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)

Estramustine phosphate (Estracyt), a combination of estradiol and nitrogen mustard given to males with prostatic carcinoma, had the same effect on serum lipids, lipoproteins, and serum phosphoglyceride fatty acid composition as ethynyl estradiol (Etivex). The characteristic effects on serum lipids caused by both drugs, i.e., a reduction in serum cholesterol and an increase in serum phospholipids, were apparently expressions for reduced low density lipoproteins and increased alpha-lipoproteins. Serum lecithin fatty acid composition revealed during the administration of both drugs a characteristic increase in palmitic acid (16:0) and a decrease in stearic acid (18:0), interpreted as evidence for a cholestatic, although subclinical, liver involvement. Similar changes have earlier been revealed in women given ethynyl estradiol; however, the increase in serum triglycerides and very low density lipoprotein cholesterol in young women was not duplicated in aged males with prostatic carcinoma. Furthermore, in aged males, the administration of these estrogens did not change carbohydrate metabolism but did produce an increase in adipose tissue lipoprotein lipase.
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PMID:Treatment of oral estramustine phosphate (Estracyt) in prostatic carcinoma: influences on lipid and carbohydrate metabolism. 59 Dec 68

Fatty acid incorporation into adipose tissue (FIAT), the metabolic process assimilating plasma triglyceride fatty acids liberated by lipoprotein lipase, was recently found to be lower in hyper- than in normotriglyceridaemia. In the present report, the relation of FIAT to glucose tolerance and adipose tissue morphology and fatty acid composition has been studied in a popoulation of men with normo- and hypertriglyceridaemia, using needle biopsy specimens. In addition, the associations between plasma triglyceride concentration and these factors as well as FIAT were examined by statistical methods. FIAT and GLIAT (glucose incorporation into adipose tissue) activities per cell were positively correlated with fat cell diameter but not with fat cell number. FIAT activities per cell and per unit surface area were lower in hyper- than in normo-triglyceridaemic subjects. The k-value of the i.v.glucose tolerance test and glycerol release from adipose tissue did not correlate with FIAT or GLIAT activities. The proportion of stearic acid in adipose tissue was negatively correlated with the serum triglyceride level and with fat cell diameter, but positively correlated with FIAT. Linolenic acid in adipose tissue correlated positively with the k-value. The negative correlation between serum triglycerides and FIAT remained when the other variables which were significantly correlated with FIAT or the serum triglycerides were entered in partial correlat-on analysis. These results suggest that although low FIAT activity is related in part to other characteristics, it occurs in hypertriglyceridaemia independent of glucose tolerance or various characteristics in fat. With serum triglyceride concentration as dependent variable, stepwise regression analysis was performed, entering all other variables as independent ones. The highest multiple --value was 0.76 (p less than 0.001) and it was obtained with three adipose tissue parameters: FIAT (or GLIAT), content of linolenic acid and of stearic acid. The other parameters did not give rise to any further improvement in the prediction of the serum triglyceride concentration which is better than 50% (R2 = 0.57).
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PMID:Serum triglycerides and fatty acid incorporation into human adipose tissue (TIAT). Their relations with adipose tissue characteristics and glucose tolerance. 98 13

