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)

The characteristics of lipoprotein lipolytic activity in lysosomes after the administration of Triton WR-1339 were studied, and the observed decrease in the density of the particles is discussed. The light mitochondrial fraction prepared from rat liver according to the method of De Duve et al. (Biochem. J. (1955) 60, 604) was used as a crude lysosomal fraction, in which acid phosphatase and lipoprotein lipase activities were concentrated. The lipoprotein lipolytic activity of lysosomes had a pH optimum of 4.0. The activity was strongly inhibited by Triton WR-1339 in vitro at low concentrations, while the acid lipase activity was almost unaffected, though relatively high concentration of the detergent significantly inhibited the latter activity. When Triton WR-1339 administered to rats (150 mg/100 g body weight), the activities of both the lipoprotein lipase and acid lipase of lysosomes from the treated rats decreased to one-third of those of control rats. Low-density and high-density lysosomes were partially purified from the light mitochondrial fraction from Triton WR-1339-treated and silver colloid-treated rats, respectively, by sucrose density gradient centrifugation. The low-density lysosomes (d = 1.00-1.13) from Triton WR-1339 administered rats had approximately 4 and 3 times higher contents of triglyceride and cholesterol, respectively, than the high-density lysosomes (d greater than 1.30) from silver colloid-treated rats. In view of these results and the fact that the density of Triton WR-1339 is quite high (at least d = 1.20), the decrease in density of hepatic lysosomes upon Triton WR-1339 administration cannot be due simply to incorporation of the detergent, and may rather be a result of incorporation and accumulation of some lipid(s) (possibly as lipoprotein) into lysosomes together with Triton WR-1339.
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PMID:Effects of Triton WR-1339 on lipoprotein lipolytic activity and lipid content of rat liver lysosomes. 724 Jan 28

A lipase from Aspergillus oryzae was purified by ammonium sulfate fractionation, anion exchange chromatography, hydrophobic interaction chromatography, and anion exchange chromatography. The purified enzyme was a monomeric protein with a molecular mass of 41 kDa estimated by SDS-PAGE and 39 kDa by gel filtration. The optimum pH at 30 degrees C and optimum temperature at pH 7.0 were 7.0 and 30 degrees C, respectively. The enzyme was stable over a pH range of 6-9 at 25 degrees C for 18 h, and up to 30 degrees C at pH 7.0 for 3 h. Ag+, Fe3+, Hg2+, Cu2+, and Zn2+ inhibited the enzyme activity severely. The enzyme was a lipase that hydrolyzed monoacylglycerols and diacylglycerols, but did not hydrolyze triacylglycerols. The N-terminal amino acid sequence of the enzyme was highly homologous with that of the mono- and diacylglycerol lipase from Penicillium camembertii U-150.
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PMID:Purification and characterization of a lipase from Aspergillus oryzae. 767 Jan 77

Apolipoproteins (apo) C-I, C-II, and C-III play crucial roles in intravascular lipid metabolism. Whereas apo C-II is an obligate cofactor for lipoprotein lipase, apo C-III was shown to inhibit its action. Apo C-I can be a potent cofactor of human lecithin:cholesterol acyltransferase. Structural mutants and deficiencies of apo C-II lead to hypertriglyceridemia. A similar phenotype is associated with apo C-III mutants and is inducible by overexpression of human apo C-III in transgenic animals. No structural variant has so far been reported for apo C-I. The present paper describes a rapid semi-automated procedure for isoelectric focusing analysis of these C-apolipoproteins from whole plasma or serum and their visualization by immunofixation and silver staining. The procedure allows detection of charged variants of C-apolipoproteins. As applied to 295 patients with coronary heart disease and 85 controls, it also serves to detect deficiency syndromes of these apolipoproteins. The procedure provides reliable, easy and quick analysis of C-apolipoproteins applicable as a routine or screening procedure not restricted to specialized laboratories.
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PMID:Semi-automated rapid isoelectric focusing of apolipoproteins C from human plasma using Phastsystem and immunofixation. 1047 72

