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)

Rabbit very low density lipoproteins (VLDL) have been fractionated by heparin sepharose chromatography into two subpopulations: an unretained fraction (UR) and a retained fraction (R). The separation profiles of VLDL from cyclophosphamide treated rabbits differed from those obtained in normal animals: UR fraction was far more important in treated rabbits than in control animals. Comparative studies of the two VLDL subfractions isolated from treated rabbits have been performed. Polyacrylamide gel electrophoresis in presence of urea showed a similar distribution in both fractions of apolipoproteins X, a group of low molecular weight apolipoproteins detected after antimitotic therapy. SDS - polyacrylamide electrophoresis revealed the presence of one form of apolipoprotein B: apo B100 in the VLDL from treated rabbits giving evidence of their hepatic origin. Relative to the R-fraction, the UR-fraction was characterized by an increased triacylglycerol content and a larger diameter as observed by electron microscopy. In vitro incubations with lipoprotein lipase and reisolation of postlipolysis particles suggest that both VLDL fractions can undergo metabolic conversion to LDL. A decrease of lipoprotein lipase activity after treatment, as previously observed, may thus explain the accumulation of the large VLDL.
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PMID:Accumulation of large VLDL in cyclophosphamide treated rabbits. Relationship with lipoprotein lipase deficiency. 340 Dec 26

Apolipoproteins play major roles in regulating lipoprotein synthesis and catabolism. Apolipoprotein AI activates the lecithin cholesterol acyltransferase, apolipoprotein CII and CIII regulate the lipoprotein lipase, and apolipoprotein B-100, B-48, and E control the cholesterol uptake into hepatic and extrahepatic cells. Therefore, investigating the alterations of lipoprotein metabolism in disease states at the apolipoprotein level may give increased insight into the underlying mechanisms of lipoprotein changes and provide better understanding about the premature development of the atherogenic process.
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PMID:Lipoproteins and apolipoproteins. Composition, metabolism, and association with coronary heart disease. 352 5

To evaluate mechanisms of diabetes-induced changes in very-low-density lipoprotein (VLDL), VLDL triglyceride (TG) and VLDL apolipoprotein B (apoB) metabolism were studied in 12 obese Pima Indian control subjects and in 15 Pima Indian obese non-insulin-dependent diabetics. Eleven of the diabetics were restudied after reduction of hyperglycemia with oral sulfonylurea therapy. In addition, adipose, muscle, and postheparin lipoprotein lipase and postheparin hepatic lipase activities were measured in all subjects. Obese diabetics as compared with obese controls showed a trend toward increased production of VLDL TG (46 +/- 4 vs. 35 +/- 6 g/day, P = .10) but not of VLDL apoB (1595 +/- 106 vs. 1597 +/- 164 mg/day, NS); production of VLDL TG declined to control levels (33 +/- 4 g/day, P less than .05) during therapy, whereas there was no change in production of VLDL apoB. Diabetics had a clearance defect for VLDL, indicated by significantly lower fractional catabolic rates for both VLDL TG (10.6 +/- .9 vs. 13.1 +/- .9 pools/day, P less than .05) and VLDL apoB (5.6 +/- .4 vs. 7.5 +/- 0.7, P less than .05) as compared with controls; fractional catabolic rates increased after therapy (to 13.3 +/- 1.5, P less than .05, and 6.7 +/- .4, P less than .05, respectively). In the diabetics, this decrease in clearance was accompanied by a lower adipose lipoprotein lipase (.30 +/- .09 vs. .92 +/- .25 mumol X g-1 X h-1, P less than .01), which increased during therapy (to .61 +/- .17, P less than .05). Hepatic lipase also decreased significantly after therapy (27.4 +/- 3.6 to 26.4 +/- 3.2, P less than .01). Composition of VLDL in diabetics was also abnormal, indicated by a higher TG/apoB ratio (14.7 +/- .6 vs. 11.7 +/- .8, P less than .01); this ratio fell during therapy (to 12.5 +/- .8, P less than .05). The data indicate there are multiple abnormalities in structure and metabolism of VLDL in non-insulin-dependent diabetics. Control of hyperglycemia with sulfonylureas has the capability of reversing some of these abnormalities.
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PMID:Effects of NIDDM on very-low-density lipoprotein triglyceride and apolipoprotein B metabolism. Studies before and after sulfonylurea therapy. 353 Aug 55