In cultured dorsal root ganglion (DRG) neurons prelabeled with [3H]arachidonic acid [( 3H]AA), bradykinin (BK) stimulation resulted in increased levels of radioactive diacylglycerol, monoacylglycerol, and free AA. The transient increases in content of radioactive diacylglycerol and monoacylglycerol preceded the increase in level of free AA, suggesting the contribution of a diacylglycerol lipase pathway to AA release. An analysis of the molecular species of diacylglycerols in unstimulated cultures revealed the presence of two primary [3H]AA-containing species, 1-palmitoyl-2-arachidonoyl and 1-stearoyl-2-arachidonoyl diacylglycerol. BK stimulation resulted in a preferential increase in content of 1-stearoyl-2-arachidonoyl diacylglycerol. When DRG cultures were labeled with [3H]stearic acid, treatment with BK increased the amount of label in diacylglycerol and free stearic acid, but not in monoacylglycerol. This result suggested that AA release occurred through the successive actions of an sn-1 diacylglycerol lipase and monoacylglycerol lipase. Other data supporting a diacylglycerol lipase pathway was the significant inhibition of [3H]AA release and consequent accumulation of diacylglycerol by RG 80267, which preferentially inhibits diacylglycerol lipase. Analysis of the molecular species profiles of individual phospholipids in DRG neurons indicated that phosphoinositide hydrolysis may account for a significant portion of the rapid increase in content of 1-stearoyl-2-arachidonoyl diacylglycerol. We were unable to obtain evidence that the phospholipase A2 pathway makes a significant contribution to BK-stimulated AA release in DRG cultures. Under our assay conditions there were no BK-stimulated increases in levels of radioactive lysophosphatidylinositol, lysophosphatidylcholine, or lysophosphatidylethanolamine in cultures prelabeled with [3H]inositol, [3H]choline, or [3H]-ethanolamine, respectively.
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PMID:Bradykinin stimulates arachidonic acid release through the sequential actions of an sn-1 diacylglycerol lipase and a monoacylglycerol lipase. 173 88

Lipid emulsions were prepared with compositions similar to the triacylglycerol-rich plasma lipoproteins, but also incorporating added small amounts of monoacylglycerols. Control emulsions without monoacylglycerol were metabolized similarly to natural chylomicrons or very-low-density lipoproteins when injected intravenously in rats. The emulsion triacylglycerols and cholesteryl esters were both removed rapidly from the bloodstream, with the removal rates of triacylglycerols faster than those of cholesteryl esters. Much of the removed cholesteryl ester was found in the liver, but only a small fraction of the triacylglycerol, consistent with hepatic uptake of the triacylglycerol-depleted remnants of the injected emulsion. Emulsions incorporating added monooleoylglycerol or stearic acid were metabolized similarly. Added 1- or 2-monostearoylglycerol had no effect on triacylglycerol removal from plasma, but the removal rate of cholesteryl esters was decreased and less cholesteryl ester was found in the liver. These effects are similar to those recently described when emulsions and chylomicrons contained triacylglycerols with a saturated acyl chain at the glycerol 2-position, suggesting that saturated monoacylglycerol produced by the action of lipoprotein lipase may cause triacylglycerol-depleted remnant particles to remain in the plasma instead of being rapidly taken up by the liver.
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PMID:The effect of added monoacylglycerols on the removal from plasma of chylomicron-like emulsions injected intravenously in rats. 271 86

It has been postulated that the diacylglycerol lipase pathway is a predominant source of the free arachidonic acid which is released from phospholipids upon the exposure of human platelets to thrombin. The amount of released arachidonic acid and other fatty acids in thrombin-stimulated platelets was determined in the presence of BW755C, the cyclooxygenase/lipoxygenase inhibitor, and in relation to phosphatidylinositol degradation and phosphatidic acid formation. A stearic acid:arachidonic acid molar ratio approaching unity would be expected in the free fatty acid fraction if the latter pathway were a major source of released arachidonic acid. Our results indicate that the diacylglycerol lipase pathway contributes a maximum of 3-4 nmol of arachidonic acid/2 X 10(9) platelets or 12-15% of the total arachidonic acid released (25.8 nmol/2 X 10(9) platelets) upon exposure to thrombin (2 units/ml) for 4 min. Trifluoperazine inhibited most of the thrombin-dependent free arachidonic acid release but only 15% of the absolute loss of arachidonic acid from phosphatidylinositol. Therefore, we conclude that the diacylglycerol lipase pathway represents only a minor source of the free arachidonic acid that is released upon thrombin stimulation of human platelets.
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PMID:Diacylglycerol lipase pathway is a minor source of released arachidonic acid in thrombin-stimulated human platelets. 308 Oct 1

