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)

Lipolysis in human adipose tissue was measured as glycerol release in isolated fat cells and in adipose tissue homogenates. In isolated fat cells lipolysis proceeded optimally at pH 7.4, was stimulated 3.5 fold by noradrenaline and was not influenced by serum or protamine. In adipose tissue homogenates lipolysis was stimulated 4 fold by serum. Serum-stimulated lipolytic activity was optimal at pH 8.0, was inhibited by 1 M sodium chloride and protamine and was not influenced by noradrenaline. Lipolytic activity in isolated fat cells is ascribed on the basis of these observations mainly to the action of hormone-sensitive lipase. whereas lipolysis in adipose tissue homogenates in the presence of serum seems to be regulated by lipoprotein lipase. Thus, the lipolytic processes involved in the mobilization of triglycerides from adipose tissue and in the uptake or triglycerides into adipose tissue can be assessed separately, using the two described methods. The re-esterification of FFA, the second pathway in the mobilization of triglycerides, has also been investigated.
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PMID:[Pathophysiology of lipolysis in human adipose tissue (author's transl)]. 2 89

Lipoprotein lipase activity was detected and characterized in the fat body of Triatoma brasiliensis one of the vector of Chagas' disease. The enzyme activity was close to a free fatty acid production of 47 mumol FFA mg protein-1-h-1 when assayed in the complete system. 2. The enzyme presented maximum activity at pH 8.5. It appeared to be activated by heparin (2 U/ml) and to require a cofactor (rat serum lipoproteins) when assayed with simple triglyceride emulsions. The requirement for a FFA acceptor (albumin or CaCl2) was also observed. 3. Inhibition of enzyme activity by pyrophosphate, HDB, protamine sulphate and 1 m NaC1 indicated further that the enzyme from fat body of T. brasiliensis had the characteristic features of lipoprotein lipase from other sources.
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PMID:Lipoprotein lipase in the fat body of Triatoma brasiliensis. 6 Sep 18

The ketogenic potential of Intralipid was studied in two groups of infants: 12 were SGA and 15 AGA; all were clinically stable and less than 48 hours of age. During four-hour Intralipid tolerance tests, the SGA infants achieved significantly higher plasma TG and FFA levels. Both groups of infants significantly increased the concentration of ketone bodies; however, there was no difference in the levels achieved. In view of the slower clearance rate of TG and the higher levels of FFA in SGA infants, it is speculated that in addition to a possible defective lipoprotein lipase system and a decrease in number and size of the adipose cells, beta-oxidation of FFA to ketones may be occurring at a slower rate. The generation of high levels of ketones during Intralipid infusion period in both groups of infants indicates that SGA infants can handle ketone bodies as readily as AGA infants.
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PMID:Lipid metabolism in the neonate. III. The ketogenic effect of Intralipid infusion in the neonate. 9 42

Fat-mobilizing lipolysis was studied in rat and human adipose tissue during incubation in vitro by following the release of glycerol into the incubation medium. Gemfibrozil as well as clofibrate consistently and readily inhibited basal as well as noradrenaline-stimulated fat-mobilizing lipolysis in rat fat. With human adipose tissue no effect was observed with gemfibrozil and clofibrate on basal lipolysis. This may be due to the comparatively low rate of the nonstimulated fat-mobilizing lipolysis in human tissue incubated in vitro. When lipolysis was stimulated with noradrenaline as well as isoprenaline, however, both gemfibrozil and clofibrate significantly reduced the fat-mobilizing lipolysis. This inhibition of lipolysis was however not observed in all studies. When lipolysis had been stimulated with theophylline, no inhibition of lipolysis was obtained with either compound. The possibility that reduced fat-mobilizing lipolysis in adipose tissue may cause a lowering of plasma triglycerides by reducing the flow of FFA to the liver is discussed in some detail. It is also suggested that inhibition of lipolysis may be accompanied by increased activity of lipoprotein lipase as well as an increase in the FIAT process. However, the pharmacological implication of the above-mentioned findings, particularly for gemfibrozil, must await further studies, as fairly large doses, around 1 mg/ml of incubation medium, were needed to obtain inhibition of fat-mobilizing lipolysis.
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PMID:Effect of gemfibrozil in vitro on fat-mobilizing lipolysis in human adipose tissue. 101 47