Plasma lipoprotein concentrations and post-heparin lipoprotein lipase, hepatic triglyceride lipase (HTGL), and lecithin:cholesterol acyltransferase (LCAT) activities were determined in 10 obese women before and after weight loss. In period I, a diet was given to maintain constant weight for 3 weeks. In period II, total calories were restricted to 600 kilocalories/day for 3 weeks. In period III, caloric intake was adjusted to maintain weight at the lower level for 6 weeks. The lower calorie diet decreased plasma very low density, low density, and high density lipoprotein (HDL), cholesterol, and apolipoprotein B and A-I concentrations and molar enzyme activities, while the percent conversion of free to esterified cholesterol by the LCAT enzyme was unchanged. During weight stabilization at a lower state (period III), the mean plasma HDL cholesterol level increased, and lipoprotein lipase and LCAT activities increased to values higher than those in period I. The mean HTGL activity remained reduced. I conclude that successful weight loss improves the possibly atherogenic plasma lipoprotein profile of obese subjects. The increase in HDL cholesterol and cholesterol esterification, possibly explained by lowered HTGL enzyme activity, may increase the capacity of HDL to transport cholesterol from peripheral cells to the liver.
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PMID:Plasma lipoproteins and lipase and lecithin:cholesterol acyltransferase activities in obese subjects before and after weight reduction. 366 89

Several parameters of lipoprotein metabolism were examined in 38 men with primary hypertriglyceridemia (phenotype IV). Family investigation showed that 17 men had familial combined hyperlipidemia (FCH), seven had familial hypertriglyceridemia (FHT), and 14 had unclassified hypertriglyceridemia (UNC). In all three groups, plasma high density lipoprotein (HDL) cholesterol and the concentrations of apolipoprotein A-I and A-II were decreased, and apolipoprotein B was increased, each to the same extent. These results are compatible with an increased risk of cardiovascular disease in both FCH and FHT patients. The mean concentration of LDL cholesterol and the ratio of LDL to HDL cholesterol were significantly higher in FCH subjects, which could explain their increased risk. Postheparin lipoprotein lipase and hepatic lipase were the same in both groups. Determination of apolipoprotein C composition, which may modulate lipoprotein lipase activity, did not reveal any abnormalities in the different groups. In both FCH and FHT, the mean turnover rate of plasma triglycerides was almost twice normal, indicating that overproduction of plasma triglyceride plays an important role in both disorders. However, there was an overlap with normal controls, indicating impaired triglyceride removal in some subjects. The underlying mechanism of hypertriglyceridemia in FCH and FHT therefore seems to be heterogeneous.
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PMID:Plasma lipoproteins, apolipoproteins, and triglyceride metabolism in familial hypertriglyceridemia. 372 96

This study was designed to investigate the response of Type III hyperlipoproteinemic subjects to bezafibrate therapy. The metabolism of apolipoprotein B was examined in four lipoprotein subclasses of Sf 60-400 (large very low density lipoprotein (VLDL)), Sf 20-60 (small VLDL), Sf 12-20 (intermediate density lipoprotein (IDL)), and Sf 0-12 (low density lipoprotein (LDL)) before and during bezafibrate therapy. Treatment reduced the plasma concentration of VLDL and raised high density lipoprotein (HDL) cholesterol. There was no net change in LDL cholesterol or its associated apolipoprotein B. The decrease in plasma VLDL derived mainly from an inhibition of synthesis of both large and small subfractions which reduced the number of particles in the circulation without normalizing their lipid composition. Catabolism of the larger VLDL also increased, presumably as a result of lipoprotein lipase activation. Although the plasma concentration of LDL was unchanged, both its synthesis and catabolism were perturbed. Its fractional catabolic rate fell by 50%, but the impact that this would have had on its steady state level in the circulation was apparently blunted by a decrease in its synthesis from Sf 12-20 IDL. In the control phase of the study, most IDL apolipoprotein B was converted to LDL. Bezafibrate therapy channelled this material towards direct catabolism.
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PMID:Effects of bezafibrate on apolipoprotein B metabolism in type III hyperlipoproteinemic subjects. 378 47

Serum lipoprotein metabolism was studied in 7 women before and after treatment for thyrotoxicosis. Of the lipoprotein lipids, the triglyceride concentration in the low density lipoproteins (LDL) (P less than 0.01) and the cholesterol concentration in both LDL (P less than 0.01) and the high density lipoproteins (HDL) (P less than 0.05) increased significantly during treatment. These changes were accompanied by increases in apolipoprotein B (P less than 0.01) and A-I (P less than 0.05) concentrations in serum. Muscle lipoprotein lipase activity (LPLA) was increased in the thyrotoxic state by 46% (P less than 0.05) compared with the value after the patients had been rendered euthyroid, but adipose tissue LPLA was only 8% higher (ns) in the former state. The capacity for removal of exogenous fat, as determined by the fractional elimination rate (K2) at an iv fat tolerance test, was 23% higher in the thyrotoxic than in the euthyroid state (ns). It is suggested that the increase in muscle LPLA in the thyrotoxic state may be due to enhanced sensitivity to catecholamines. This may contribute to the increased capacity for plasma triglyceride turnover in thyrotoxicosis.
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PMID:High muscle lipoprotein lipase activity in thyrotoxic patients. 383 38

