The most recent information on LPL is here. Click here for the function of LPL. Edit this page in Wiki Genes - LPL or see Wiki Gene. There was no change in LPL, HTGL, or LCAT. Paper-7510344. TNF is known to inhibit LPL activity. Paper-219221. The CII apoprotein was found to activate LPL. Paper-2266232. In addition, TNF-alpha action is associated with the LPL activity. Paper-383654. Insulin resistance is associated with decreased plasma LPL mass. Paper-12211153. Apolipoprotein CII (apoCII) activates lipoprotein lipase ( LPL). Paper-9155568. The apoC content of TRLP regulated the docking of TRLP to LPL. Paper-833765. Apolipoprotein C-II (C-II) had no effect on the esterase activity of LPL. Paper-4399820. We therefore speculated that adiponectin may directly affect LPL in humans. Paper-10654541. In addition to LpL, hepatic lipase ( HL) has been shown to bind to LRP. Paper-805859. In this model, GH has little or no effect on LPL activity in adipose tissue. Paper-1998709. Both polyaspartate and polyglutamate blocked LPL and chylomicron binding to GPIHBP1. Paper-13041320. CD23, usually of dim intensity, and CD11c are expressed commonly in LPL/WM. Paper-10989177. However, the magnitude of the increase in LPL did not correlate with the decrease in TNF. Paper-219221. Insulin stimulates LPL and inhibits HSL; the opposite is true for catecholamines. Paper-8894168. Both LPL and GST-LPLC promoted binding of VLDL to LDL receptor-coated wells. Paper-619349. Testosterone and GH inhibit LPL and stimulate lipolysis markedly. Paper-1304748. C-reactive protein enhances macrophage lipoprotein lipase expression. Paper-12911091. Apolipoprotein CII was biologically active and could activate lipoprotein lipase. Paper-3348849. Modulation of lipoprotein lipase activity by apolipoproteins. Effect of apolipoprotein C-III. Paper-4896706. Furthermore, we found that PRL also inhibited the cortisol- induced LPL activity. Paper-9878011. Thus, LPL S447X genotype influenced exercise- induced changes in LV mass and SBP. Paper-11364863. This antibody thus appears to recognize the apo-C-II binding site of lipoprotein lipase. Paper-4892535. The Acidic Domain of GPIHBP1 Is Important for the Binding of Lipoprotein Lipase and Chylomicrons. Paper-13041320. Effect of lipid transfer proteins on lipoprotein lipase induced transformation of VLDL and HDL. Paper-746402. In contrast, ANGPTL4 suppressed LPL by accelerating the irreversible inactivation of LPL. Paper-13570812. The decrease in lipoprotein lipase activity correlated with the amount of bound apolipoprotein C-II. Paper-5158835. ApoE enhances lipid uptake by macrophages in lipoprotein lipase deficiency during pregnancy. Paper-805861. Peroxisome proliferator-activated receptor-alpha ligands inhibit cardiac lipoprotein lipase activity. Paper-9018326. Serum from FH patients also enhances the levels of LPL secreted by macrophages from control subjects. Paper-9385659. Freshly harvested cells stimulated with lipoprotein lipase (LPS) released TNF and IL-1. Paper-7393955. Plasma adiponectin appears to be a determinant of plasma triglycerides via an effect on LPL activity. Paper-11248183. In order to test this hypothesis, lipolysis experiments were performed using HSPG- bound LPL. Paper-1414709. Gastric inhibitory polypeptide enhanced lipoprotein lipase activity in cultured preadipocytes. Paper-3269099. LPL release by TNF required endothelial cell metabolic event(s) which involved cell secretion. Paper-6539266. We conclude that post-heparin plasma LPL activity, but not HL activity, is related with plasma adiponectin. Paper-11248183. This indicates that trout LPL carries out functions that hepatic lipase has evolved to take over in mammals. Paper-9511564. IgGs purified from these three antisera also block hTNF- induced cytolysis and lipoprotein lipase suppression. Paper-5649414. When both LPL and HL were included in the same incubation, however, LPL prevented the effects of HL. Paper-6526397. Heparin-bound lipoprotein lipase is catalytically active and can be stimulated by apolipoprotein CII. Paper-3825018. These experiments show that LPL enhances the CETP-mediated transfer of cholesteryl esters from HDL to VLDL. Paper-4624125. Deletion of LpL residues 380-384 abolished the binding to LRP, whereas binding to heparin was unperturbed. Paper-946681. A hallmark of GPIHBP1 is the ability to bind lipoprotein lipase, chylomicrons, and apolipoprotein (apo-) AV. Paper-13445608. Thus, bacterial LPS potently decreases macrophage LPL activity and mass independent of an autocrine effect of TNF. Paper-6080056. Furthermore, LPL promoted binding of 125I-lipoproteins to highly purified LRP in a solid-phase assay. Paper-7865842. In contrast, LPL synergistically enhanced IFN-gamma-induced gene expression in HAECs. Paper-10746839. The current study investigated the potential for this region of LPL to promote cellular catabolism of VLDL via LRP. Paper-125583. Effect of lipoprotein lipase on binding of chylomicrons to LDL receptor-deficient Chinese hamster ovary cells. Paper-8771185. By contrast, PPAR activators decrease secreted LPL mass and enzyme activity in differentiated macrophages. Paper-9380659. The PHP- LPL activity decreases in hypophysectomized rats and this effect is reversed by growth hormone ( GH) therapy. Paper-1998709. There is evidence that CR contain LPL and it has been demonstrated that LPL binds with high affinity to LRP. Paper-8227627. OBJECTIVE: GPIHBP1 is an endothelial cell protein that binds lipoprotein lipase ( LPL) and chylomicrons. Paper-13796945. The data indicate that IFN-gamma is inhibiting macrophage LPL at least in part via a reduction of LPL synthesis. Paper-6540600. Calreticulin promotes folding/ dimerization of human lipoprotein lipase expressed in insect cells (sf21). Paper-9810347. There is evidence that CR contains LPL and it has been demonstrated that LPL binds with high affinity to LRP. Paper-628006. Human recombinant TNF suppresses lipoprotein lipase activity and stimulates lipolysis in 3T3-L1 cells. Paper-5487121. ApoA-I and apoC-I activate lecithin/ cholesterol acyltransferase; apoC-II is an activator of lipoprotein lipase. Paper-3290271. HDL2 cholesterol was associated positively with LPL and negatively with VLDL triglyceride in the model. Paper-7202654. In adipose tissue, GIP interacts with insulin to increase lipoprotein lipase activity and lipogenesis. Paper-13643286. Here we demonstrate that LPL binds to the alpha-chain of purified alpha 2MR/ LRP immobilized on microtiter plates. Paper-7881971. These studies confirm that the VLDL receptor binds to and mediates the catabolism of LpL and uPA.PAI-1 complexes. Paper-414460. Treatment of human macrophages with up to 1000 U/ml of recombinant human TNF had no effect on macrophage LPL activity. Paper-6080056. The amount of LDL bound to the cells in the presence of LPL far exceeded the capacity for LDL binding via the LDL receptor. Paper-7494874. The aim of the present study was to investigate if parathyroid hormone ( PTH) had an inhibitory effect on LPL activity. Paper-170105. Therefore, the presence of TNF-alpha might lead to the increase in plasma TG mediated by LPL in tumor-bearing hamsters. Paper-383654. Dimeric LPL could mediate binding of beta-VLDL to immobilized alpha 2MR/ LRP and to cells, e.g. monocytes. Paper-7881971. Growth-hormone- induced changes in postheparin plasma lipoprotein lipase and hepatic triglyceride lipase activities. Paper-4575188. TNF may not cause the cachexia of cancer or chronic infection by directly inhibiting LPL in adipose tissue. Paper-5920153. Purified LRP bound specifically to microtiter wells coated with LPL or LPLC with KD values of 2.8 and 5 nM, respectively. Paper-115484. Immobilized LPL bound alpha 2MR/ LRP in solution as well as beta-VLDL prepared from cholesterol-fed rabbits. Paper-7881971. Lipoprotein lipase ( LpL) activity is enhanced by apolipoprotein C-II ( apoC-II), a 79 amino acid residue peptide. Paper-5450576. To localize the portion of LPL that is responsible for interacting with LRP, fragments of LPL were expressed in bacteria. Paper-115484. GIP stimulated significant increases in the lipoprotein lipase activity released into the culture medium and in cells. Paper-3269099. Furthermore, mean LPL and HTGL activities in the low-HDL patients with elevated CETP activities were in the normal range. Paper-234451. Correlations were calculated between the cholesterol concentration of each fraction and plasma PLTP, HL, and LPL activity. Paper-9603843. Cyanogen bromide fragments of apoC-II corresponding to residues 1--9 and 10--59 had little ability to activate LPL. Paper-2840756. The APOC3 polymorphism presented additive effects to the LPL variants on TG and HDL-C levels in men, and on TG in women. Paper-9402257. Treatment with phosphatidylinositol-specific phospholipase C ( PIPLC) inhibited 125I- labeled LPL degradation by 13%. Paper-918168. Since lipoprotein lipase and apolipoprotein C-II are already present in fish, this lipase probably evolved before hepatic lipase. Paper-188719. A lipoprotein lipase mutation (Asn291Ser) is associated with reduced HDL cholesterol levels in premature atherosclerosis. Paper-326865. Taken together, these data establish that LPL binds with high affinity to LRP and undergoes LRP-mediated cellular uptake. Paper-78131. Peroxisome proliferator-activated receptor alpha and gamma agonists upregulate human macrophage lipoprotein lipase expression. Paper-9574709. Consistent with this possibility, we found that LPL promoted in vitro binding of 125I-lipoproteins to gp330. Paper-7881255. The higher expression level of LPL was also associated with higher level of ZAP-70 and CD38, and more aggressive Binet stage. Paper-13526680. Overall, TNF may function to make the subject less obese by inhibiting LPL and rendering the animal more insulin resistant. Paper-1177744. These studies indicate that DHT may alter HSL and LPL expression, whereas only LPL