The short tandem repeat (STR) polymorphism of the lipoprotein lipase (LPL) locus was amplified by PCR and analyzed using denaturing polyacrylamide gel electrophoresis followed by silver staining. Among 158 DNA samples from the Japanese population, six alleles were observed. When the sequences of the allelic products were compared, each allelic segment contained 7 and 9-13 TTTA tetranucleotide repeat motifs. Genotypic distribution met Hardy-Weinberg expectations, and included heterozygosity was 48.8%. Most of the Japanese genotypes allele 10. When PCR amplification efficiency for the LPL locus from degraded DNA was compared with that for the D21S11 locus in terms of amplification size, increase in amplification size showed a considerable influence on amplification efficiency, producing inaccurate amplification, such as unbalanced amplification, or amplification of non-target PCR products. These results suggest that reduction in amplification size increases the accuracy and efficiency of PCR amplification from highly degraded DNA.
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PMID:Polymorphism of LPL Locus in Japanese and comparison of PCR amplification efficiency from degraded DNA between LPL locus and the D21S11. 1682 10

Reduced levels of high-density lipoproteins (HDL) in non-obese and obese states are associated with increased risk for the development of coronary artery disease. Therefore, it is imperative to determine the mechanisms responsible for reduced HDL in obese states and, conversely, to examine therapies aimed at increasing HDL levels in these individuals. This paper examines the multiple causes for reduced HDL in obese states and the effect of exercise and diet--two non-pharmacologic therapies--on HDL metabolism in humans. In general, the concentration of HDL-cholesterol is adversely altered in obesity, with HDL-cholesterol levels associated with both the degree and distribution of obesity. More specifically, intra-abdominal visceral fat deposition is an important negative correlate of HDL-cholesterol. The specific subfractions of HDL that are altered in obese states include the HDL2, apolipoprotein A-I, and pre-beta1 subfractions. Decreased HDL levels in obesity have been attributed to both an enhancement in the uptake of HDL2 by adipocytes and an increase in the catabolism of apolipoprotein A-I on HDL particles. In addition, there is a decrease in the conversion of the pre-beta1 subfraction, the initial acceptor of cholesterol from peripheral cells, to pre-beta2 particles. Conversely, as a means of reversing the decrease in HDL levels in obesity, sustained weight loss is an effective method. More specifically, weight loss achieved through exercise is more effective at raising HDL levels than dieting. Exercise mediates positive effects on HDL levels at least partly through changes in enzymes of HDL metabolism. Increased lipid transfer to HDL by lipoprotein lipase and reduced HDL clearance by hepatic triglyceride lipase as a result of endurance training are two important mechanisms for increases in HDL observed from exercise.
Obesity (Silver Spring) 2007 Dec
PMID:Effect of obesity on high-density lipoprotein metabolism. 1819 93

Adipocyte dysfunction is strongly associated with the development of obesity, which is a major risk factor for many disorders including diabetes, hypertension, and heart disease. It is generally accepted that the regulation of adipogenesis or adipokines expression prevents obesity. In this study, we show that isorhamnetin inhibits adipocyte differentiation, as evidenced by reduced triglyceride (TG) accumulation and glycerol-3-phosphate dehydrogenase (GPDH) activity. At the molecular level, the mRNA expression levels of peroxidase proliferator-activated receptor-gamma (PPAR-gamma) and CCAAT/enhancer-binding protein-alpha (C/EBP-alpha), which are the major adipogenic transcription factors, were markedly reduced by isorhamnetin. However, the mRNA levels of C/EBP-beta and -delta, the upstream regulators of PPAR-gamma and C/EBP-alpha, were not reduced by isorhamnetin. 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. We also showed that isorhamnetin inhibits the expression and secretion of adiponectin, and the results of adiponectin promoter assays suggest the inhibition of PPAR-gamma expression as a possible mechanism underlying the isorhamnetin-mediated effects. Taken together, these results indicate that isorhamnetin inhibits adipogenesis through downregulation of PPAR-gamma and C/EBP-alpha.
Obesity (Silver Spring) 2009 Feb
PMID:Isorhamnetin represses adipogenesis in 3T3-L1 cells. 1894 72