A systematic study was undertaken to observe the effects of dietary (dioleoyl) triacyl-sn-glycerol structure on chylomicron composition and metabolism. First studied was a series of 1,2-dioleoyl-3-(saturated)acyl-sn-glycerols, where the fatty acid esterified at the 3-position was varied from 14 to 24 carbons. Next a series of 1,3-dioleoyl-2-acyl glycerols was studied, with various fatty acids esterified at the glycerol 2-position. These stereospecific triacyl-sn-glycerols were fed to donor rats and lymph chylomicrons were isolated, analyzed, and reinjected into recipient rats to study their disappearance from plasma and delivery to tissues. As shown by their compositions, chylomicrons obtained after feeding triacylglycerols containing all sn-3 fatty acid of chain length greater than 20 carbons were under-represented, possibly due to poorer digestion by lipases, or poorer absorption by the intestine. The 18-carbon saturated chain fatty acid (stearic acid) was equally well represented in chylomicrons whether in the 2- or 3-position of the fed triacylglycerol. The presence of increased amounts of long-chain saturated fatty acids in donor chylomicron triacylglycerols affected the metabolism of chylomicrons injected into the bloodstream of recipient rats. In particular the rate of removal of labeled cholesteryl esters, tracing removal of the partially degraded chylomicron remnants was slowed by the saturated chains, with palmitic acid and the 20-carbon fatty acid, arachidic acid, showing the most severe effects. There were clear differences in the removal from plasma of injected lymph chylomicrons derived from fed triacylglycerols containing stearic acid in either the 2- or 3-position, with evidence for remnants from the symmetrical triacylglycerols being less rapidly removed from the circulating blood. This effect was investigated further by injected model emulsions of chylomicrons, where the 2-position was substituted with saturated or transunsaturated acyl chains. Quantitation of removal from the blood stream of these model lipoproteins confirmed that a saturated or transunsaturated long chain fatty acid at the 2-position of the emulsion triacylglycerols slowed remnant removal from the blood. In some cases, with both lymph chylomicron and with emulsions, the lipolytic step mediated by lipoprotein lipase was also slowed.
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PMID:The effect of triacyl-sn-glycerol structure on the metabolism of chylomicrons and triacylglycerol-rich emulsions in the rat. 335 83

The possible role of Mg in the pathogenesis of vascular disease has recently received increasing attention. Accumulating evidence indicates that Mg strongly influences vascular tone and responsiveness to pressor agents and that Mg deficiency may be associated with an increased risk of hypertension. Moreover, experimental Mg deficiency produces vascular lesions with calcifications while increasing the dietary intake of Mg has been shown to prevent atheroma and thrombotic complications. The modifications of lipid metabolism during experimental Mg deficiency have been recently characterized. Severe Mg deficiency in weanling rats produces a marked hypertriglyceridemia and a decrease in the percentage of cholesterol transported by high-density lipoprotein. The decreased clearance of circulating triglycerides appears to be the major mechanism contributing to hyperlipemia. The same animals were found to have a reduced insulin response after intravenous glucose challenge and a slight reduction in heparin release lipoprotein lipase. A marked reduction in plasma activity of LCAT and a significant decrease in esterified/total plasma cholesterol ratio have also been reported. Severe Mg deficiency in weanling rats produces marked changes in the fatty acid pattern of total plasma lipids, as shown by decreased levels of stearic acid, increased of oleic acid and linoleic acid, and decreased levels of arachidonic acid. Platelets from Mg-deficient rats become more sensitive to thrombin. Such an increased sensitivity of platelets may in turn play an important role in initiating the vascular lesion as well as in thrombotic complications. In view of these experimental data in animal models, more work seems necessary in man to assess the effect of Mg on lipid metabolism and vascular disease.
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PMID:Magnesium, lipids and vascular diseases. Experimental evidence in animal models. 352 56