expression appears mediated by AR. Paper-9477051. Thus, compositional differences alone can not explain the differences in lipolysis rates observed with HSPG- bound LPL. Paper-1414709. The angiopoietin-like proteins ANGPTL3 and ANGPTL4 inhibit lipoprotein lipase activity through distinct mechanisms. Paper-13570812. We suggest that the S447X polymorphism of the LPL gene may modify the risk of atherogenic sdLDL fraction in an ApoE-dependent fashion. Paper-13718148. TNF is expressed at higher levels in muscle cells of insulin-resistant subjects, and TNF may inhibit LPL expression. Paper-1177744. TNF concentrations up to 1000 pM had no effect on either LPL activity or LPL immunoreactive mass in the human adipocytes. Paper-5920153. The results showed that Lp(a) can be enriched with apoE and that this resulted in increased LPL- enhanced binding to HSPG. Paper-1048275. Lipoprotein lipase ( LPL) induces macrophage tumor necrosis factor-alpha ( TNF-alpha) gene expression and protein secretion. Paper-230969. Furthermore, up- and down regulation of the LDL receptor did not influence the binding of these lipoproteins in the presence of LPL. Paper-7456703. Insulin, exercise, alcohol, fats, drugs, and diet affect lipoprotein lipase and consequently influence levels of LDL and HDL2 indirectly. Paper-6565988. Lipoprotein lipase ( LPL) is bound to heparan sulphate proteoglycans ( HSPG) at the luminal surface of endothelium. Paper-1414709. This suggested that, like a number of other heparin-binding proteins, LPL binding to cells also involves non- HSPG proteins. Paper-116911. Hydrolysis of phospholipids by purified milk lipoprotein lipase. Effect of apoprotein CII, CIII, A and E, and synthetic fragments. Paper-2102416. The patient's LpL hydrolysed triolein emulsified with lysophospholipid at a normal rate in the presence of apolipoprotein CII. Paper-6180135. In contrast, the same TNF in the same concentrations progressively inhibited LPL activity and immunoreactive mass in 3T3-L1 cells. Paper-5920153. Lipoprotein lipase HindIII polymorphism influences HDL-cholesterol levels in statin-treated patients with coronary artery disease. Paper-13405357. Apolipoprotein CII enhances hydrolysis of monoglycerides by lipoprotein lipase, but the effect is abolished by fatty acids. Paper-3393280. These observations indicate that the uptake of LPL- mediated HSPG- bound LDL and VLDL mainly proceeds via the LDL receptor. Paper-7862949. Acute dyslipoproteinemia induced by interleukin-2: lecithin:cholesteryl acyltransferase, lipoprotein lipase, and hepatic lipase deficiencies. Paper-995532. LPL catalyzed the complete hydrolysis of triolein to free oleate and monooleate in the presence of apolipoprotein C-II. Paper-6275702. LPL- induced hydrolysis of VLDL in vitro was not influenced by TFPI neither in suspension nor at the endothelial surface. Paper-11311118. HTGL hydrolyzed triolein substrate at a rate much slower than LPL, and produced mainly free oleate with little monooleate. Paper-6275702. TNF (400 ng/ml) produced a fall of approx. 50% in LPL activity after 2 h of incubation and of approx. 30% in LPL mRNA levels after 3 h. Paper-6584561. Also, a rabbit antiserum against the acidic domain of GPIHBP1 blocked LPL and chylomicron binding to GPIHBP1-expressing cells. Paper-13041320. Levels of apolipoprotein C-III were reduced significantly (P <.03), as were ratios of postheparin hepatic lipase to lipoprotein lipase (P <.05). Paper-9826712. These compounds do not inhibit other hydrolases such as hepatic lipase, lipoprotein lipase, pancreatic lipase, and butyrylcholine esterase. Paper-10301761. The addition of a surplus of either apolipoprotein E or inactivated lipoprotein lipase to the remnants led to an increase in particle uptake. Paper-823762. Because LRP has also been shown to bind LPL, the present findings further extend the functional similarities between gp330 and LRP. Paper-7881255. VCAM-1 expression was stimulated by LPS (395 +/- 221%) and similarly by CH- LPL (322 +/- 136%) but considerably stronger by CH (1245 +/- 324). Paper-1172328. Genotypes of the FABP-2, HL, LPL, APOE, and PPARgamma genes and the APOC-III, APOC-III/A-IV intergenic region were determined. Paper-10785627. Growth hormone but not gonadal steroids influence lipoprotein lipase and hepatic lipase activity in hypophysectomized rats. Paper-8084561. The extracellular lipolysis is regulated by lipoprotein lipase and the intracellular lipolysis is regulated by hormone-sensitive lipase. Paper-8568104. ApoC-II would enhance the apparent catalytic rate constant of lipoprotein lipase by functioning as a specific acyl-enzyme hydrolase. Paper-4389995. In addition, LPL enhances the binding in LDL-receptor negative fibroblasts to the same extent as it does in normal fibroblasts. Paper-7456703. The mutation eliminated the ability of GPIHBP1 to bind LPL and chylomicrons, strongly suggesting that it caused the patient's chylomicronemia. Paper-13796945. We have shown previously that macrophage lipoprotein lipase expression is suppressed by interferon-gamma ( IFN-gamma) at the transcriptional level. Paper-9159118. LPL- mediated lipolysis of VLDL induces an upregulation of AU-rich mRNAs and an activation of HuR in endothelial cells. Paper-12292864. To identify the region of HL involved in the interaction with LRP, we used a C-terminal fragment of LpL, known to inhibit LpL-mediated uptake. Paper-805859. ApoCIII inhibits lipoprotein lipase as well as binding of lipoproteins to cell surface heparan sulfate proteoglycans and receptors. Paper-12832343. Lipoprotein lipase activity was also inhibited by the addition of a large excess of lipid-free apolipoprotein C-III to the artificial particles. Paper-5158835. Effect of apolipoprotein E variants on lipolysis of very low density lipoproteins by heparan sulphate proteoglycan- bound lipoprotein lipase. Paper-1414709. CONCLUSION: Lipoprotein lipase S447X stop codon mutation is associated with lower levels of interleukin 8 after coronary artery bypass grafting. Paper-13360655. These data indicate that the COOH-terminal domain of LPL may function both in binding lipoproteins and mediating their interaction with LRP. Paper-115484. In combination with E(2) 10(-7) mol/L, anti-E 10(-8) mol/L did not abrogate the inhibitory effect on LPL expression relative to control (P <.05). Paper-9658847. At equal protein concentration of added lipoproteins the ratio of HDL3 to VLDL bridging via EL was 0.092 compared with 0.174 via HL and 0.002 via LpL. Paper-9977877. ApoCIII decreases TRL catabolism by inhibiting lipoprotein lipase activity and reducing ApoE-dependent hepatic uptake of TRL and remnants. Paper-1741332. Addition of TNF to the culture medium for 20 h caused a dose-dependent inhibition of LPL activity to an average of 37% of controls at 50 U/ml TNF. Paper-6253306. These data suggest that binding occurs by direct interaction of VLDL with LPL but the subsequent catabolism of the VLDL is mediated by the LDL receptor. Paper-654851. ApoC-II exerts no effect on the activity of LpL for soluble substrates, suggesting that activation occurs via the formation of a lipid-bound complex. Paper-2186132. Replacing the acidic amino acids within GPIHBP1 residues 38-48 with alanine eliminated the ability of GPIHBP1 to bind LPL and chylomicrons. Paper-13041320. The increased lipoprotein lipase activity produced by GIP could provide a mechanisms for clearance of chylomicron triglyceride after feeding in man. Paper-3269099. The implication of these findings for lipoprotein catabolism in vivo may be important if LRP binding is preserved when LPL is attached to lipoproteins. Paper-78131. Therefore, LPL may represent a link between low adiponectin levels and dyslipidemia in both nondiabetic individuals and patients with type 2 diabetes. Paper-10654541. However, neither RAP nor PIPLC treatment of adipocytes significantly increased the amount of endogenously produced LPL activity in the media. Paper-918168. Presence of lipoprotein lipase S447X stop codon affects the magnitude of interleukin 8 release after cardiac surgery with cardiopulmonary bypass. Paper-13360655. These data were dependent upon neither the type of LPL inhibitor (E600 or THL) nor the source of CETP (delipidated plasma or partially purified CETP). Paper-2086991. Anti-E 10(-8) mol/L alone reduced LPL protein expression relative to control (P <.05) and increased HSL protein expression relative to control (P >.05). Paper-9658847. We conclude that oxandrolone increases the activities of postheparin plasma hepatic lipase and phospholipase A1 but has little influence on lipoprotein lipase. Paper-2347660. V(max) of the apoC-III complex containing no apoC-II was 9.2 nmol/min per mg LpL vs. 482 nmol/min per mg LpL for the complex containing only apoC-II. Paper-4351820. The evidence suggests that in the adipocyte, TNF alpha is the unique molecule that suppresses LPL through the selective inhibition of mRNA production. Paper-6239089. Crosslinking experiments on cells with 125I-labeled apoE liposomes or lipoprotein lipase showed that both proteins were able to bind to LRP on the cell surface. Paper-7134920. GPIHBP1 binds lipoprotein lipase and chylomicrons and is expressed along the luminal surface of microvascular endothelial cells. Paper-13058845. The relation between LPL and HL and components of HDL in the paraoxonase genotypic subgroups in general reflected the associations seen in the group as a whole. Paper-713198. The LPL S447X and apolipoprotein E ( APOE) exon 4 polymorphisms affect TG levels, and the APOC3 -455T>C polymorphism affects LPL activity. Paper-12136586. SUBJECTS: Altogether 17 consecutive postmenopausal female patients with RA and 16 age and sex matched controls were enrolled for the initial determination of LPL. Paper-855696. However, high Apo E levels may interfere with lipolysis by interacting with the lipoprotein lipase ( LPL) activator, apolipoprotein C2 (Apo