Abdominal visceral tissue (VAT) and subcutaneous adipose tissue (SAT), comprised of superficial-SAT (sSAT) and deep-SAT (dSAT), are metabolically distinct. The antidiabetic agents thiazolidinediones (TZDs), in addition to their insulin-sensitizing effects, redistribute SAT suggesting that TZD action involves adipose tissue depot-specific regulation. We investigated the expression of proteins key to adipocyte metabolism on differentiated first passage (P1) preadipocytes treated with rosiglitazone, to establish a role for the diverse depots of abdominal adipose tissue in the insulin-sensitizing effects of TZDs. Adipocytes and preadipocytes were isolated from sSAT, dSAT, and VAT samples obtained from eight normal subjects. Preadipocytes (P1) left untreated (U) or treated with a classic differentiation cocktail (DI) including rosiglitazone (DIR) for 9 days were evaluated for strata-specific differences in differentiation including peroxisome proliferator-activated receptor-gamma (PPAR-gamma) and lipoprotein lipase (LPL) expression, insulin sensitivity via adiponectin and glucose transport-4 (GLUT4), glucocorticoid metabolism with 11 beta-hydroxysteroid dehydrogenase type-1 (11 beta HSD1), and alterations in the adipokine leptin. While depot-specific differences were absent with the classic differentiation cocktail, with rosiglitazone sSAT had the most potent response followed by dSAT, whereas VAT was resistant to differentiation. With rosiglitazone, universal strata effects were observed for PPAR-gamma, LPL, and leptin, with VAT in all cases expressing significantly lower basal expression levels. Clear dSAT-specific changes were observed with decreased intracellular GLUT4. Specific sSAT alterations included decreased 11 beta HSD1 whereas secreted adiponectin was potently upregulated in sSAT with respect to dSAT and VAT. Overall, the subcompartments of SAT, sSAT, and dSAT, appear to participate in the metabolic changes that arise with rosiglitazone administration.
Obesity (Silver Spring) 2008 Sep
PMID:Subcutaneous abdominal adipose tissue subcompartments: potential role in rosiglitazone effects. 1918 24

We have previously shown that combined amylin + leptin agonism elicits synergistic weight loss in diet-induced obese (DIO) rats. Here, we assessed the comparative efficacy of amylin, leptin, or amylin + leptin in the maintenance of amylin + leptin-mediated weight loss. DIO rats pretreated with the combination of rat amylin (50 microg/kg/day) and murine leptin (125 microg/kg/day) for 4 weeks were subsequently infused with either vehicle, amylin, leptin, or amylin + leptin for an additional 4 weeks. Food intake, body weight, body composition, plasma parameters, and the expression of key metabolic genes in liver and white adipose tissue (WAT) were assessed. Amylin + leptin treatment (weeks 0-4) reduced body weight to 87.5% of baseline. Rats subsequently maintained on vehicle or leptin regained all weight (to 104.2 and 101.2% of baseline, respectively), those maintained on amylin had partial weight regain (97.0%). By contrast, weight loss was largely maintained with continued amylin + leptin treatment (91.4%), associated with a 10% decrease in adiposity. Cumulative food intake (weeks 5-8) was reduced by amylin and amylin + leptin, but not by leptin alone. Amylin + leptin, but not amylin or leptin alone, reduced plasma triglycerides (by 55%), total cholesterol (by 19%), and insulin (by 57%) compared to vehicle. Amylin + leptin also reduced hepatic stearoyl-CoA desaturase-1 (Scd1) mRNA, and increased WAT mRNA levels of adiponectin, fatty acid synthase (Fasn), and lipoprotein lipase (Lpl). We conclude that, in DIO rats, maintenance of amylin + leptin-mediated weight loss requires continued treatment with both agonists, and is accompanied by sustained improvements in body composition, and indices of lipid metabolism and insulin sensitivity.
Obesity (Silver Spring) 2010 Jan
PMID:Interaction of leptin and amylin in the long-term maintenance of weight loss in diet-induced obese rats. 1954 17