Infection causes disturbances in lipid metabolism that may be mediated by cytokines. Therefore we studied plasma lipids, lipoproteins, triglyceride (TG) metabolism, and serum cytokines in three groups: patients with the acquired immunodeficiency syndrome (AIDS) without active secondary infection, patients with evidence of human immunodeficiency virus infection but without clinical AIDS (HIV+), and controls. Plasma TGs and FFA were increased in AIDS, while plasma cholesterol, high density lipoprotein (HDL) cholesterol, apolipoprotein-A-1 (Apo-A-1), low density lipoprotein (LDL) cholesterol, and Apo-B-100 levels were decreased. Increased TG levels in AIDS were primarily due to increases in very low density lipoprotein of normal composition; in addition, LDL and HDL were TG enriched. In HIV+, TGs and FFA were not increased, but total cholesterol, HDL cholesterol, Apo-A-1, and Apo-B-100 were significantly decreased. Interferon-alpha (IFN alpha) and C-reactive protein levels were increased in AIDS, but tumor necrosis factor and haptoglobin levels were not. There was a significant correlation between plasma TGs and IFN alpha levels (r = 0.477; P less than 0.01), but not between TGs and tumor necrosis factor, C-reactive protein, haptoglobin, or P-24 antigen. In addition, there was no relationship between circulating IFN alpha levels and plasma cholesterol, HDL cholesterol, Apo-A-1, LDL cholesterol, Apo-B-100, or FFA. TG clearance time and postheparin lipase were significantly decreased in AIDS and HIV+. There was a strong correlation between serum IFN alpha levels and TG clearance time in AIDS and HIV+ (r = 0.783; P less than 0.001). In summary, decreases in cholesterol and cholesterol containing lipoproteins (including HDL) in both AIDS and HIV+ precede the appearance of hypertriglyceridemia and are not related to IFN alpha or TG levels. Our data raise the possibility that with development of AIDS, subsequent increases in IFN alpha may contribute to increases in plasma TG levels in part by decreasing the clearance of TG.
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PMID:Lipids, lipoproteins, triglyceride clearance, and cytokines in human immunodeficiency virus infection and the acquired immunodeficiency syndrome. 137 35

A man whose weight is near 70 kg has approximately 15 kg of fat as triglycerides in adipose tissue, representing about 140,000 kcal. With such a quantity of stored fat, the question is to know why triglycerides are not the only fuel for exercise. Probably because this fuel cannot sustain maximal rates of exercise. The ability to sustain maximal exercise is dependent on carbohydrate use. The reason for the limited rate at which energy can be derived from fat store is not clear. We can examine successively: 1) The rate of release from adipose tissue. Hydrolysis of the adipose tissue triglyceride is regulated by hormonal and nervous influence. It has recently been shown that 70% of fatty acids released from adipose tissue at rest are reesterified. This value decreases to 25% at the onset of submaximal exercise at 40% of VO2max. One part of the increase in fat oxidation could therefore result from the reduced reesterification. 2) The capacity of transport and muscle extraction. A close correlation has been shown between the increase in FFA concentration and FFA uptake during increased energy expenditure under the effect of exercise. Exercise increases lipoprotein lipase (LPL) activity in muscle. This causes increase in muscle and cardiac FFA uptake and a decrease in LPL activity in adipose tissue. The control of this enzyme is coordinated by hormonal mechanisms resulting from the reduction of insulin and the increase in catecholamines induced by exercise.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Role of lipids on endurance capacity in man. 148 46

