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)

To delineate the factors that may affect triglyceride capture in brown adipose tissue, we have determined the lipoprotein lipase activity (LPS) under conditions known to modulate this activity in other tissues. Acclimation temperature (28 degree C or 5 degree C) had no effect on circadian variations of white adipose tissue and heart LPL activity, LPL activity in brown adipose tissue of 28 degree C rats was similar to that in white adipose tissue (peak activity between 21:00 and 07:00 h), whereas LPL activity of the former was four times higher in 5 degree C rats and rhythmicity was altered (peak activity at 17:00 h as for heart). Brown adipose tissue LPL activity was increased in 28 degree C rats but not in 5 degree C rats after a single injection of insulin to fasting animals. A single injection of dexamethasone increased brown adipose tissue LPL activity only in 5 degree C rats, whereas enzyme activity was increased in both 28 degree C and 5 degree C rats by a single injection of norepinephrine to fed animals. These variations were discussed with relation to the role of brown adipose tissue at 5 degrees C and 28 degrees C.
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PMID:Circadian rhythm and hormonal sensitivity of lipoprotein lipase activity in cold acclimated rats. 701 9

Insulin may be important in regulating adipose tissue lipoprotein lipase in the rat. Insulin appears to be necessary for the maintenance of enzyme activity in adipose tissue in humans since it is decreased in untreated diabetes and returns to normal with anti-hyperglycemic therapy. Other than this permissive role of insulin in maintenance of adipose tissue LPL activity in humans, there is little evidence that insulin, by itself, plays a primary role in the regulation of adipose-tissue lipoprotein lipase in man.
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PMID:Insulin and adipose tissue lipoprotein lipase activity in humans. 703 52

71 healthy women aged 20-35, nonobese and who had received 1 of 3 different combinations of ethinyl estradiol and D-norgestrel for more than 6 months were studied to observe the influence of the drugs on the plasma lipids and lipoprotein lipase. The 3 combinations were: 1) 30 mcg ethinyl estradiol and 250 mcg D-norgestrel; 2) 50 mcg ethinyl estradiol and 250 mcg D-norgestrel; and 3) 50 mcg ethinyl estradiol and 500 mcg D-norgestrel. Results were compared to data from a similar study on 24 normal females who were not on OC. Patients in groups 1 and 2 had significantly elevated total plasma cholesterol and LDL-C (high density lipoprotein cholesterol) as compared to the controls. In group 2 total plasma LPL (lipoprotein lipase) activator property was significantly lower than in controls, but total plasma triglycerides level was significantly higher. Patients in group 3 has significantly lower total plasma triglycerides but high LPL activating property than women in group 2. These results show that OC may affect plasma triglycerides through the influence of apolipoproteins that modulate lipoprotein lipase activity.
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PMID:Plasma lipids and lipoprotein lipase activating property in women on three different combinations of estrogens and progestins. 727 64

Post-heparin lipoprotein lipase (PH-LPL)-high density lipoprotein cholesterol (HDL-C) interrrelationships were assessed in 9 subjects with documented familial hyperalphalipoproteinemia (FHA) and in 8 controls to focus on potential biochemical etiologies of FHA and relationships of HDL-C to triglyceride hydrolysis and PH-LPL. FHA subjects had mean HDL-C and HDL2-C levels > twice controls; their PH-LPL levels (mean +/- SEM) (3.14 +/- 2.3 mumol FFA/h/ml) were also > twice that of controls (15.0 +/- 1.6) (P < 0.01), but post-heparin hepatic lipase levels (PH-HL) in the FHA and control subjects did not differ (18.1 +/- 1.6 vs 26.6 +/- 4.3, P > 0.1). For all subjects (FHA and controls) PH-LPL was positively correlated with HDL-C (r = 0.79, P < 0.01) and with HDL2-C (r = 0.90, P < 0.01), but not with HDL3-C (r = --0.02). There were no significant PH-HL and HDL-C interrelationships, P > 0.1. The amount of apo CII (the primary activator of PH-LPL) in HDL2 was greater in the FHA (mean +/- SEM) (16.1 +/- 2.5 microgram/ml plasma) than in control subjects (4.7 +/- 0.9, P < 0.01). There were strong positive correlations between HDL2 apo CII and both PH-LPL (r = 0.79, P < 0.01) and HDL2-C (r = 0.80, P < 0.01). Apo CII as a percentage of HDL2 protein was higher in FHA than control subjects (mean +/- SEM) (1.2 +/- 0.3% vs 0.5 +/- 0.2%, P < 0.01). Apo CII as a percentage of HDL3 protein was similar in FHA and control subjects. We postulate that increased turnover rate of triglyceride-rich lipoproteins due to high LPL activity may be an important factor leading to the elevation of HDL-C in FHA. The highly significant positive correlation between HDL2-C and PH-LPL provides strong clinical evidence for the theory that HDL2 is formed during the hydrolysis of triglycceride-rich lipoproteins. The high concentration of HDL2 apo CII in FHA subjects may be caused by increased catabolism of triglyceride-rich lipoproteins in the presence of high endothelial LPL, with transfer of apo CII from very low to high density lipoproteins.
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PMID:Post-heparin plasma lipoprotein and hepatic lipases. Relationships to high density lipoprotein cholesterol and to apolipoprotein CII in familial hyperalphalipoproteinemic and in normal subjects. 742 98