Apolipoprotein A5 (APOA5) and lipoprotein lipase (LPL) proteins interact functionally to regulate lipid metabolism, and single-nucleotide polymorphisms (SNPs) for each gene have also been associated independently with obesity risk. Evaluating gene combinations may be more effective than single SNP analyses in identifying genetic risk, but insufficient minor allele frequency (MAF) often limits evaluations of potential epistatic relationships. Populations with multiple ancestral admixtures may provide unique opportunities for evaluating genetic interactions. We examined relationships between LPL m107 (rs1800590) and APOA5 S19W (rs3135506) and lipid and anthropometric measures in Caribbean origin Hispanics (n = 1,019, aged 45-75 years) living in the Boston metropolitan area. Significant interaction terms between LPL m107 and APOA5 S19W were observed for BMI (P = 0.003) and waist circumference (P = 0.019). Higher BMI (P = 0.001), waist (P = 0.011) and hip (P = 0.026) circumference were observed in minor allele (G) carriers for LPL m107 who also carried the APOA5 S19W minor allele (G). Additionally, extreme obesity (BMI > or = 40 kg/m(2)) risk was higher (odds ratio = 4.02; 95% confidence interval: 1.81-8.91; global P = 0.008) for minor allele carriers for both SNPs (LPL TG+GG, APOA5 CG+GG) compared to major allele carriers for both SNPs. In summary, we identified significant interactions for APOA5 S19W and LPL m107 for obesity in Caribbean Hispanics. Population-specific MAFs increase the difficulties of replicating gene-gene interactions, but may support the hypothesis that combinations of frequencies in selected genes could heighten obesity susceptibility in a given population. Analyses of gene-gene interactions may improve understanding of genetically based obesity risk, and underscore the need for further study of groups with multiple ancestral admixtures.
Obesity (Silver Spring) 2010 Feb
PMID:Apolipoprotein A5 and lipoprotein lipase interact to modulate anthropometric measures in Hispanics of Caribbean origin. 1962 56

The relative release in vitro of endothelin-1, zinc-alpha2-glycoprotein (ZAG), lipocalin-2, CD14, RANTES (regulated on activation, normal T cell expressed and secreted protein), lipoprotein lipase (LPL), osteoprotegerin (OPG), fatty acid-binding protein 4 (FABP-4), visfatin/PBEF/Nampt, glutathione peroxidase-3 (GPX-3), intracellular cell adhesion molecule 1 (ICAM-1), and amyloid A was examined using explants of human adipose tissue as well as the nonfat cell fractions and adipocytes from obese women. Over a 48-h incubation the majority of the release of LPL was by fat cells whereas that of lipocalin-2, RANTES, and ICAM-1 was by the nonfat cells present in human adipose tissue. In contrast appreciable amounts of OPG, amyloid A, ZAG, FABP-4, GPX-3, CD14, and visfatin/PBEF/Nampt were released by both fat cells and nonfat cells. There was an excellent correlation (r = 0.75) between the ratios of adipokine release by fat cells to nonfat cells over 48 h and the ratio of their mRNAs in fat cells to nonfat cells at the start of the incubation. The total release of ZAG, OPG, RANTES, and amyloid A by incubated adipose tissue explants from women with a fat mass of 65 kg was not different from that by women with a fat mass of 29 kg. In contrast that of ICAM-1, FABP-4, GPX-3, visfatin/PBEF/Nampt, CD14, lipocalin-2, LP, and endothelin-1 was significantly greater in tissue from women with a total fat mass of 65 kg.
Obesity (Silver Spring) 2010 May
PMID:Release of 12 adipokines by adipose tissue, nonfat cells, and fat cells from obese women. 1983 60


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