Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

---

Query: EC:3.1.1.34 (lipoprotein lipase)
7,025 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We have studied the capacity of human neutrophils to release arachidonic acid from diacylglycerol, employing 1-stearoyl-2-[1-14C]arachidonoyl-sn-glycerol and 1-[1-14C]stearoyl-2-arachidonoyl-sn-glycerol as exogenous substrates. We have found that arachidonic acid is removed from diacylglycerol by the sequential action of two enzymes. First, the sn-1 position is split by 1-diacylglycerol lipase activity, and then, arachidonic acid is released from the resulting 2-monoacylglycerol by a 2-monoacylglycerol lipase. The specific activity of the 2-monoacylglycerol lipase, using 2-[1-14C]arachidonoyl-sn-glycerol as exogenous substrate, was at least 9-fold higher than that of 1-diacylglycerol lipase, indicating that the action of the 1-diacylglycerol lipase is the rate-limiting step in arachidonic acid release from diacylglycerol. Postnuclear supernatants from A23187-treated cells showed a 2.5-fold increase in both lipase activities. The arachidonic acid-releasing diacylglycerol lipase system showed an optimum pH of 4.5 and was not inhibited by EGTA or stimulated by Ca2+, Mg2+, Mn2+, Zn2+, or Co2+. However, arachidonic acid release was inhibited by Hg2+, suggesting the involvement of sulfhydryl groups in catalytic activity. The subcellular distribution of both 1-diacylglycerol lipase and 2-monoacylglycerol lipase activities was examined in resting and A23187-treated human neutrophils by fractionation of postnuclear supernatants on continuous sucrose gradients. Both lipases were localized mainly in the membrane of gelatinase-containing granules, which were resolved from cytosol, plasma membrane, phosphasomes, and specific and azurophilic granules. When neutrophils were stimulated by the calcium ionophore A23187, a drastic shift of the 1-diacylglycerol lipase and 2-monoacylglycerol lipase toward the plasma membrane was detected. This shift was due to fusion of gelatinase-containing granules with the plasma membrane upon neutrophil stimulation. As a result of the membrane fusion process, the capacity to release arachidonic acid from diacylglycerol was increased. This translocation from the membrane of gelatinase-containing granules to the plasma membrane may play an important role in regulating the diacylglycerol level in stimulated human neutrophils.
...
PMID:Arachidonic acid release from diacylglycerol in human neutrophils. Translocation of diacylglycerol-deacylating enzyme activities from an intracellular pool to plasma membrane upon cell activation. 190 58

The activities of lipoprotein lipase in postheparin plasma, retroperitoneal adipose and gastrocnemius muscle tissues were determined in the rats fed 2.8 ppm of dietary zinc for eight weeks, as compared with pair-fed and ad libitum-fed rats given 30.8 ppm of zinc. The postheparin lipoprotein lipase activity, as determined by using a lipid emulsion labeled with [3H]triolein as the substrate, was significantly lower in the first group of rats, relative to that in the second and third groups. Tissue lipoprotein lipase activities were compared using the lipid emulsion and activator serum obtained from the zinc-deficient rats and the ad libitum-fed rats. The activator sera were devoid of very low density and low density lipoproteins, but enriched in high density lipoproteins. Muscle lipoprotein lipase activities were significantly lower when assayed with the activator serum from the zinc-deficient compared with the activities determined with the activator serum from the ad libitum-fed. Similarly, muscle lipoprotein lipase activities were lower in all groups when [3H]-triolein-labeled chylomicrons from the zinc-deficient were used as the substrate, compared with the activities determined using the chylomicrons from the ad libitum-fed. Lipoprotein lipase activities in the adipose tissues were not affected by the different sources of the activator sera and chylomicrons. The results strongly suggest that the decrease in postheparin lipoprotein lipase activity in zinc deficiency is not due to changes in tissue lipoprotein lipase enzyme per se, but to compositional alterations in chylomicrons and high density lipoprotein, particularly, with regard to C apolipoproteins, modulators of lipoprotein lipase activity.
...
PMID:Effect of marginal zinc deficiency on lipoprotein lipase activities in postheparin plasma, skeletal muscle and adipose tissues in the rat. 275 1