The enzymes lipoprotein lipase (LPL, EC 3.1.1.34) and hormone-sensitive lipase (HSL, EC 3.1.1.3) apparently catalyze opposing functions in white adipose tissue: the former is concerned with fat storage, the latter with fat mobilization. We have studied their regulation in vivo in normal subjects in the postabsorptive state and after eating meals of different compositions, by measurement of arteriovenous concentration differences for triacylglycerol, non-esterified fatty acids and glycerol across a subcutaneous adipose depot. The two enzymes are regulated in a broadly reciprocal manner: in the overnight-fasted state, HSL is more active, but after a meal HSL is suppressed whilst LPL is activated. The movement of fatty acids in and out of adipose tissue appears to be driven by concentration gradients generated by regulation of these two enzymes, and also by activation, in the postprandial period, of the process of fatty acid esterification. The results show some interesting and perhaps unexpected features of metabolic regulation. Of the fatty acids generated by the action of LPL on circulating TAG, a large proportion is released directly into the venous plasma: close to 100% in the overnight-fasted state, and 50% or more at the peak of LPL action after a meal, making what appear reasonable assumptions. We suggest that this apparent 'inefficiency' of fat storage reflects the energetic cost of maintaining precise control over such a fundamental process. Although LPL is usually thought of as the enzyme regulating fat deposition, in fact the fatty acids and glycerol it releases from circulating TAG represent a substantial proportion of those released from adipose tissue, especially in the postprandial state. In addition, although HSL is considered the enzyme responsible for fat mobilization, suppression of its activity is essential to normal regulation of fat deposition. Thus, fat storage and fat mobilization during normal daily life are controlled by coordinated regulation of a number of enzymatic processes in white adipose tissue.
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PMID:Coordinated regulation of hormone-sensitive lipase and lipoprotein lipase in human adipose tissue in vivo: implications for the control of fat storage and fat mobilization. 757 42

We have studied low density lipoprotein (LDL) subclass distribution in a group of male patients with non-insulin-dependent diabetes mellitus (NIDDM) and investigated its relationships to fasting and postprandial triglyceride (TG)-rich lipoproteins, insulin resistance, lipoprotein lipase (EC 3.1.1.3; LPL), hepatic lipase (EC 3.1.1.34; HL), lecithin:cholesterol acyl transferase (EC 2.3.1.43; LCAT) and cholesteryl ester transfer protein (CETP) activities. LDL was subfractionated by density gradient ultracentrifugation. Postprandial lipoproteins were measured after an oral fat load using retinyl palmitate as a marker for intestinal TG-rich lipoproteins. Hypertriglyceridaemic NIDDMs (HTG) had a preponderance of small dense LDL particles present in the plasma and reduced amounts of large buoyant species when compared to normotriglyceridaemic patients (NTG) and controls. Both groups of diabetics were more insulin resistant than the controls (P < 0.05) and had raised concentrations of proinsulin (P < 0.05), although insulin content did not differ significantly. 32-33 split proinsulin (SPI) was the major insulin-like molecule present in HTG and was present in significantly higher amounts in these patients (P < 0.05) than either NTG or control subjects and correlated significantly with the presence of small dense LDL particles. After a test meal, the postprandial chylomicron response was greater in HTG than either NTG diabetics or controls (P < 0.05). Chylomicron remnants were present to a greater extent in HTG than in NTG and controls (P < 0.05), although in this case NTG also contained more chylomicron remnants than control subjects (P < 0.05). There was no difference in the LPL activity, CETP and LCAT between diabetics and controls, whereas an increase in hepatic lipase activity was seen in the HTG diabetics (P < 0.05). Both CETP and LCAT activities increased postprandially. Multivariate analysis showed that TG, HDL content and HL activity were the most important determinants of small dense LDL concentration in the fasting state (R2 = 67%). Postprandially, chylomicron remnant clearance, HL and insulin resistance were the major determinants (R2 = 61%) of LDL-III.
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PMID:Fasting and postprandial determinants for the occurrence of small dense LDL species in non-insulin-dependent diabetic patients with and without hypertriglyceridaemia: the involvement of insulin, insulin precursor species and insulin resistance. 760 66

By aligning nucleotide and amino acid sequences of lipoprotein lipase in eight species (man, pig, cow, sheep, mouse, rat, guinea-pig and chicken), we found that the main domains (catalytic, N-glycosylation and putative heparin binding sites) are well conserved. The longest identical amino acid chain was encoded by a sequence between the end of exon 2 and the beginning of exon 3, emphasizing the importance of this region which encodes the beta 5-loop of the active site, among other domains. Exon 10 is entirely untranslated in the seven mammals studied here and contains species-characteristic deletions, insertions or elements rich in A or A + T. In chicken, the beginning of exon 10 is translated. These eight previously unreported alignments could be a useful tool for further studies on LPL function.
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PMID:Comparison of the cDNA and amino acid sequences of lipoprotein lipase in eight species. 761 63