C2). Paper-9324164. Interestingly, either LPLC or LPL when added in excess could block LPL- induced 125I-VLDL degradation presumably by interacting directly with LRP. Paper-125583. LPL positively associated only with HDL in most of subgroups and LCAT correlated with low-density lipoprotein (LDL) in all subgroups but with HDL only in males. Paper-9886432. LPL significantly suppressed TNF-alpha-induced gene expression, and this suppression was reversed by tetrahydrolipstatin and heparinase. Paper-10746839. The cholesterol content of the low-density lipoprotein (LDL) and HDL2 subfractions and endothelial- bound lipoprotein lipase activity (LPLA) were calculated. Paper-1387175. Cleavage of apoC-II by MMP-14 markedly decreased LPL activity and would thus impair hydrolysis of triglycerides in plasma and transfer of fatty acids to tissues. Paper-11335456. Previous studies have demonstrated that cachectin/tumor necrosis factor ( TNF) inhibits lipoprotein lipase ( LPL) activity in cultures of 3T3-L1 cells. Paper-5920153. The action of lipoprotein lipase on triglyceride-rich lipoproteins produces remnant lipoprotein particles enriched in cholesterol and apolipoprotein E (apo E). Paper-1795933. We conclude that the C-terminal folding domain of human LpL has a site for binding to heparin and to HSPG, presumably involving amino acids within residues 404-430. Paper-946681. We hypothesize that apo E mutations may cause a diminished interaction of VLDL with HSPG leading to impaired lipolysis of VLDL by HSPG- bound LPL. Paper-1414709. However, we found that gp330 (purified from human or rat) bound the lipolytic enzyme lipoprotein lipase ( LPL) with high affinity (Kd = 6.1 and 2.7 nM, respectively). Paper-7881255. Finally, mutation of the positively charged heparin-binding domains within LPL and apolipoprotein AV abolished the ability of these proteins to bind to GPIHBP1. Paper-13041320. These results indicated that neither TG solubility nor amount of apoC-II binding were determinate factors in LPL-mediated lipolysis under physiological conditions. Paper-1349129. These results disagree with the putative enhanced apo AI FCR in LPL deficient patients and suggest the need to reconsider the effects of LPL activity on HDL metabolism. Paper-12022177. Apolipoprotein E effectively inhibits lipoprotein lipase-mediated lipolysis of chylomicron-like triglyceride-rich lipid emulsions in vitro and in vivo. Paper-585471. Insulin sensitisation affects lipoprotein lipase transport in type 2 diabetes: role of adipose tissue and skeletal muscle in response to rosiglitazone. Paper-12211153. Identification of functional prolactin (PRL) receptor gene expression: PRL inhibits lipoprotein lipase activity in human white adipose tissue. Paper-9878011. Furthermore, in human adipose tissue cultured in vitro, prolactin ( PRL) inhibited lipoprotein lipase ( LPL) activity via functional PRL receptors. Paper-12894033. In samples drawn 10 days after myocardial infarction we found marked changes in the ability of the patients' sera to enhance the activity of purified lipoprotein lipase. Paper-4110939. In addition, our results demonstrate that UCP-2 and UCP-3 are differentially regulated in response to LPL-mediated NEFA uptake in skeletal muscle of mice. Paper-8784910. We conclude from these studies that both apolipoprotein C-II and heparin interact with immobilized lipoprotein lipase and that they have different binding sites. Paper-3480017. The increase in lipoprotein lipase activity probably mediated the fall in serum triglycerides after exercise and may also account for the increase in HDL cholesterol. Paper-4596690. It is proposed that LPL binds primarily to cell surface heparan sulfate in monocytes and is presented for endocytosis and degradation by alpha 2MR/ LRP. Paper-7881971. Transcriptional control of triglyceride metabolism: fibrates and fatty acids change the expression of the LPL and apo C-III genes by activating the nuclear receptor PPAR. Paper-763485. In contrast, one in vitro study indicates that TFPI may enhance lipoprotein lipase ( LPL) activity, thereby increasing triglyceride hydrolysis. Paper-11311118. On co-expression of LPL with human molecular chaperones, we found that calreticulin had the most pronounced effects on LPL activity, but calnexin was also effective. Paper-9810347. This was further supported by observing that an immunoaffinity-isolated polyclonal antibody against LRP blocked cellular degradation of 125I- LPL in a dose-dependent manner. Paper-78131. On the one hand there is likely to be a synergism between CETP and the non-esterified fatty acids (NEFA) released by LPL; this will favour a reduction in HDL particle size. Paper-7398938. 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. Paper-360652. Moreover, the lipoprotein lipase fragment completely inhibited the binding of several alpha 2MR/ LRP ligands in a pattern similar to that of carboxyl-terminal RAP fragments. Paper-377111. GH was not found to have opposite effects on the activity of LPL in adipose tissue and muscle, since GH treatment reduced them both (by 65% and 20%, respectively). Paper-8402594. To verify the role of 2 different LPL gene mutations on HDL metabolism, we studied the in vivo turnover of the apo AI and apo AII in heterozygous carriers of LPL deficiency. Paper-12022177. Cachectin/tumor necrosis factor and interleukin-1 show different modes of combined effect on lipoprotein lipase activity and intracellular lipolysis in 3T3-L1 cells. Paper-6197597. The effects of normal heparin on factor Xa, thrombin, aPTT, lipoprotein [ LPL] and hepatic triglyceride lipase [ HTGL] activities were neutralized immediately by i.v. protamine. Paper-4958066. Intravascular free tissue factor pathway inhibitor is inversely correlated with HDL cholesterol and postheparin lipoprotein lipase but proportional to apolipoprotein A-II. Paper-2073652. In conclusion, GH treatment of GH-deficient men influenced adipose tissue LPL and postheparin plasma HL activity, as well as serum lipoprotein concentrations. Paper-522616. Is decreased activity of C-II activated lipoprotein lipase in type III hyperlipoproteinemia ( broad-beta-disease) a cause or an effect of increased apolipoprotein E levels? Paper-2658502. To determine the minimal sequence requirements for activation, we have prepared both native and synthetic fragments of apoC-II and tested them for their ability to activate LPL. Paper-2840756. We investigated the mechanism by which the endotoxin-induced macrophage secretory protein cachectin is able to suppress the activity of lipoprotein lipase in 3T3-L1 adipocytes. Paper-5335721. Infected fibroblasts that express the VLDL receptor mediate the cellular internalization of 125I- labeled LpL and uPA.PAI-1 complexes, leading to their degradation. Paper-414460. These observations indicate that for physiological hypertrophy AMPK phosphorylation does not mediate the enhanced translocation of LPL to cardiac endothelium. Paper-13035891. Protein synthesis was required for the induction of NOS mRNA, and a TNF-alpha- mediated effect of LPL on NOS gene expression and NO production was observed. Paper-230969. Using TRLP coated to microtiter wells and associated with LPL, the b-HS displacement patterns were comparable to those obtained with coated LDL in the presence or absence of LPL. Paper-833765. Lipoprotein lipase was effective in substantially augmenting the HDL mass including cholesteryl while the major effect of HL was the selective hydrolysis of HDL triglycerides. Paper-677745. LPL associated with sex (females>males) and LCAT with alcohol intake (drinkers>non-drinkers) although neither enzyme demonstrated direct correlation with coronary stenosis. Paper-9886432. This paper considers how apolipoprotein CII from human plasma lipoproteins and T1 and T2 proteins from egg yolk lipoproteins stimulate the activity of lipoprotein lipase. Paper-3578590. We show, by chemical cross-linking and surface plasmon resonance analysis, that soluble sortilin binds lipoprotein lipase with an affinity similar to that of LRP. Paper-1808100. Indeed, previous studies have shown that the rare S2 allele of the APOC3 Sst I polymorphism was associated with higher concentrations of TG levels in noncarriers of LPL defect. Paper-10995245. We investigated the effect of weight loss together with GH treatment on the activity and gene expression of LPL and hormone-sensitive lipase ( HSL) in AT and muscle tissue. Paper-8402594. These results show that hypertriglyceridemia with low HDL cholesterol results from a reduction of LPL activity without affecting apolipoprotein CII after STZ administration. Paper-1585829. TNF addition induced rapid (maximum release at 45 minutes) dissociation of LPL protein and activity from its binding sites on cultured porcine aortic endothelial cells. Paper-6539266. TNF effects were studied in human adipose tissue fragments maintained in organ culture in the presence of insulin and dexamethasone to induce high LPL activity. Paper-6253306. The alpha 2-macroglobulin receptor/low density lipoprotein receptor-related protein binds lipoprotein lipase and beta-migrating very low density lipoprotein associated with the lipase. Paper-7881971. CONCLUSIONS: The results of this study suggest that the EPO supplement therapy may reduce plasma RLP-C levels by increasing the plasma LPL and HTGL levels in maintenance-stage HD patients. Paper-1970835. There are a number of potential thrifty genes, including those that regulate lipolysis or code for the beta3-adrenergic receptor, the hormone-sensitive lipase, and lipoprotein lipase. Paper-11594429. ApoE-rich and apoE-poor Type IV VLDL subfractions induced similar increments in cellular esterified cholesterol in the presence of LPL, despite a 4-fold difference in apoE content. Paper-7509479. In conclusion, two different PPAR-alpha ligands (Wy-14643 and BM-17.0744) inhibited cellular LPL activity in cultured cardiomyocytes by a