Rats were given daily injections of protamine-zinc insulin (PZI) that increased food intake and body weight. Termination of insulin treatment resulted in transient hypophagia and weight loss. Simultaneously with the weight loss, plasma levels of glycerol, free fatty acids, glucose, and ketones increased, whereas adipose tissue lipoprotein lipase activity and liver glycogen decreased. These changes in food intake and metabolism after termination of PZI treatment were accentuated in streptozotocin-diabetic rats. Two antilipolytic drugs (nicotinic acid and 3,5-dimethylpyrazole) blocked the elevation in plasma glycerol while having no effect on food intake. A 1-day fast after termination of insulin treatment equalized insulin-treated and control groups for plasma glycerol and ketones and reversed group differences in free fatty acids; the elevation in plasma glucose persisted despite starvation. Following starvation, previously PZI-treated rats ate less than controls on refeeding. The results show that enhanced lipolysis does not invariably accompany hypophagia during excess weight loss and suggest that a disturbance in carbohydrate metabolism or an increase in hepatic fatty acid oxidation may underlie this decrease in food intake.
...
PMID:Metabolic concomitants of hypophagia during recovery from insulin-induced obesity in rats. 635 32

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.
...
PMID:Purification and characterization of a lipase from Aspergillus oryzae. 767 Jan 77

The present study was performed to investigate the effect of zinc deficiency on the activities of lipoprotein lipase in postheparin serum and tissues of rats fed diets containing either coconut oil or fish oil as dietary fat, using a bifactorial experimental design. To ensure an adequate food intake, all the rats were force-fed by gastric tube. Experimental diets contained either 0.8 mg zinc/kg (zinc-deficient diets) or 40 mg zinc/kg (zinc-adequate diets). The effects of zinc deficiency on the activities of lipoprotein lipase in postheparin serum and postprandial triglyceride concentrations and distribution of apolipoproteins in serum lipoproteins depended on the type of dietary fat. Zinc-deficient rats fed the coconut oil diet exhibited a reduced activity of lipoprotein lipase in postheparin serum and adipose tissue, markedly increased concentrations of triglycerides in serum, and a markedly reduced content of apolipoprotein C in triglyceride-rich lipoproteins and high density lipoproteins compared with zinc-adequate rats fed coconut oil. By contrast, zinc-deficient rats fed the fish oil diet did not exhibit reduced activities of lipoprotein lipase in postheparin serum and adipose tissue and increased concentrations of serum lipids compared with zinc-adequate rats fed the fish oil diet. This study suggests that a reduced activity of lipoprotein lipase might contribute to increased postprandial concentrations of serum triglycerides observed in zinc-deficient animals. However, it also demonstrates that the effects of zinc deficiency on lipoprotein metabolism are influenced by dietary fatty acids.
...
PMID:Zinc deficiency and the activities of lipoprotein lipase in plasma and tissues of rats force-fed diets with coconut oil or fish oil. 1074 57

Chronic highly elevated expression of a growth hormone (GH) transgene enhances overall body growth with minimal adipose accretion, while moderate levels of circulating GH fail to enhance body growth yet promote adipose deposition. These findings suggest that the growth response to GH can be dissociated from adipose effects. This hypothesis was tested in the oMtla-oGH transgenic mouse model by titrating circulating GH levels through variable induction of transgene expression. Circulating GH levels in female transgenics were approximately 49, 132, and 750 ng/ml in response to the transgene stimulus at 0, 15, and 25 mM zinc sulfate, respectively. The highest level of circulating GH generated the largest body weight with the smallest fat accrual while the intermediate GH level generated a body weight equivalent to that for the highest GH but the heaviest gonadal fat pads. The lowest GH levels did not increase body size but did enlarge fat depots. Animals exposed to the highest level of GH had an extended growth phase relative to lower GH levels and the nontransgenic controls. In contrast, the duration of the growth phase for the 0 and 15 mM zinc stimulated transgenics was abbreviated relative to the growth phase of the control animals. The two highest levels of circulating GH increased all forms of the GH receptor, IGF-I, and hepatic lipoprotein lipase mRNA. The growth differential observed for the 0 vs. the 15 mM zinc stimulated transgenics may reflect the preferential increase in the full length GH receptor mRNA and the induction of the smaller IGF-I transcripts with the higher circulating GH while the lipid accrual paralleled the disproportionate induction of the truncated GH receptor mRNA form. Liver and bone content of zinc, manganese, copper, and iron primarily reflected dietary zinc supplementation and did not appear to play a role in the differential growth response. The dissociation of GH effects on growth and adipogenesis as a function of circulating GH levels suggests that the level of GHR and IGF-I expression acts through a threshold mechanism and low expression results in adipogenesis while high expression generates body growth.
...
PMID:Dissociation of body growth and adipose deposition effects of growth hormone in oMt1a-oGH transgenic mice. 1530 63

