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

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

Phosphorylated glucosamine (glucosamine-6-phosphate, PGlc) was synthesized using methanesulfonic acid, phosphorus pentoxide (P(2)O(5)), NH(2)NH(2) and DMF. Its inhibitory effect on lipid accumulation in cultured 3T3-L1 adipocytes was investigated by measuring triglyceride contents and Oil Red O staining. In order to understand the mechanism by which lipid accumulation in adipocytes is decreased by PGlc, we examined the expression levels of several genes and proteins associated with adipogenesis and lipolysis using reverse transcription polymerase chain reaction, real-time polymerase chain reaction and Western blot analysis. Treatment with PGlc significantly reduced lipid accumulation during adipocyte differentiation and induced down-regulation of peroxisome proliferator-activated receptor-gamma, sterol regulatory element binding protein 1 and CCAAT/enhancer binding protein-alpha in a dose-dependent manner. Moreover, treatment with PGlc during adipocyte differentiation induced significant up-regulation of preadipocyte factor 1 mRNA and down-regulation of such adipocyte-specific gene promoters as adipocyte fatty acid binding protein, fatty acid synthase, lipoprotein lipase and leptin. According to the lipolytic response, PGlc up-regulated hormone-sensitive lipase mRNA expression and suppressed the expression levels of tumor necrosis factor-alpha mRNA compared with fully differentiated adipose tissue. These results suggest that the inhibitory effect of PGlc on adipocyte differentiation might be mediated through the down-regulation of adipogenic transcription factors, such as peroxisome proliferator-activated receptor-gamma, sterol regulatory element binding protein 1 and CCAAT/enhancer binding protein-alpha, which are related to the downstream adipocyte-specific gene promoters.
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PMID:Phosphorylated glucosamine inhibits adipogenesis in 3T3-L1 adipocytes. 1942 83

Three kinds of photoreactive polyelectrolytes of polyallylamine (PAAm), poly(acrylic acid) (PAAc), and poly(vinyl alcohol) (PVA) were synthesized by the introduction of azidophenyl groups in the respective polymers. The photoreactive PAAm, PAAc, and PVA were micropatterned on polystyrene surfaces by photolithography. Observation with optical microscopy and scanning probe microscopy demonstrated the formation of a striped pattern of polyelectrolytes with a width of 200 microm. The micropatterned polyelectrolytes swelled in water. The micropatterned surfaces were used for cell culture of mesenchymal stem cells (MSCs) and their effects on adipogenic differentiation were investigated. The MSCs adhered to and proliferated evenly on the PAAm- and PAAc-patterned surfaces while they formed a cell pattern on the PVA-patterned surface. The PAAm-, PAAc-grafted, and polystyrene surfaces supported cell adhesion while the PVA-grafted surface did not. When cultured in adipogenic differentiation medium, the adipogenic differentiation of MSCs on the polyelectrolyte-patterned surfaces was demonstrated by the formation of lipid vacuoles and gene expression analysis. Oil Red-O-positive cells showed an even distribution on the PAAm- and PAAc-patterned surfaces, while they showed a pattern on the PVA-patterned surface. The fraction of Oil RedO-positive cells increased with culture time. The MSCs cultured on the PAAm-, PAAc-grafted, and polystyrene surfaces in adipogenic differentiation medium expressed the adipogenesis marker genes of peroxisome proliferator-activated receptor gamma2 (PPARgamma2), lipoprotein lipase (LPL), and fatty acid binding protein 4 (FABP4). These results indicate that the PAAm-, and PAAc-grafted, and polystyrene surfaces supported the adipogenesis of MSCs while a PVA-grafted surface did not.
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PMID:Adipogenic differentiation of mesenchymal stem cells on micropatterned polyelectrolyte surfaces. 1944 1

Exposure to maternal overnutrition increases the expression of peroxisome proliferator-activated receptor-gamma (PPARgamma) in adipose tissue before birth, and it has been proposed that the precocial activation of PPARgamma target genes may lead to increased fat deposition in postnatal life. In this study, we determined the effect of intrafetal administration of a PPARgamma agonist, rosiglitazone, on PPARgamma target gene expression in fetal adipose tissue as well indirect actions of rosiglitazone on fetal liver and skeletal muscle. Osmotic pumps containing rosiglitazone (n = 7) or vehicle (15% ethanol, n = 7) were implanted into fetuses at 123-126 d gestation (term = 150 +/- 3 d gestation). At 137-141 d gestation, tissues were collected and mRNA expression of PPARgamma, lipoprotein lipase (LPL), adiponectin, and glycerol-3-phosphate dehydrogenase (G3PDH) in adipose tissue, PPARalpha and PPARgamma-coactivator 1alpha (PGC1alpha) in liver and muscle and phosphoenolpyruvate carboxykinase (PEPCK) in liver determined by quantitative real-time RT-PCR. Plasma insulin concentrations were lower in rosiglitazone-treated fetuses (P < 0.02). Rosiglitazone treatment resulted in increased expression of LPL and adiponectin mRNA (P < 0.01) in fetal adipose tissue. The expression of PPARalpha mRNA in liver (P < 0.05) and PGC1alpha mRNA (P < 0.02) in skeletal muscle were also increased by rosiglitazone treatment. Rosiglitazone treatment increased expression of PPARgamma target genes within fetal adipose tissue and also had direct or indirect actions on the fetal liver and muscle. The effects of activating PPARgamma in fetal adipose tissue mimic those induced by prenatal overnutrition, and it is therefore possible that activation of PPARgamma may be the initiating mechanism in the pathway from prenatal overnutrition to postnatal obesity.
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PMID:Rosiglitazone increases the expression of peroxisome proliferator-activated receptor-gamma target genes in adipose tissue, liver, and skeletal muscle in the sheep fetus in late gestation. 1952 Jul 84