posttranscriptional and posttranslational mechanism. Paper-9018326. In addition, the mRNAs for GM-CSF and TNF-alpha - established ARE-containing targets for HuR- mediated regulation - were upregulated by LPL-mediated lipolysis in ECAP. Paper-12292864. Thus, retention of LDL in the artery wall is initiated by direct LDL-proteoglycan binding but shifts to indirect binding with bridging molecules such as LPL. Paper-12487373. Comparison of apolipoprotein C-II-deficient triacylglycerol-rich lipoproteins and trioleoylglycerol/ phosphatidylcholine- stabilized particles as substrates for lipoprotein lipase. Paper-5158835. Pertussis toxin also significantly reduced TNF- induced inhibition of lipoprotein lipase activity in 3T3-L1 adipocytes and TNF blockade of 3T3-L1 preadipocyte differentiation. Paper-6599105. Given the predominant role of macrophage LPL in atherogenesis, LPL might represent a novel factor underlying the adverse effect of CRP on the diabetic vasculature. Paper-12911091. Under these conditions HL promoted marked reduction in HDL particle size in a process dependent on the concentration of VLDL triacylglycerol while LPL was virtually without effect. Paper-6526397. Suppression of CETP along with the putative activation of lipoprotein lipase due to peripheral hyperinsulinism appears to induce synergistically the increase in HDL-C in IDDM children. Paper-8337671. The results demonstrate that sortilin is a multifunctional receptor that binds lipoprotein lipase and, when expressed on the cell surface, mediates its endocytosis and degradation. Paper-1808100. The maturation of lipoprotein lipase ( LPL) into a catalytically active enzyme was believed to occur only after its transport from the endoplasmic reticulum (ER) to the Golgi apparatus. Paper-9158132. Cachectin/tumor necrosis factor ( TNF-alpha) is a macrophage- secreted cytokine initially found to be a lipoprotein lipase-suppressing serum factor in cachectic, parasite-infected animals. Paper-6581462. Our experiments demonstrate that LCAT promotes HDL3/HDL2 interconversion in native serum irrespective of the presence or absence of triglyceride-rich lipoproteins and lipoprotein lipase. Paper-4173228. LPL increases the cellular uptake of apoE via LRP, and polymorphisms in LPL alter its ability to mediate apoE- LRP interactions, with potential implications for AD pathogenesis. Paper-9516989. For lipoprotein lipase measurement, hepatic lipase is inactivated by a specific antiserum, whereas hepatic lipase is measured after lipoprotein lipase is inactivated by NaCl, 1.0 mol/L. Paper-4302321. Several SNPs (e.g. in APOE, CETP, LPL, APOB and LDLR) influenced multiple phenotypes, while others (e.g. in F7, CRP and FBB) showed restricted association to the index marker. Paper-13802531. In addition, 125I- LPL bound to highly purified LRP in a solid-phase assay with a KD of 18 nM, and this binding could be partially displaced with alpha 2M* (KI = 7 nM) and RAP (KI = 3 nM). Paper-78131. The finding that ANGPTL3 and ANGPTL4 inhibit LPL activity through distinct mechanisms indicates that the two proteins play unique roles in modulation of lipid metabolism in vivo. Paper-13570812. Since TNF-alpha can increase interferon gamma (IFN-gamma)-dependent nitric oxide (NO) production, we studied whether LPL may synergize with IFN-gamma for the induction of macrophage NO production. Paper-230969. ApoC enrichment of TRLP resulted in a reduced capacity to bind LPL and therefore a subsequently reduced capacity to bind b-HS, compared with control TRLP associated with LPL. Paper-833765. To determine whether TNF also inhibits LPL in human adipocytes, primary cultures of isolated human adipocytes were exposed to a spectrum of concentrations of recombinant human TNF. Paper-5920153. The maximal reaction velocity (V(max)) of LPL- induced hydrolysis of n-VLDL was not affected by the addition of increasing concentrations of r- TFPI to the reaction mixture in vitro. Paper-11311118. Addition of NaCl (final concentration 1 M) during the course of lipolysis inhibited lipoprotein lipase as well as the enhancing effect of hepatic lipase on triacylglycerol lipolysis. Paper-7013443. Moreover, the mRNA levels of PPAR-gamma target genes such as lipoprotein lipase ( LPL), CD36, aP2, and liver X receptor-alpha ( LXR-alpha) were downregulated by isorhamnetin. Paper-13587823. Also, apolipoprotein A-II, A-I and apolipoprotein C-I inhibited lipoprotein lipase activity, whereas only apolipoprotein A-II was able to decrease hepatic triacylglycerol activity. Paper-4103234. Lipoprotein lipase- induced lipolysis of human plasma VLDL usually does not yield a complete conversion of VLDL to LDL due to insufficient loss of surface and core lipids and apolipoprotein E. Paper-746402. To determine whether direct uptake of LPL bound to HSPG could account for the non-RAP sensitive LPL uptake and degradation, proteoglycan metabolism was assessed by labeling cells with 35SO4. Paper-918168. Testosterone stimulates lipid mobilization through transcriptional expression of beta-adrenergic receptors via a specific androgen receptor and also inhibits lipoprotein lipase activity. Paper-56568. We also conclude that the VLDL receptor (VLDLr) may contribute significantly to the HASMC binding capacity for postprandial TRL mediated by lipoprotein lipase ( LPL) or LPL-binding molecules. Paper-8867462. To begin localization of these domains, a chimeric lipase was constructed composed of the N-terminal 329 residues of rat hepatic lipase linked to the C-terminal 136 residues of human lipoprotein lipase. Paper-7038670. Cellular catabolism of normal very low density lipoproteins via the low density lipoprotein receptor-related protein/ alpha 2-macroglobulin receptor is induced by the C-terminal domain of lipoprotein lipase. Paper-125583. Human TRLP was enriched with apoE and apoCs and the ability to bind biotin-conjugated heparan sulfate (b-HS) was studied in the presence or absence of heat- inactivated lipoprotein lipase ( LPL). Paper-833765. TNF-alpha, known as an endogenous inhibitor of LPL activity, was detected in both the sera and the extract of tumors from DMBA-treated hamsters, whereas it was not detectable in any control samples. Paper-383654. GH promotes lipolysis via inhibition of lipoprotein lipase, which hydrolyzes triglycerides in the circulation to make them available for triglyceride accumulation in adipose tissue. Paper-10584159. The LPL mass was inversely associated with vWF, suggesting that widespread endothelial cell damage results in a reduction in LPL bound to endothelium in diabetic subjects with microalbuminuria. Paper-1970786. The carboxy-terminal domain of lipoprotein lipase induces cellular catabolism of normal very low density lipoproteins via the low density lipoprotein receptor-related protein/ alpha 2-macroglobulin receptor. Paper-135323. These effects did not require altered skeletal muscle lipoprotein lipase activity but did include differential effects of insulin and leptin on liver apolipoprotein (apo) B and TG metabolism. Paper-13728445. Lactoferrin blocked the LRP-dependent stimulation of cholesteryl ester synthesis in cultured human fibroblasts elicited by apoprotein E-beta-VLDL or lipoprotein lipase-beta-VLDL complexes. Paper-78251. The hTNF-synthetic peptides and hTNF fragments were tested in hTNF receptor binding assays and in two biologic assays: cytolysis of tumor cells and suppression of lipoprotein lipase in adipocytes. Paper-5649414. Our results suggest that variants of APOAV combined with increased triglyceridemia are associated with lower LPL activity in vivo and with disturbances of regulation of NEFA concentration after glucose load. Paper-12932422. Angiopoietin-like protein 4 ( ANGPTL4) is a secreted protein that modulates the disposition of circulating triglycerides ( TG) by inhibiting lipoprotein lipase ( LPL). Paper-13748638. High levels of large HDL2 reflect effective catabolism of triglyceride-rich lipoproteins by LPL whereas low levels of this lipoprotein reflect inadequate LPL activity or elevated hepatic lipase activity. Paper-1633666. Inhibition of insulin, glucose-dependent insulinotropic polypeptide ( GIP) and glucagon-like peptide-1 ( GLP-1) secretion by octreotide has no effect on post-heparin plasma lipoprotein lipase activity. Paper-1884656. Fasting blood samples were taken for glucose (FPG), insulin, HbA(1c), lipids, apolipoproteins (apo), lipoprotein ( LPL) and hepatic lipase ( HL), and cholesterol ester transfer protein ( CETP) activity. Paper-13321346. Although directional changes in lipoprotein lipase ( LpL) and hepatic triglyceride lipase ( HTGL) similar to those found in IDDM after MDI and IP were observed, they were not statistically significant. Paper-905163. Apolipoprotein B metabolism in subjects with deficiency of apolipoproteins CIII and AI. Evidence that apolipoprotein CIII inhibits catabolism of triglyceride-rich lipoproteins by lipoprotein lipase in vivo. Paper-5134296. Recently, using ligand blotting and affinity chromatography we identified a 116-kDa heparin-releasable LPL- binding protein (hrp-116) from endothelial cells which was not a HSPG (Sivaram, P., Klein, M. Paper-116911. These data suggest that the CD14-positive cells are a subpopulation of foam cells that express low levels of lipoprotein lipase, and the lipid content could be a major factor for downregulation of LPL. Paper-7840347. Concomitantly, lipoprotein lipase and hepatic lipase activities increased by 90%, low density lipoprotein receptor activity was stimulated significantly, apoE2 was redistributed to HDL, and HDL were converted to HDL1. Paper-1158281. LS14 cells express many adipose-associated genes, such as adipocyte fatty acid-binding protein (aP(2)), hormone-sensitive lipase, lipoprotein lipase, preadipocyte factor 1, adiponectin, leptin, and IL-6. Paper-10832185. We investigated postheparin plasma activities of hepatic lipase ( HL) and LPL, and plasma activities