Osterix (Osx) is a zinc-finger-containing transcription factor that is expressed in osteoblasts of all endochondral and membranous bones. In Osx null mice osteoblast differentiation is impaired and bone formation is absent. In this study, we hypothesized that overexpression of Osx in murine bone marrow stromal cells (BMSC) would be able to enhance their osteoblastic differentiation and mineralization in vitro. Retroviral transduction of Osx in BMSC cultured in non-differentiating medium did not affect expression of Runx2/Cbfa1, another key transcription factor of osteoblast differentiation, but induced an increase in the expression of other markers associated with the osteoblastic lineage including alkaline phosphatase, bone sialoprotein, osteocalcin, and osteopontin. Retroviral transduction of Osx in BMSC also increased their proliferation, alkaline phosphatase activity, and ability to form bone nodules. These events occurred without significant changes in the expression of alpha1(II) procollagen or lipoprotein lipase, which are markers of chondrogenic and adipogenic differentiation, respectively.
...
PMID:Osterix enhances proliferation and osteogenic potential of bone marrow stromal cells. 1646 99

Nutrigenomics examines nutrient-gene interactions on a genome-wide scale. Increased dietary fat or higher non-esterified fatty acids (NEFA) from starvation-induced mobilisation may enhance hepatic oxidation and decrease esterification of fatty acids by reducing the expression of the fatty acid synthase gene. The key factors are the peroxisome proliferator-activated receptors (PPARs). Dietary carbohydrates--both independently and through insulin effect--influence the transcription of the fatty acid synthase gene. Oleic acid or n-3 fatty acids downregulate the expression of leptin, fatty acid synthase and lipoprotein lipase in retroperitoneal adipose tissue. Protein-rich diets entail a shortage of mRNA necessary for expression of the fatty acid synthase gene in the adipocytes. Conjugated linoleic acids (CLAs) are activators of PPAR and also induce apoptosis in adipocytes. Altered rumen microflora produces CLAs that are efficient inhibitors of milk fat synthesis in the mammary gland ('biohydrogenation theory'). Oral zinc or cadmium application enhances transcription rate in the metallothionein gene. Supplemental CLA in pig diets was found to decrease feed intake and body fat by activating PPARgamma-responsive genes in the adipose tissue. To prevent obesity and type II diabetes, the direct modulation of gene expression by nutrients is also possible. Nutrigenomics may help in the early diagnosis of genetically determined metabolic disorders and in designing individualised diets for companion animals.
...
PMID:Veterinary aspects and perspectives of nutrigenomics: a critical review. 1755 88

Zinc is a structural and functional component of PPAR and zinc deficiency may be associated with an increased risk for cardiovascular diseases. We tested the hypothesis that zinc deficiency compromises lipid metabolism in rosiglitazone (RSG)-treated mice lacking the LDL-receptor (LDL-R) gene. LDL-R-deficient mice were maintained for 3 wk on low-fat (7 g/100 g) diets that were either zinc deficient or zinc adequate. Subsequently, diets were adjusted to a high-fat (HF) (15 g/100 g) regimen for 1 wk to produce a biological environment of mild oxidative and inflammatory stress. One-half of the mice within each zinc group was gavaged daily with the PPARgamma agonist RSG starting 2 d prior to the HF feeding. Selected lipid parameters were studied. Zinc deficiency increased plasma total cholesterol, which was also elevated by RSG. Zinc deficiency also caused an increased lipoprotein-cholesterol distribution toward the non-HDL fraction (VLDL, intermediate density lipoprotein, LDL). Plasma total fatty acids tended to increase during zinc deficiency and RSG treatment resulted in similar changes in the fatty acid profile in zinc-deficient mice. Fatty acid translocase (FAT/CD36) expression in abdominal aorta was upregulated by RSG only in zinc-deficient mice. In contrast, RSG treatment markedly increased lipoprotein lipase (LPL) expression only in zinc-adequate mice. In vitro studies confirmed that adequate zinc is required for RSG-induced PPARgamma activity to transactivate target genes. These data suggest that in this atherogenic mouse model treated with RSG, lipid metabolism can be compromised during zinc deficiency and that adequate dietary zinc may be considered during therapy with the antidiabetic medicine RSG.
...
PMID:Zinc deficiency alters lipid metabolism in LDL receptor deficient mice treated with rosiglitazone. 1795 67

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.
...
PMID:Release of 12 adipokines by adipose tissue, nonfat cells, and fat cells from obese women. 1983 60


1 2 Next >>

---