In patients with familial lipoprotein lipase deficiency (FLPL-d) and glycogen storage disease type I (GSD-I), hypertriglyceridaemia (1445 +/- 247 and 1082 +/- 312 mg dl-1, n = 5 per group) was associated primarily with reduced extrahepatic lipoprotein lipase (LPL) activity (0.33 +/- 0.33 and 1.69 +/- 0.38 mumol FFA ml-1 h-1) when compared with controls (4.83 +/- 0.90). Hypercholesterolaemia was characterized by elevated LDL cholesterol (191 +/- 30 and 344 +/- 34 vs. 115 +/- 5 mg dl-1 in controls P less than 0.01) and low HDL cholesterol (12 +/- 2 and 22 +/- 2 vs. 56 +/- 3 in controls, P less than 0.001). In order to ascertain the role of LPL in the interconversion and remodelling of lipoproteins in these disorders, we analysed lipid and lipoprotein profiles before and following in vitro incubation of patient plasma with purified milk LPL (EC 3.1.1.34) for 6 h at 37 degrees C. The efficiency of exogenous LPL in vitro was demonstrated by the extent of hydrolysis of chylomicrons and of VLDL-TG in both groups. Concomitant with the disappearance of TG-rich lipoprotein particles, a consistent per cent increment of IDL (99.2 +/- 30.8 and 43.9 +/- 70.5), LDL (152.8 +/- 36.2 and 137.0 +/- 36.1) and of HDL2 (144.8 +/- 29.4 and 99.8 +/- 18.7) was observed in both groups of patients. The enhancement of the latter fractions contrasted with the decline of HDL3 mass concentration (25.4 +/- 7.7 and 51.4 +/- 5.8%), suggesting that a major shift of HDL3----HDL2 occurs following in vitro lipolysis by LDL. Simultaneous compositional and morphological changes of individual lipoprotein particles were noted, confirming the dynamic movement and exchange of neutral lipids and proteins. Specificity of LPL results was demonstrated by experiments in which incubation of the whole plasma at 37 degrees C without exogenous lipolytic enzyme did not cause any substantial changes. The present study, therefore, demonstrates a correction of the major lipoprotein abnormalities associated with FLPL-d and GSD-I by exogenous LPL. No substantial difference was noted between primary (FLPL-d) and secondary (GSD-I) hyperlipidaemias. These studies allow us to conclude that a simple in vitro system, utilizing an exogenous source of LPL and plasma from patients, may serve as a suitable model for the study of the metabolic relationships of lipoproteins. However, in view of the fact that the extent of lipolysis achieved in vitro did not differ between FLPL-d and GSD-I, it may not be able to separate primary from secondary hyperlipaemias.
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PMID:In vitro remodelling of plasma lipoproteins in whole plasma by lipoprotein lipase in primary and secondary hypertriglyceridaemia. 212 2

Hypertriglyceridemic (HTG) serum, lipolyzed in vitro by purified bovine milk lipoprotein lipase, was found to be cytotoxic to cultured macrophages. Surviving macrophages contained numerous lipid inclusions similar to those found in foam cells. Individual lipoprotein fractions isolated from the lipolyzed HTG serum, including HDL, were also cytotoxic. Lipolysis of isolated lipoprotein fractions (either HTG or normal) allowed localization of cytotoxicity to postlipolysis remnant VLDL and chylomicron particles. The presence of a critical concentration of HDL in either the lipolysis mixture or the culture dishes inhibited the cytotoxicity. Below this critical concentration HDL itself became cytotoxic, producing lipid inclusions in surviving macrophages. The lipid fraction of the cytotoxic remnants contained the cytotoxic factor(s); neither FFA nor lysolecithin alone could account for this cytotoxicity. Postprandial lipemic sera from subjects with a brisk chylomicron response, when lipolyzed in vitro, were cytotoxic to cultured macrophages; neither fasted sera from these subjects, nor postprandial sera from normolipidemic subjects with a normal chylomicron response, were cytotoxic. Postheparin (in vivo lipolyzed) serum and its isolated lipoprotein fractions obtained 30 min after heparin injection in subjects with HTG were shown to be cytotoxic to macrophages; by 60 min most of the cytotoxicity had disappeared. The postprandial and postheparin observations support an in vivo significance for remnant-associated cytotoxicity. We hypothesize that cytotoxic remnants of lipolyzed VLDL and chylomicrons may be one of the major atherogenic lipoproteins. Further, we suggest that inhibition of the cytotoxicity of these remnants may be one important way that HDL prevents atherosclerosis.
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PMID:Lipolytic surface remnants of triglyceride-rich lipoproteins are cytotoxic to macrophages but not in the presence of high density lipoprotein. A possible mechanism of atherogenesis? 270 36