of CETP and phospholipid transfer protein ( PLTP) in 191 individuals from 37 Finnish FCHL families. Paper-9408601. Apolipoprotein E (apoE) and lipoprotein lipase ( LPL), key proteins in the regulation of lipoprotein metabolism, bind with high affinity to heparin and cell-surface heparan sulfate proteoglycan ( HSPG). Paper-2073636. Semb et al (1987. J. Biol Chem. 262: 8390-8394) have shown that administration of murine TNF to rats decreases lipoprotein lipase ( LPL) in the epididymal fat pad with maximal inhibition requiring several hours. Paper-6382913. These data implicated LRP as mediating LPL- induced lipoprotein degradation and were confirmed by showing that LPL's effects were prevented by an immunoaffinity-isolated polyclonal antibody against LRP. Paper-7865842. Postheparin plasma lipoprotein lipase activity was significantly higher in the IDDM group than in the control group (P < 0.001), whereas postheparin plasma hepatic lipase activities were similar in both groups. Paper-7644118. We conclude that while guinea pig apoC-II is fully competent to stimulate lipoprotein lipase, the sum of several different factors explains the low ability of guinea pig plasma to accomplish stimulation. Paper-1272736. Overall, this study demonstrates that macrophages from FH subjects overproduce LPL and that PDGF present in the serum from FH patients stimulates LPL secretion by control macrophages. Paper-9385659. The independent roles of human lipoprotein lipase ( LPL) and hepatic triglyceride lipase ( HTGL) in determining the distribution of apolipoprotein E (apo E) among the plasma lipoproteins has been studied in vitro. Paper-5973521. It is concluded that proteins I, II and apoprotein E have no effect on the degradation of chylomicrons by lipoprotein lipase and that the hepatic recognition of remnants does not appear to be affected by proteins I and II. Paper-5236593. The effect of apo very low density lipoprotein (apo VLDL) and apoprotein C-II on the phospholipase A1 activity associated with lipoprotein lipase (E.C.3.1.1.3) was studied using purified bovine milk lipoprotein lipase. Paper-3557595. Lipoprotein lipase activity in postheparin plasma was clearly depressed in all patients with Cushing's disease and was associated with moderate hypertriglyceridaemia and slightly lowered HDL cholesterol levels. Paper-6531816. However, the abnormalities observed involve impaired function of LPL in IRS and impaired function of HSL in FCHL, suggesting separate etiologies for the altered lipolysis in these conditions, at least in male subjects. Paper-1212814. The 39.4% increase in reaction velocity of LPL catalysis produced by 10 nM full length recombinant TFPI was comparable to 38.9% increase produced by 5 microM of the basic peptide under the same conditions. Paper-2074878. Furthermore, LPL inhibited the cellular degradation of 125I- alpha 2M* at 37 degrees C. Because both alpha 2M* and RAP interact with LRP, these data suggest that LPL binds specifically to this receptor. Paper-78131. The finding of an increase in the amount of LPL bound to LDL suggests an important mechanism to facilitate the uptake of diabetic LDL by endothelial proteoglycans and collagen in the atherosclerotic plaque. Paper-11022376. In this study, we created a human GPIHBP1 expression vector, introduced the G56R mutation, and tested the ability of the mutant GPIHBP1 to reach the cell surface and bind lipoprotein lipase, chylomicrons, and apo-AV. Paper-13445608. Adiponectin receptor expression is increased by beta cell exposure to the unsaturated FFA oleate, and treatment of insulin-producing cells with globular adiponectin induces lipoprotein lipase expression. Paper-10105035. Fat cells were also enriched by at least 26-fold in the mRNAs for proteins involved in lipolysis such as hormone-sensitive lipase, lipoprotein lipase, adipose tissue triglyceride lipase, and FAT/ CD36. Paper-12832144. Taken together, LPL causes the enhancement of triglyceride-rich lipoproteins binding to the VLDL receptor via both the formation of bridge between lipoproteins and heparan sulfate proteoglycans and its lipolytic effect. Paper-274363. High density lipoproteins with differing apolipoproteins: relationships to postprandial lipemia, cholesteryl ester transfer protein, and activities of lipoprotein lipase, hepatic lipase, and lecithin: cholesterol acyltransferase. Paper-8216001. LPL 447X-containing genotypes (447X+) were significantly decreased in DN patients [18.6 vs 25.6%, odds ratio (OR) = 0.66, p = 0.02], as were APOE epsilon3/epsilon3 genotypes (64.8 vs 73.1%, OR = 0.68, p = 0.01). Paper-12136586. In hepatocytes, fibrates, unlike the thiazolidinediones, induce LPL mRNA levels, whereas in preadipocyte cell lines the PPAR gamma ligand induces LPL mRNA levels much quicker and to a higher extent than fibrates. Paper-1129175. In summary, GH is involved in the regulation of both LPL and HL activity but the effects and mechanisms of action of GH in the regulation of LPL and HL activity in different tissues are not yet fully elucidated. Paper-1998709. We investigated variation in the HMG CoA reductase ( HMGCR), 7-dehydrocholesterol reductase ( DHCR7), lipoprotein lipase ( LPL), low-density lipoprotein receptor ( LDLR), and apolipoprotein E ( APOE) genes. Paper-10263125. Lipoprotein lipase- enhanced binding of lipoprotein(a) [Lp(a)] to heparan sulfate is improved by apolipoprotein E (apoE) saturation: secretion-capture process of apoE is a possible route for the catabolism of Lp(a). Paper-1048275. The carboxyl-terminal domain of lipoprotein lipase binds to the low density lipoprotein receptor-related protein/ alpha 2-macroglobulin receptor ( LRP) and mediates binding of normal very low density lipoproteins to LRP. Paper-115484. Furthermore, intermittent but not continuous PTH treatment suppressed markers of differentiated adipocytes such as mRNA expression of lipoprotein lipase and PPARgamma as well as glycerol 3-phosphate dehydrogenase activity. Paper-12341881. The effect of a synthetic steroid, oxandrolone, on total postheparin plasma lipolytic activity, postherpain hepatic lipase activity, lipoprotein lipase and phospholipase A1 was studied in seven patients with hypertriglyceridemia. Paper-2347660. Whereas thiazolidinediones predominantly affect adipocyte LPL production through activation of PPAR gamma, fibrates exert their effects mainly in the liver via a PPAR alpha- mediated reduction in apo C-III production. Paper-1129175. We found a significant and independent effect of the following polymorphisms on: (i) plasma LDL-C ( Apo E, MTP and Apo B); (ii) plasma HDL-C (HL, FABP-2 and LPL S447X); (iii) plasma triglycerides ( Apo E and Apo A-V). Paper-10425175. We also review in more detail studies that have revealed the association with MI or CHD of polymorphisms in MTHFR, LPL, and APOE by the candidate gene approach and those in LTA and at chromosomal region 9p21.3 by genome-wide scans. Paper-12972001. Studies with purified lipoprotein lipase ( LPL) and hepatic triglyceride lipase ( HTGL) clearly revealed that both enzymes interacted with apoE-2 VLDL (binding, hydrolysis) to a lesser degree compared to control preparations. Paper-4913035. Lipoprotein lipase ( LPL) binds to the low density lipoprotein receptor-related protein (LRP)/alpha 2-macroglobulin receptor and induces catabolism of normal human very low density lipoproteins (VLDL) via LRP in vitro. Paper-125583. The different expression of LPL gene in tissues associated with the increased levels of insulin and TNF-alpha possibly elucidate the underlying mechanisms involving the postprandial hyperlipidemia observed in visceral obesity. Paper-8594559. Structure of heparin fragments with high affinity for lipoprotein lipase and inhibition of lipoprotein lipase binding to alpha 2-macroglobulin-receptor/low-density-lipoprotein-receptor-related protein by heparin fragments. Paper-202443. GPIHBP1 is expressed along the luminal surface of endothelial cells of heart, skeletal muscle, and adipose tissue, and GPIHBP1- expressing cells bind lipoprotein lipase ( LPL) and chylomicrons avidly. Paper-13041320. CONCLUSIONS: Genetic variation in lipoprotein lipase is associated with differences in plasma triglycerides greater than 1 mmol/liter and differences in HDL cholesterol greater than 0.5 mmol/liter. Paper-11772495. Inhibition of cleavage did not interfere with oligomerization of ANGPTL4 or with its ability to inhibit LPL, whereas mutations that prevented oligomerization severely compromised the capacity of the protein to inhibit LPL. Paper-13748638. LOD scores were -14.63, -5.03, and -5.70 for the three LPL polymorphisms (theta=0.00); -9.40, -6.30, and -4.74 for the three HL polymorphisms (theta=0.00); and -15.29 for the HSL polymorphism (theta=0.00). Paper-1020565. Using immunofluorescence it was shown that apoprotein E and lipoprotein lipase follow a distinct route from the sorting compartment to the surface, which is clearly distinguishable from the perinuclear transferrin recycling compartment. Paper-1781066. This study investigated the role of DHT and androgen receptors ( AR) in the regulation of lipolysis and lipogenesis by examining the key enzymes hormone sensitive lipase ( HSL) and lipoprotein lipase ( LPL) respectively. Paper-9477051. Also, LPL- induced binding to cells was blocked by an anti- LPL monoclonal antibody but not by antibodies that are known to block apolipoprotein E- or B-100-mediated binding to low density lipoprotein (LDL) receptors. Paper-7865842. Lipoprotein lipase bound to LDL may facilitate cholesterol accumulation in the artery wall through the attachment of LDL to the proteoglycans expressed on endothelial cells and collagen. Paper-11022376. Preincubation of human macrophages with antioxidants, protein kinase C ( PKC), and mitogen-activated protein kinase ( MAPK) inhibitors prevented CRP- induced LPL expression. Paper-12911091. The anti-inflammatory response of LPL in