Once brain ischemia was induced in the gerbil cerebral fronto-parietal cortex, serial changes occurred in energy metabolites and various lipids. The amounts of inositol-containing phospholipids began to decrease immediately after energy failure, followed by an increase in the amount of 1,2-diacylglycerol with a subsequent liberation of arachidonic acid and other free fatty acids. The fatty acid compositions of inositol-containing phospholipids, of 1,2-diacylglycerols produced by ischemia, and of free fatty acids liberated during ischemia were quite similar. The amount of stearic acid liberated was much larger than that of arachidonic acid between 30 s and 1 min of ischemia. On the other hand, there was no significant decrease in the amount of the other phospholipids except for phosphatidic acid. Furthermore, there was also no change in the fatty acid composition of phosphatidylcholine or phosphatidylethanolamine throughout 15 min of ischemia. The amount of cytidine-monophosphate reached a peak (36.7 nmol/g wet wt) at 2 min of ischemia. These results indicated that arachidonic acid was predominantly liberated from inositol-containing phospholipids by phospholipase C, and by the diglyceride lipase and monoglyceride lipase system rather than from phosphatidylcholine or phosphatidylethanolamine by phospholipase A2 or plasmalogenase or choline phosphotransferase during the early period of ischemia.
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PMID:Mechanism of arachidonic acid liberation during ischemia in gerbil cerebral cortex. 379 19

The prolonged incubation of dilute plasma on ice in the presence of added sulphatide vesicles or the long-chain saturated fatty acids (FA) stearic acid (C18:0) or behenic acid (C22:0) induced a concentration-dependent increase in factor VII coagulant activity (VIIc). The addition of FA at various ratios to human serum albumin showed the micellar non-bound pool to be responsible for this effect, FA bound to the high-affinity or low-affinity binding sites of albumin having no influence on VIIc. Plasma VIIc also increased following addition of behenate-enriched lipoprotein particles produced by incubation of the d < 1.006 g/ml lipoprotein fraction with this FA, or addition of lipoprotein remnants produced by pre-incubation of the d < 1.006 g/ml fraction with lipoprotein lipase. Long-chain saturated fatty acids in the interface of lipoprotein remnants, produced by the interaction of triglyceride-rich lipoprotein particles with lipoprotein lipase, appear to provide a surface that activates the contact system of coagulation and subsequently factor VII.
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PMID:The activation of factor VII in citrated plasma by charged long-chain saturated fatty acids at the interface of large triglyceride-rich lipoproteins. 814 88

The triacylglycerol emulsion Intralipid was infused into six normal subjects to investigate the metabolism of individual fatty acids in subcutaneous adipose tissue and forearm muscle, by measurement of arteriovenous differences. The composition of plasma nonesterified fatty acids changed steadily after passage through adipose tissue and became similar to that of the emulsion, reflecting hydrolysis of the Intralipidtriacylglycerol by lipoprotein lipase, since endogenous lipolysis (hormone-sensitive lipase activity plus lipoprotein lipase hydrolysis of very low density lipoprotein triacylglycerol) was decreased. There was no significant net release of total or individual fatty acids from forearm muscle although there was a tendency for the composition of the fatty acids in forearm venous plasma to change during passage through the tissue to reflect the composition of the emulsion. This may reflect hydrolysis of emulsion particles by lipoprotein lipase situated in capillaries which drain into the forearm vein. The behavior of stearic acid in the plasma nonesterified fatty acid pool was consistently aberrant, with arterialized concentrations considerably higher than predicted from adipose tissue release, both before and during Intralipid infusion. We conclude that there are no significant differences in the metabolism of specific fatty acids, with the exception of stearic acid.
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PMID:Metabolism of individual fatty acids during infusion of a triacylglycerol emulsion. 1040 65


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