Obesity is an increasingly prevalent problem, and long-term maintenance of the weight-reduced state is difficult for the obese individual. Following weight reduction, many metabolic changes occur. Among these is an increase in adipose tissue lipoprotein lipase (ATLPL), which predicts an alteration in lipid fuel partitioning which may then contribute to resumption of the obese state. The purpose of this study was to test whether changes in skeletal muscle LPL (SMLPL) and its response to insulin/glucose after sustained weight reduction also indicate a potential altered partitioning of lipid fuels away from oxidative pathways in muscle to storage in adipose tissue. Biopsies of vastus lateralis muscle were carried out in premenopausal obese women (n = 11, 94 +/- 4 kg, mean +/- SEM) before and after consumption of a 900 kcal day-1 diet for 3 months followed by 3 months of isocaloric maintenance of the reduced weight (n = 11, 82 +/- 4 kg). SMLPL activity was measured in the fasted state and after 6 h insulin/glucose infusion, before and after sustained weight loss. SMLPL activities were also measured in six normal weight women. Fasting SMLPL activity in obese women (3.9 +/- 0.3 nmol FFA min-1 g-1) was similar to that measured in normal weight control women (4.4 +/- 0.5). Unlike normal weight controls in whom a 6 h insulin/glucose infusion decreased SMLPL activity, in obese women the response of SMLPL was positive (normal weight vs. obese: delta -0.8 +/- 0.3 vs. delta 1.6 +/- 0.5, P = 0.002). Following maintained weight reduction, fasting SMLPL in the obese group was reduced to 1.2 +/- 0.3 (obese before weight loss vs. obese after: P = 0.0001). This change in fasting SMLPL activity following weight loss/maintenance correlated with the resultant change in percent body fat (r s = 0.663, P = 0.026).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Sustained weight reduction in moderately obese women results in decreased activity of skeletal muscle lipoprotein lipase. 765 17

Polymorphic alleles at loci such as LPL (lipoprotein lipase) and MSR (macrophage scavenger receptor) in chromosome band 8p22 are frequently lost during the genesis of several types of human cancer, including colorectal, non-small cell lung, hepatocellular, and prostatic carcinomas. A physical map of 31 published or novel probes and sequence-tagged sites in this genetic region was constructed using a radiation hybrid panel and the CEPH (Centre d'Etude du Polymorphisme Humain) yeast artificial chromosome (YAC) library. Thirty-six overlapping YACs defined a physical order for the following polymorphic markers: tel-D8S26-D8S511-D8S549-MSR-D8S254-D8S233- D8S261-D8S21-LPL-D8S258-cen. These maps unify small consensus regions of allelic loss on chromosome 8p defined by restriction fragment length polymorphisms with more informative PCR-based polymorphisms and widely available YAC mapping resources.
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PMID:Yeast artificial chromosome and radiation hybrid map of loci in chromosome band 8p22, a common region of allelic loss in multiple human cancers. 769 54

Previous studies have demonstrated that some cytokines induce a coordinate catabolic response in adipose cells which leads to decreased fat storage. The mechanisms by which cytokines cause these effects are unknown. The primary purpose of the present study was to determine the effects of TNF, IL-1, IFN-alpha and IFN-alpha on the mRNA levels of the key enzymes involved in fat metabolism in 3T3-F442A adipocytes. TNF, IL-1, IFN-alpha and IFN-gamma decreased lipoprotein lipase activity and increased lipolysis in adipocytes. TNF, IFN-alpha and IFN-gamma decreased fatty acid synthesis while IL-1 increased fatty acid synthesis. However, the cytokine effects on mRNA levels were not always consistent with the observed changes in activity and were unique for each cytokine. Specifically, while all cytokines decreased LPL activity, only TNF and IFN-gamma decreased LPL mRNA levels. In addition, while TNF, IFN-alpha and IFN-gamma decreased fatty acid synthesis, only TNF significantly decreased the mRNA levels of both acetyl CoA carboxylase and fatty acid synthase, the key enzymes in fatty acid synthesis. IFN-alpha and IFN-gamma decreased fatty acid synthase mRNA levels without significantly altering acetyl CoA carboxylase mRNA. IL-1 caused a slight increase in fatty acid synthesis and increased acetyl CoA carboxylase mRNA levels. Finally, while all cytokines increased lipolysis, hormone sensitive lipase mRNA levels were decreased by TNF, IFN-alpha and IFN-gamma treatment. These results indicate that the regulation of adipocyte lipid metabolism by cytokines is complex and that coordinate changes in mRNA levels cannot account for the observed metabolic changes.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cytokines induce catabolic effects in cultured adipocytes by multiple mechanisms. 782 85


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