suppressing TNF-alpha-induced gene expression was a result of its inhibition of NF-kappaB activity by the abrogation of IkappaB-alpha degradation and phosphorylation of the p65 subunit. Paper-10746839. These results indicate that decreased LPL mass and activity in the animal model with visceral obesity is possibly caused by decreased expression of LPL gene in tissues mediated by the increased levels of insulin and TNF-alpha. Paper-8594559. GH treatment decreases adiposity, reduces triglyceride accumulation by inhibiting lipoprotein lipase and enhances lipolysis both via increased hormone-sensitive lipase activity and via induction of beta adrenoreceptors. Paper-8649145. Thus, the VLDL receptor may play a unique role on the vascular endothelium in lipoprotein catabolism by regulating levels of LpL and in the regulation of fibrinolysis by facilitating the removal of urokinase complexed with its inhibitor. Paper-414460. A further reduction in insulin and increase in glucagon secretion occurs during starvation and mild sympathetic activation stimulates hormone.sensitive lipoprotein lipase to increase the release of free fatty acids (FFAs) from adipose tissue. Paper-11436370. The low-density lipoprotein receptor-related protein ( LRP) is a multifunctional receptor that binds to apolipoprotein E-rich lipoproteins, lipoprotein lipase, alpha 2-macroglobulin, lactoferrin, and tissue plasminogen activator. Paper-8232190. Genetic factors contributing to the expression of type III HLP were investigated in 113 hyper- and 52 normolipidemic E2/2 subjects, by testing for polymorphisms in APOC3, APOA5, HL ( hepatic lipase) and LPL ( lipoprotein lipase) genes. Paper-13730626. Total post-heparin lipolytic activity (PHLA), hepatic triglyceride lipase ( HTGL) and protamine inactivated lipoprotein lipase ( LPL) and plasma lipoprotein pattern were investigated in 8 patients with acute renal failure (ARF). Paper-4982450. Each of the ovine activator proteins was as effective as human apolipoprotein C-II ( apo C-II) in activating LPL, with 1 microgram/ml giving near to maximum activation, and in lowering the apparent Km of LPL for triolein substrate. Paper-5669810. Addition of apolipoprotein C-II-deficient triacylglycerol-rich lipoproteins or high-density lipoproteins to trioleoylglycerol/phospholipid particles in the presence of apolipoprotein C-II inhibited lipoprotein lipase activity. Paper-5158835. The reduction in absolute amounts of Apo C-II was also reflected in a reduction of the ratio Apo C-II/Apo C-III in very low density lipoproteins (VLDL) and in a reduction in the ability of the sera to activate skim milk lipoprotein lipase. Paper-4093128. All apoC-III proteins inhibited LPL in the presence or absence of apoC-II, with F64A/W65A displaying the most inhibition, suggesting that apoC-III inhibition of LPL is independent of lipid binding and therefore of apoC-II displacement. Paper-8377933. The activator potency of apoC-II is independent of the method of enrichment of VLDLp with apoC-II: delipidated human apoC-II and apoC-II transferred from human high density lipoproteins activate lipoprotein lipase to equal extents. Paper-3826904. This indicates that the inhibition of the binding of lipoprotein lipase to alpha 2-macroglobulin-receptor/low-density-lipoprotein receptor-related protein by heparin is exclusively mediated by binding of heparin to lipoprotein lipase. Paper-202443. Mixed acyl chain phosphatidylcholine molecules in Triton N-101 micelles were employed as substrates for lipoprotein lipase to test which substrate acyl chain has the greatest effect on activation of the enzyme by apolipoprotein C-II. Paper-5253229. Tumor necrosis factor ( TNF) has been proposed to mediate the hypertriglyceridemic response to infection by either increasing hepatic lipid synthesis or decreasing clearance of triglyceride-rich particles through inhibition of lipoprotein lipase. Paper-6713881. Fenofibrate is a peroxisome proliferator-activated receptor alpha (PPARalpha) agonist which regulates the transcription of genes encoding proteins involved in triglyceride (TG)-rich lipoproteins and lipoprotein lipase ( LPL) metabolism. Paper-9573986. We conclude that VLDL isolated from apo E2 homozygotes and apo E3-Leiden heterozygotes display decreased lipolysis by HSPG- bound LPL due to a defective binding of these lipoproteins to the HSPG- LPL complex. Paper-1414709. Inhibition of PARP-1 enhanced the DNA binding and transactivation of PPAR gamma and increased the transcription of PPAR gamma- target genes including CD36, lipoprotein lipase, and leptin in cultured fibroblasts. Paper-13495637. Heparan sulfate has been further implicated in presentation and stabilization of lipoprotein lipase and hepatic lipase on cell surfaces and in the transport of lipoprotein lipase from extravascular cells to the luminal surface of the endothelia. Paper-11594357. When alcolhol was administered to fed subjects in the evening the postheparin plasma hepatic lipase was significantly decreased in the next morning as compared to corresponding control value but the lipoprotein lipase and Intralipid clearance were not changed. Paper-3107427. Neither LPL activity nor protein was found in medium of cells expressing the mutant hLPL and all detectable protein was present exclusively in the ER identified witha specific antibody against the protein disulfide isomerase ( PDI), an ER marker. Paper-339795. The results provide evidence that lipoprotein lipase binds to the site on alpha2MR/ LRP also available for binding of the carboxyl-terminal domain of RAP and suggest that pro-uPA may bind to or overlap the site available for the amino-terminal domain of RAP. Paper-377111. The current study was conducted to investigate how native VLDL influenced the synthesis and release of TFPI in endothelial cells, and how TFPI affected the LPL-induced hydrolysis of VLDL in vitro and at the endothelial surface. Paper-11311118. Bovine milk LPL displaced both 125I- labeled alpha 2M* and 39-kDa alpha 2M receptor-associated protein (RAP) from the surface of cultured mutant fibroblasts lacking LDL receptors with apparent KI values at 4 degrees C of 6.8 and 30 nM, respectively. Paper-78131. Several candidate gene loci, namely, apolipoprotein (APO) A1, APOA4, APOC3, APOB, APOE, CETP, LPL, and FABP2, have been shown to explain a significant, but still rather small, proportion of the interindividual variability in dietary response. Paper-11594036. Adipose tissue LPL activity decreased and postheparin plasma HL activity increased after 14 days of GH treatment irrespective of the mode of GH administration, whereas GH treatment had no effect on postheparin plasma LPL activity. Paper-522616. Functional studies revealed that all mutant alleles of ANGPTL3 and ANGPTL4 that were associated with low plasma TG levels interfered either with the synthesis or secretion of the protein or with the ability of the ANGPTL protein to inhibit LPL. Paper-13566492. 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. Paper-5187940. Prolactin stabilizes and promotes transcription of casein mRNA; may stimulate synthesis of alpha-lactalbumin, the regulatory protein of the lactose synthetase enzyme system; and increases lipoprotein lipase activity in the mammary gland. Paper-6784220. This receptor is a large endocytotic receptor that mediates the catabolism of a number of molecules known to be important in vascular biology, including apolipoprotein E- and lipoprotein lipase-enriched lipoproteins, thrombospondin, and plasminogen activators. Paper-295652. Although LPL alone had no effect on Stat1 activation, LPL enhanced IFN-gamma-induced phosphorylation of Stat1 on tyrosine 701 and serine 727, as well as Stat1-mediated transactivation. Paper-10746839. We conclude that lipoprotein lipase strongly enhances the binding of apoE-containing lipoproteins to LRP and therefore might play an important role in chylomicron catabolism not only because of its lipolytic activity but also because of its structural properties. Paper-7134920. APO A1 (A/G -75 and C/T +83) and APO C3 (C/G 3'UTR) non-coding sequences, CETP (Taq 1B), LPL (D9N), APO E (varepsilon2, varepsilon3, varepsilon4,), PON-1 (Q192R), and two LCAT variants Arg(147)-->Trp and Tyr(171)-->Stop were tested by PCR-RFLP. Paper-13541065. These studies suggest that arterial LDL- CE delivery via SU can be an important mechanism in vivo and that dietary influences on arterial LPL levels and atherogenesis modulate arterial LDL- CE delivery, cholesterol deposition, and SU. Paper-10800993. Changes in HL activity seem to be an important mechanism for the disturbance of cholesterol metabolism in thyroid dysfunction while the thyroid hormone influence on LPL seems to be of importance mainly for the disturbance in triglyceride metabolism. Paper-4387287. We suggest that while the binding of apoC-II to the lipid surface promotes the formation of a high-affinity complex of apoC-II and LpL, activation occurs via direct helix-helix interactions between apoC-II39-62 and the loop covering the active site of LpL. Paper-2186132. Apoprotein-free heparin- binding and non- binding chylomicrons were used as substrates to test the effects on lipoprotein lipase activity of (a) chylomicron protein I; (b) the mixture of proteins I, II and apoprotein E and (c) human beta 2-glycoprotein I. Paper-5236593. We also found that the cytotoxic activity of TNF on A673 cells and its inhibitory effect on lipoprotein lipase were parallel with the cytotoxic activity on L929 cells, but the growth-enhancing activity on FS-4 cells and the cytotoxic activity on endothelial cells were not. Paper-5536373. The effects that PPAR alpha exerts on triglyceride-rich lipoproteins is due to their stimulation of lipoprotein lipase and repression of apolipoprotein CIII expression, while the effects on high-density lipoproteins depend upon the regulation of apolipoproteins AI and AII. Paper-8659018. 