The effects of obesity, weight loss and weight maintenance on the serum lipid levels and lipoprotein lipase and hepatic triglyceride lipase were investigated in rats. Obesity induced by high-fat (HF) feeding was associated with decreased serum triglyceride levels (HF: 70.3 +/- 8.2, control (CON): 140.0 +/- 26.9 mg/dl, P less than 0.05), increased lipoprotein lipase (LPL, HF: 593.2 +/- 10.6 vs CON: 280 +/- 19.5 nmol FFA/min per mg tissue, P less than 0.05) and suppressed hepatic triglyceride lipase activities (HTGL, HF: 14.2 +/- 0.5 vs CON: 18.0 +/- 0.4 nmol FFA/min per mg tissue, P less than 0.01). After a weight loss to the level of control rats, weight maintenance was achieved either by high-protein (HP) or chow feedings (CH). Both high-protein (HFHP) and chow (HFHC) groups had similar weights but only high-protein feeding restored the normal body compositions. Both groups of rats had higher total (TC, HFHP: 146 +/- 10.7; HFCH: 104.8 +/- 5.1 mg/dl), and high density lipoprotein cholesterol levels (HDL-C, HFHP: 100.8 +/- 15.6; HFCH: 75.5 +/- 5.5 mg/dl) and lower lipoprotein lipase (HFHP: 238.2 +/- 15.8, HFCH: 354.8 +/- 34.9 nmol FFA/min per mg tissue) and hepatic triglyceride activities (HFHP: 16.3 +/- 1.1; HFCH: 14.5 +/- 0.6 nmol FFA/min per mg tissue) than control rats (TC: 70.1 +/- 4.7 mg/dl; HDL-C: 14.2 +/- 4.3 mg/dl; LPL: 742.4 +/- 82.3 nmol FFA/min per mg tissue; HTGL: 20.5 +/- 1.0 nmol FFA/min per mg tissue, P less than 0.05 to 0.005) or the rats who regained weight by resuming high-fat feeding (TC: 59.5 +/- 6.7 mg/dl; HDL-C: 10.2 +/- 6.7 mg/dl; LPL: 1284.3 +/- 90 nmol FFA/min per mg tissue; HTGL: 22.2 +/- 1.9 nmol FFA/min per mg tissue, P less than 0.05 to 0.005). The high protein-group had significantly higher total and high-density-lipoprotein cholesterol levels than the chow fed animals despite comparable body weights in both groups. The findings of this study suggest that weight maintenance induced by high protein feeding is more successful in restoring the normal body composition. However, high protein feeding is also associated with high serum cholesterol levels. The clinical applications of these findings need to be evaluated further.
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PMID:Effects of weight loss and weight maintenance on the serum lipids, lipoprotein lipase and hepatic triglyceride lipase activities in obese rats. 276 81

The effects of sepsis on lipid metabolism may be summarized as follows: The increased plasma catecholamine concentration stimulates adipose tissue FFA release. The increased FFA mobilization and plasma concentration results in an enhanced FFA uptake by the liver which promotes TGFA synthesis and output. Thus, triglyceride appearance rate also can be increased during hypermetabolic sepsis. In severe sepsis, the regulatory signals to increase FFA release from adipose tissue may be counterbalanced by blood flow limitations that inhibit FFA release, possibly due to the inadequate availability of the plasma carrier, albumin. Under such conditions, the arterial FFA concentration may be unchanged or decreased along with similar changes in the rate of peripheral FFA utilization. Triglyceride metabolism can also be altered during septic conditions in which plasma levels of cytokines are very high. Cytokines, notably TNF and IL-1, suppress synthesis of lipoprotein lipase which decreases the rate of TGFA clearance. Thus, hypertriglyceridemia can develop in the absence of elevated plasma FFA levels. The plasma concentration of cytokines necessary to inhibit LPL and how often this form of hypertriglyceridemia occurs in human sepsis are unknown at present. The sequence of events describing the influence of sepsis on carbohydrate metabolism is postulated to be the following: The presence of bacteria, or their products (eg, endotoxin) either directly or indirectly (via stimulating mononuclear phagocytes to release cytokines) activate the immune tissues. Glucose utilization by these tissues, which are predominantly glycolytic, is thereby stimulated resulting in increased lactate production. At the same time, glucose uptake by skeletal muscle and lactate release are also elevated.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Alterations in lipid and carbohydrate metabolism in sepsis. 306 39


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