Lipoprotein lipase is the rate-limiting factor for hydrolyzing triglycerides to glycerol and fatty acids. Carnitine is a cofactor in the transport of long-chain fatty acids through the mitochondrial membrane for oxidation. To assess these determinants of fat utilization during total parenteral nutrition, lipoprotein and hepatic lipase activities and carnitine concentrations of nine newborn infants, operated on because of gastrointestinal anomalies during the first day of life, were measured with specific methods. Total parenteral nutrition was built up in 3 days whereafter the infants received 3 g/kg of fat at a constant rate of infusion for 24 h/day. Lipoprotein lipase activity of post-heparin plasma increased from 14 to 35 mumol free fatty acids/ml/h during parenteral nutrition whereas hepatic lipase activity remained unchanged at 40 mumol free fatty acids/ml/h. Serum free carnitine and acylcarnitine levels decreased significantly during parenteral nutrition; urinary excretion of carnitine decreased also. In addition, serum cholesterol and phospholipids increased markedly during parenteral nutrition whereas serum triglycerides, free fatty acids, and blood beta-hydroxybutyrate remained unchanged. Serum apolipoprotein A-I concentrations were unaltered, apolipoprotein A-II underwent a transient increase, and apolipoprotein B increased monotonically during parenteral nutrition. The results suggest that under the present circumstances neither lipoprotein lipase activity nor carnitine resources are rate-limiting for the utilization of fat in newborn infants during total parenteral nutrition.
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PMID:Postheparin plasma lipases and carnitine in infants during parenteral nutrition. 392 Jun 39

Previous work has shown that nascent hepatic very-low-density lipoproteins (VLDL) in the rat are biosynthesized without the obligatory co-factor (apolipoprotein C-II) for lipoprotein lipase-mediated hydrolysis of their core triacylglycerols. Upon secretion, apolipoproteins C-II and C-III are rapidly transferred to the particles from high-density lipoprotein (HDL) within the space of Disse and upon the entry into the plasma. Here we extend those studies to include observations on the apolipoprotein E content and lipid composition of nascent hepatic VLDL before and after exposure to plasma components. We have elected to use hepatic secretory vesicle VLDL rather than liver perfusate VLDL as truly representative of the nascent lipoproteins. Nascent VLDL from fed rats has an apolipoprotein B/E ratio of 6.6 +/- 0.5, whereas that from fasted animals is 13.9 +/- 2.3. Incubation of nascent VLDL from fed and fasted rats with d greater than 1.063 g/ml rat serum, HDL or the d greater than 1.21 g/ml fraction resulted in a mass transfer of apolipoprotein E to the VLDL such that the apolipoprotein B/E ratio decreased to at least that of serum VLDL (3.4 +/- 0.3). The d greater than 1.21 g/ml fraction appeared to contain a species of apolipoprotein E which most actively transferred to VLDL. The acquisition of apolipoprotein E by nascent secretory vesicle VLDL was attended by a loss of phospholipids, particularly the C40 (stearoylarachidonyl) molecular species, and an increase in the cholesterol-to-phospholipid ratio from 0.11 +/- 0.01 to 0.18 +/- 0.03. No evidence was obtained to suggest a simultaneous acquisition of cholesteryl esters upon incubation of nascent VLDL with VLDL-free serum. We conclude that nascent hepatic VLDL is modified after secretion by acquisition of apolipoproteins C-II, C-III and E with a concomitant loss of phospholipids.
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PMID:Post-secretory acquisition of apolipoprotein E by nascent rat hepatic very-low-density lipoproteins in the absence of cholesteryl ester transfer. 394 May 34

Twenty-five obese women were put on low-calorie diet for one month. The mean weight loss was 2.7 kg and was accompanied by a 9% decrease of LDL-cholesterol. LDL-apolipoprotein B (in 13 subjects) showed a 16% fall and LDL-triglyceride levels did not change. The results suggest both a decrease of LDL concentration and a relative increase of triglyceride-rich particles in the density range of 1.006-1.063. HDL2-cholesterol showed a 17% decrease and HDL3-cholesterol a 16% increase. Total and lipoprotein triglycerides were not modified. The changes of lipoprotein pattern suggest a sluggish VLDL catabolism by lipoprotein lipase. In 10 women followed for 6 months the decrease of LDL-cholesterol seen after one month of diet was no more present at the 6th month, while the decrease of HDL2-cholesterol and the increase of HDL3-cholesterol were still evident. At the end of the 6th month a slight but significant decrease of total and VLDL-triglycerides also occurred.
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PMID:Serum lipoprotein subfractions before and during low-calorie diet in obese women. 408 20


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