3. Inhibition of lipoprotein lipase synthesis in similar experiments in mammals has been attributed to the effects of TNF-alpha and/or IL-1, but recombinant human TNF-alpha and IL-1 had no effect on lipoprotein lipase activity in chicken adipocytes. Paper-6440955. Maximum likelihood linkage analyses were performed to test for linkage between serum apoB levels and several candidate gene markers including apolipoprotein B, lipoprotein lipase, hepatic lipase, cholesterol ester transfer protein, and apolipoprotein AI in a large pedigree. Paper-124255. Recent studies demonstrate that LPL binds to three members of the low density lipoprotein (LDL) receptor family, including the LDL receptor-related protein ( LRP), GP330/ LRP-2, and very low density lipoprotein (VLDL) receptors and induces receptor-mediated lipoprotein catabolism. Paper-619349. These include alpha 2-macroglobulin-protease complexes, free plasminogen activators as well as plasminogen activators complexed with their inhibitors, and beta-migrating very low density lipoproteins complexed with either apolipoprotein E or lipoprotein lipase. Paper-8200060. These genes include scavenger receptor, 15-lipoxygenase, monocyte chemoattractant protein-1, macrophage colony stimulating factor-1, lipoprotein lipase, platelet-derived growth factor, tissue factor, apolipoprotein E, stromelysin, different adhesion molecules and various cytokines. Paper-7250370. Most missense mutations of the lipoprotein lipase ( LPL) gene identified among LPL-deficient subjects cluster in a segment of the sequence that encodes the catalytic triad as well as functional elements involved in the activation of the lipase at lipid-water interfaces. Paper-7299522. To elucidate the mechanism by which apolipoprotein C-II ( apoC-II) enhances the activity of lipoprotein lipase ( LpL), discoidal phospholipid complexes were prepared with apoC-III and di[(14)C]palmitoyl phosphatidylcholine (DPPC) and containing various amounts of apoC-II. Paper-4351820. These data are consistent with a model for activation of lipoprotein lipase in which residues 56-79 bind to lipoprotein lipase and alter the interaction of the sn-2 acyl chain of the phosphatidylcholine (PC) substrate or the lysoPC product within the activated state complex. Paper-5253229. Plasma lipoprotein levels and the postheparin activities of hepatic lipase and lipoprotein lipase were measured in 28 women with systemic lupus erythematosus ( SLE) who were treated with prednisone, 10 women with SLE not treated with prednisone, and 15 normal women. Paper-5909175. In pulse-chase experiments, addition of LPL during the chase period produced a decrease in secretion of apoprotein E from human monocyte-derived macrophages, from the human monocytic THP1 cell line, and from J774 cells transfected to constitutively express a human apo E cDNA. Paper-1027210. Common variants in the cholesteryl ester transfer protein (CETP-629C/A), lipoprotein lipase ( LPL S447X), hepatic lipase (HL-480C/T) and apolipoprotein E (apoE e2/ e3/e4) genes were studied in relation to LDL particle size distribution in 377 healthy, middle-aged men. Paper-9753557. A cohort of 1002 heterozygous FH patients was genotyped for polymorphisms in the genes encoding for ATP-binding cassette transporter A1, apolipoprotein (apo) AIV, apoCIII, apoE, cholesteryl transfer ester protein, hepatic lipase, lipoprotein lipase, and two paraoxonases. Paper-10995262. In vitro experiments indicated that, although sera from the apo CIII-apo-AI deficient patients were able to normally activate purified LPL, increasing volumes of these sera did not result in the progressive inhibition of LPL activity demonstrable with normal sera. Paper-5134296. In contrast, LPL monomers were not able to mediate binding to immobilized alpha 2MR/ LRP, presumably because of cross-inhibition due to close relation between the binding regions for the lipoprotein and for the receptor in the carboxyl-terminal domain of the LPL monomer. Paper-7881971. Lp (a) binding to platelets mediated by apo (a) increases platelet intracellular c-AMP levels in resting platelets, and decreases platelet production of thromboxane A2 and fibrinogen binding to platelets all of which reduce platelet aggregation. Paper-12626149. These results are consistent with a proposition that HL has a direct effect on HDL particle size in a process which is dependent on concurrent lipid transfers between HDL and VLDL and that LPL reduces the effect of HL by reducing the concentration of VLDL triacylglycerol. Paper-6526397. We now show in approximately 1 in 20 males with proven atherosclerosis that an Asn291Ser mutation in the human lipoprotein lipase ( LPL) gene is associated with significantly reduced HDL levels (P = 0.001) and results in a significant decrease in LPL catalytic activity (P < 0.0009). Paper-326865. The inverse relationship between TFPI and LPL suggests that increased free TFPI concentrations as a compensatory response of the endothelium to prevent atherothrombotic processes compete with and displace LPL on endothelial surface, resulting in reduced LPL and low HDL-C. Paper-2073652. Loss of apoprotein C-peptides from HDL2 associated with activation of lipoprotein lipase, and clearance of VLDL, could have caused redistribution of C-apoproteins between HDL3 leading to the changes seen, with the establishment of a new equilibrium with continued training by 10 weeks. Paper-3746422. The binding of gp330 to apoJ could be competitively inhibited with excess apoJ as well as with the gp330 ligands apolipoprotein E, lipoprotein lipase, and the receptor-associated protein, a 39-kDa protein that acts to antagonize binding of all known ligands for gp330 and LRP. Paper-246449. SorLA binds several ligands, including neurotensin, platelet-derived growth factor-bb, and lipoprotein lipase, and via complex-formation with the amyloid precursor protein it downregulates generation of Alzheimer's disease- associated Abeta-peptide. Paper-12557359. Lipoprotein lipase ( LpL) can mediate cellular uptake of chylomicron and VLDL remnants via binding to heparan sulfate proteoglycans ( HSPG) and the endocytic alpha2-macroglobulin receptor/low density lipoprotein receptor-related protein (alpha2MR/ LRP). Paper-946681. RESULTS: Of the 12 genes previously associated with CHD risk, in stepwise multivariate risk analysis, uncoupling protein 2 ( UCP2; P = 0.0001), apolipoprotein E ( APOE; P = 0.0003), lipoprotein lipase ( LPL; P = 0.007), and apolipoprotein AIV ( APOA4; P = 0.04) remained in the model. Paper-12392604. In parallel, a rapid and dramatic decrease in the level of mRNA encoding for several adipocyte-specific proteins such as adipocyte lipid-binding protein, hormone-sensitive lipase, lipoprotein lipase, and peroxisome proliferation activating receptor-gamma2 was observed in isolated adipocytes. Paper-10023593. OBJECTIVE: The aim of the study was to examine the impact of the leucine7 to proline7 (Leu7Pro) polymorphism of the NPY gene on postprandial (PP) lipemia, post-heparin plasma lipoprotein lipase ( LPL) and hepatic lipase ( HL) activities, and the response of serum lipids to a reduced fat diet. Paper-9382983. To date, transgenes for human apo(a), apoA-I, apoB, apoE2, apoE3, hepatic lipase, lecithin: cholesterol acyltransferase ( LCAT), lipoprotein lipase, 15-lipoxygenase, as well as for rabbit apolipoprotein B mRNA-editing enzyme catalytic polypeptide 1 ( APOBEC-1), have been expressed in rabbits. Paper-10587422. CONCLUSION: Since cachectin/ TNF suppresses lipoprotein lipase in adipocytes in vitro, and causes weight loss under experimental conditions, the findings of raised levels of cachectin/ TNF in patients with AIDS may have relevance to the pathogenesis of cachexia. Paper-5906264. To study the effects of diabetes on lipoprotein profiles and atherosclerosis in a rodent model, we crossed mice that express human apolipoprotein B ( HuB), mice that have a heterozygous deletion of lipoprotein lipase ( LPL1), and transgenic mice expressing human cholesteryl ester transfer protein ( CETP). Paper-9249431. The OSM- induced down-regulation of adiponectin expression was correlated with the down-regulation of PPARgamma2 and lipoprotein lipase, markers for adipogenic differentiation, and depletion of intracellular lipid droplets, suggesting dedifferentiation of adipocytes in response to OSM. Paper-12373977. Based on our structure we suggest a new mechanism of lipoprotein lipase activation in which both helices of apoC-II(44-79) remain lipid bound, while the seven-residue interhelical linker extends away from the lipid surface in order to project Tyr63 into the apoC-II binding site of lipoprotein lipase. Paper-8477951. Among three lipases in the lipase gene family, hepatic lipase ( HL), lipoprotein lipase, and pancreatic lipase, HL exhibits the lowest intracellular specific activity (i.e. minimal amounts of catalytic activity accompanied by massive amounts of inactive lipase mass in the endoplasmic reticulum (ER)). Paper-10369012. The 5 gene SNPs were cholesteryl ester transfer protein ( CETP) TaqIB (N = 3219), ATP-binding cassette ( ABCA1) G596A (N = 3302), lipoprotein lipase ( LPL) HindIII (N = 909), plasminogen activator inhibitor, type 1 ( PAI1), 4G/5G (N = 1142), and hepatic lipase ( HL) C-541T (N = 4704). Paper-10781391. After overnight culture (16 h), 1 microM Wy-14643 and 10 microM BM-17.0744 decreased total cellular LPL activity to approximately 50% of control with no change in enzyme synthesis or mass; as a consequence, PPAR-alpha activation produced a significant decrease in LPL specific activity (mU/ng LPL protein). Paper-9018326. Treatment of heparinase reduced the effect of LPL-mediated binding at 4 degrees C, but the inhibitory effect was lower at 37 degrees C. Pseudomonas LPL also enhanced the binding of human fasted VLDL to the VLDL receptor at 37 degrees C in CHO cells overexpressing the human VLDL receptor. Paper-274363. PATIENTS AND METHODS: