IV hyperlipoproteinemia. Mean plasma triglyceride levels were reduced after acipimox compared to placebo (434 +/- 60 vs 777 +/- 224 mg/dl, P less than 0.01). Serum total cholesterol fell also significantly after acipimox compared to placebo. No significant alteration was observed in the HDL2/HDL3 ratio or in the concentration or composition of the HDL subfractions. Six patients with severe hypertriglyceridemia (2 type IV and 4 type V) and low lipoprotein lipase (LPL) activity took part in a second, open study, lasting for 9 months. Acipimox was given at a dose of 750 mg/day for the first 6 months and 1200 mg/day for the last period. The response of serum total and VLDL triglycerides was inconsistent. HDL cholesterol was significantly raised (+33.3%) after 9 months of treatment due to changes of HDL2 and HDL3 cholesterol, phospholipid and protein concentrations. LPL activity was markedly reduced in adipose tissue at 9 months. No significant changes occurred in postheparin plasma LPL activity. In contrast, hepatic lipase activity showed a reduction of about 25% from 6 months of treatment onwards.
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PMID:Effects of acipimox on serum lipids, lipoproteins and lipolytic enzymes in hypertriglyceridemia. 327 68

Insulin is essential to the physiological regulation of high density lipoprotein (HDL) cholesterol metabolism. It acts directly at the hepatic level by favouring HDL2 to HDL3 conversion (by its action on hepatic lipase). In the peripheral circulation, it induces HDL2 formation by allowing triglyceride-rich lipoprotein catabolism by lipoprotein lipase (LPL) and free cholesterol esterification by lecithin acyl cholesterol transferase (LCAT). In the case of insulin deficiency or peripheral insulin resistance, there is a reduction of HDL cholesterol related to HDL2 decrease, partly due to LPL deficiency. In the case of endogenous hyperinsulinism, there is an intrahepatic disturbance of HDL metabolism partly related to excessive synthesis of VLDL-TG and leading to the decrease of HDL2/HDL3 and enhanced formation of HDL2 TG. When hepatic hyperinsulinism is associated with peripheral insulin resistance, HDL cholesterol decrease is the consequence of both intrahepatic action of insulin and diminution of its peripheric action. Optimized insulin therapy can normalize HDL cholesterol in case of true insulin deficiency. When there is preservation of insulin secretion, HDL cholesterol remains lower than controls. Insulinopenia as well as hyperinsulinism can favour atherogenic lipoprotein disturbances.
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PMID:Insulin and HDL-cholesterol metabolism. 330 70


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