Lipoprotein profile and major lipoprotein regulators such as lecithin:cholesterol acyltransferase ( LCAT), hepatic triglyceride lipase ( HTGL), lipoprotein lipase, and cholesteryl ester transfer protein in a Japanese patient with BRIC were serially examined during a bout of cholestasis. Paper-13316101. The concept that adipose cells behave as secretory cells is now emerging from in vitro data, since secretion of various proteins ( LPL, adipsin, CETP) and important metabolites (fatty acids, monobutyrin, androgens, estrogens, prostaglandins) takes place both constitutively and upon hormonal stimulation. Paper-7447158. CONCLUSIONS: We conclude that the LPL Ser447-Stop mutation has a significant positive effect on LPL activity and HDL cholesterol and triglyceride levels and that certain subgroups of CAD patients carrying the Ser447-Stop mutation will have less adverse metabolic effects when placed on beta-blockers. Paper-1062798. Phospholipid transfer protein ( PLTP), hepatic lipase ( HL), and lipoprotein lipase ( LPL) have all been reported to be intricately involved in HDL metabolism but the effect of PLTP on the apolipoprotein B-containing lipoproteins relative to that of HL and LPL has not been established. Paper-9603843. We therefore sought conclusive evidence for these allegations by investigating the effects of the LPL Ser447-Stop mutation on LPL and hepatic lipase ( HL) activity, HDL cholesterol, and triglycerides in a large group of CAD patients (n = 820) with normal to mildly elevated total and LDL cholesterol levels. Paper-1062798. In vitro lipoprotein lipase enhances the cholesteryl ester transfer protein (CETP)- mediated transfer of cholesteryl esters from high density lipoproteins (HDL) to very low density lipoproteins as a result of lipolysis- induced alterations in lipoprotein lipids that lead to increased binding of CETP. Paper-5222648. In this study we investigated the associations between polymorphisms of CETP (mutations in intron 14 and exon 15, and Taq1B), hepatic lipase (C-514T), lipoprotein lipase ( PvuII and HindIII), and ATP-binding cassette transporter 1 (R219K) loci and longevity in 256 centenarians and 190 healthy younger controls. Paper-9893051. METHODS AND RESULTS: Using an information theory-based model, we measured the individual information content (R(i), in bits) of splice sites adjacent to 289 mutations (including 31 splice-site mutations) in the atherosclerosis candidate genes APOAII, APOB, APOCII, APOE, CBS, CETP, LCAT, LIPA, LDLR, and LPL. Paper-1956493. In an attempt to determine whether the increased import of triacylglycerol-derived NEFAs can also affect UCP expression, we determined the mRNA levels of UCP-1, UCP-2 and UCP-3 in BAT and muscle of induced mutant mouse lines that overexpressed or lacked lipoprotein lipase ( LPL) in these tissues. Paper-8784910. Using a selective immunochemical method, the activities of postheparin plasma lipoprotein lipase ( LPL) and hepatic triglyceride lipase ( HTGL) were measured in 7 children with newly diagnosed IDDM, 39 on a conventional subcutaneous insulin regimen (CSC), and 11 children receiving continuous subcutaneous infusion of insulin (CSII). Paper-4502237. These kinetic studies suggest that apoC-II enhances phospholipid hydrolysis by LpL in apoC-III-DPPC discoidal complexes and VLDL(p) mainly by increasing the V(max) of the enzyme for the substrates, whereas the activator protein primarily causes a decrease in the apparent K(m) for triacylglycerol hydrolysis.-Shirai, K., T. Paper-4351820. Lipoprotein lipase ( LPL) plays a central role in triglyceride metabolism, and the LPL gene T495G HindIII polymorphism has been associated with variations in lipid levels and heart disease in Caucasians with the more common H+ allele being associated with adverse lipid profiles and increased risk of CHD. Paper-9862026. Confirming previous reports, HL preferentially hydrolysed high density lipoprotein (HDL) triacylglycerol while LPL hydrolysed predominantly very low density lipoprotein (VLDL) triacylglycerol; however, neither lipase altered HDL particle size unless both VLDL and cholesteryl ester transfer protein ( CETP) were present. Paper-6526397. Up-regulation of LDL receptors by lovastatin treatment of normal human foreskin fibroblasts (FSF cells) resulted in an increase in LPL- induced VLDL binding and catabolism to a level that was 10-15-fold greater than in LDL receptor-negative fibroblasts, despite similar LRP activity in both cell lines. Paper-619349. Linkage analyses with penetrance parameter estimates from the segregation analysis excluded tight linkage between the detected major locus and markers for the following candidate loci: the apoAI/apoCIII genomic region (P < .05), apoB (P < .01), hepatic lipase (P < .001), lipoprotein lipase (P < .001), and the LDL receptor (P < .001). Paper-387216. We found complete cross-competition between carboxyl-terminal RAP fragments and fragments of lipoprotein lipase containing the recently identified binding domain for alpha 2MR/ LRP (Nykjaer, A., Nielsen, M., Lookene, A., Meyer, N., Røigaard, H., Etzerodt, M., Beisiegel, U., Olivecrona, G., and Gliemann, J. (1994) J. Biol. Chem. 269, 31747-31755). Paper-377111. Synthetic peptide 56-79, which does not associate with lipid, did not activate LpL at surface pressures greater than 30 mN/m; apoC-II is active up to 34 mN/m. However, acylation of the NH2-terminus of peptide 56-79 with palmitoyl chloride gave nearly identical LpL activating properties as compared to apoC-II. Paper-5292536. Genotyping of angiotensin-converting enzyme, adrenergic receptor beta(3), aldehyde dehydrogenase 2, calpastatin, connexin 37, hepatic lipase, lipoprotein lipase, peroxisome proliferator-activated receptor gamma, thyrotropin-releasing hormone receptor, and von Willebrand factor also was performed in these subjects. Paper-12918536. We conclude that in LDL receptor-positive cells, the LPL- mediated binding of LDL and VLDL to HSPG is followed by internalization of the lipoproteins mainly through the rapid process of the classical LDL receptor recycling system, whereas only a minor portion is internalized via the much slower process of HSPG uptake. Paper-7862949. The CRF-induced hypertriglyceridemia, abnormal composition, and impaired clearance of triglyceride-rich lipoproteins and their remnants are primarily due to downregulation of lipoprotein lipase, hepatic lipase, and the very-low-density lipoprotein receptor, as well as, upregulation of hepatic acyl-CoA cholesterol acyltransferase ( ACAT). Paper-10825984. With a synthetic emulsion of long-chain triacylglycerols, both the wild-type guinea pig apoC-II and the insertion mutant stimulated lipoprotein lipase similar to human apoC-II, but with chylomicrons from an apoC-II-deficient patient, 5- to 10-fold more of both wild-type guinea pig apoC-II and the insertion mutant were needed. Paper-1272736. OBJECTIVE: To evaluate the effect of a moderate dose of fish oil on glycemic control and in vivo insulin action in type 2 diabetic men with elevated plasma triacylglycerols and to determine the effect of the same treatment on gene expression of GLUT4, lipoprotein lipase ( LPL), and hormone-sensitive lipase ( HSL) in the abdominal adipose tissue. Paper-1478174. We investigated genes involved in carbohydrate and fatty acid handling [ lipoprotein lipase, acetyl-coenzyme A carboxylase ( ACC) 2, hormone-sensitive lipase, hexokinase II, and glucose transporter 4] and measured protein levels of CD36 and phosphorylated and unphosphorylated ACC2 and the activity of adenosine monophosphate-activated kinase. Paper-11474373. The chi(2) test and multivariable logistic regression analysis revealed that seven polymorphisms of APOA5, APOC3, APOA1, ACAT2, and LPL were significantly associated with hypertriglyceridemia, six polymorphisms of APOA5, LIPC, and CYP3A4 with low HDL-cholesterol, and three polymorphisms of APOE and CCR2 with high LDL-cholesterol in subject panel A. Paper-12594234. Mice carrying the combined lipase deficiency (cld) mutation show severe hypertriglyceridemia owing to a decrease in the activity of LPL and a related enzyme, hepatic lipase ( HL), caused by impaired maturation of nascent LPL and hepatic lipase polypeptides in the endoplasmic reticulum ( ER). Paper-12548545. In differentiated 3T3-L1 adipocytes, GIP, in the presence of insulin, increased LPL activity and triglyceride accumulation through a pathway involving increased phosphorylation of protein kinase B ( PKB) and reductions in phosphorylated LKB1 and AMP-activated protein kinase (AMPK). Paper-12459872. Analyses of covariance adjusting for age, body mass index, hyperlipidemia, diabetes, smoking, drinking, and antihypertensive medication revealed that 17 polymorphisms in 16 genes ( APOB, CAST, CLCNKB, CTNS, GHR, GYS1, HF1, IKBKAP, KCNJ11, LIPC, LPL, P2RY2, PON2, SLC4A1, TRH, VWF) were significantly associated with blood pressure variations. Paper-12339895. These synonyms are used for gene LPL (lipoprotein lipase): Lipoprotein lipase, LIPD, HDLCQ11. These accession numbers are used for gene LPL: X54516 (NCBI_GENBANK__AC), Q53HW6 (UNIPROT__AC), CR605471 (NCBI_GENBANK__AC), B2R5T9 (UNIPROT__AC). LPL is a homologue of LPL (lipoprotein lipase) from Bos taurus. LPL is a homologue of LPL (lipoprotein lipase) from Pan troglodytes. LPL is a homologue of LPL (lipoprotein lipase) from Gallus gallus. LPL is a homologue of LPL (lipoprotein lipase) from Canis lupus familiaris. LPL is a homologue of Lpl (lipoprotein lipase) from Mus musculus. LPL is a homologue of Lpl (lipoprotein lipase) from Rattus norvegicus. LPL is a homologue of lpl (lipoprotein lipase) from Danio rerio. LPL is a homologue of LOC568880 (similar to lipoprotein lipase) from Danio rerio. LPL is a homologue of AgaP_AGAP003749 (AGAP003749-PA) from Anopheles gambiae str. PEST. Important links ! iHOP - Information Hyperlinked over Proteins . Concept & Implementation by Robert Hoffmann.