Omega-3 fatty acids (FAs) are natural ligands of the peroxisome proliferator-activated receptor-alpha (PPARalpha), a nuclear receptor that modulates expression levels of genes involved in lipid metabolism. The L162V polymorphism of the PPARalpha gene is associated with a deteriorated metabolic profile. We postulate that subjects carrying the PPARalpha-V162 allele exhibit differences in the expression of PPARalpha and its target genes after incubation with omega-3 FAs compared with L162 homozygotes. Peripheral blood monocytes from six men carrying the PPARalpha-V162 allele paired for age and for body mass index with six L162 homozygotes were differentiated into macrophages and activated with eicosapentaenoic acid (EPA), docosahexaenoic acid (DHA), or mixtures of EPA:DHA. Data demonstrates that gene expression levels of PPARalpha and apolipoprotein AI (APOA1) were significantly lower for carriers of the PPARalpha-V162 allele compared to L162 homozygotes after the addition of DHA and a mixture of EPA:DHA. Additionally, lipoprotein lipase (LPL) gene expression displayed a tendency to be lower in the PPARalpha L162V polymorphism subgroup after the addition of a mixture of EPA:DHA. Consequently, individuals carrying the PPARalpha-V162 allele may demonstrate inferior improvements in their lipid profile due to alterations in gene expression rates in response to omega-3 FA supplementation.
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PMID:Omega-3 fatty acids regulate gene expression levels differently in subjects carrying the PPARalpha L162V polymorphism. 1958 64

Women oxidize more fat as compared to men during endurance exercise and several groups have shown that the mRNA content of selected genes related to fat oxidation are higher in women (e.g. hormone sensitive lipase, beta-hydroxyacyl-CoA dehydrogenase, CD36). One of the possible mechanisms is that women tend to have a higher area percentage of type I skeletal muscle fibers as compared with men. Consequently, we hypothesized that sex would influence the basal mRNA and protein content for genes involved in metabolism and the determination of muscle fiber type. Muscle biopsies from the vastus lateralis were collected from healthy men and women. We examined mRNA content globally using Affymetrix GeneChips, and selected genes were examined and/or confirmed by RT-PCR. Furthermore, we examined protein content by Western blot analysis. Stringent gene array analysis revealed 66 differentially expressed genes representing metabolism, mitochondrial function, transport, protein biosynthesis, cell proliferation, signal transduction pathways, transcription and translation. Stringent gene array analysis and RT-PCR confirmed that mRNA for; acyl-coenzyme A acyltransferase 2 (ACAA2), trifunctional protein beta (HADHB), catalase, lipoprotein lipase (LPL), and uncoupling protein-2 (UCP-2) were higher in women. Targeted gene analysis revealed that myosin heavy chain I (MHCI), peroxisome proliferator-activated receptor (PPAR)delta were higher in women compared with men. Surprisingly, there were no significant sex based differences in protein content for HADHB, ACAA2, catalase, PPARdelta, and MHC1. In conclusion, the differences in the basal mRNA content in resting skeletal muscle suggest that men and women are transcriptionally "primed" for known physiological differences in metabolism however the mechanism behind sex differences in fiber type remains to be determined.
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PMID:Sex differences in global mRNA content of human skeletal muscle. 1962 54

In this study, we isolated the phloroglucinol derivative, 1-(3',5'-dihydroxyphenoxy)-7-(2'',4'',6-trihydroxyphenoxy)-2,4,9-trihydroxydibenzo-1,4-dioxin (1), from Ecklonia cava and evaluated its potential inhibition on adipocyte differentiation in 3T3-L1 cells. Lipid accumulation along with the expression of several genes associated with adipogenesis and lipolysis was examined at the end of differentiation. Lipid accumulation level was examined by measuring triglyceride content and Oil-Red O staining. The expression levels of several genes and proteins were examined using reverse-transcription polymerase chain reaction (RT-PCR), real-time RT-PCR, and Western blot analysis. Compound 1 significantly reduced lipid accumulation and downregulated peroxisome proliferator-activated receptor-gamma, sterol regulatory element-binding protein 1c, and CCAAT/enhancer-binding proteins alpha in a dose-dependent manner. Moreover, the presence of compound 1 induced downregulation of adipogenic target genes such as fatty acid binding protein 4, fatty acid transport protein 1, fatty acid synthase, acyl-CoA synthetase 1, lipoprotein lipase, and leptin. According to the lipolytic response, compound 1 downregulated perilipin and hormone-sensitive lipase while upregulating tumor necrosis factor alpha. Therefore, these results suggest that compound 1 might decrease lipid accumulation during adipocyte differentiation by modulating adipogenesis and lipogenesis. Furthermore, compound 1 could be developed as a functional agent effective in improving obesity.
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PMID:1-(3',5'-dihydroxyphenoxy)-7-(2'',4'',6-trihydroxyphenoxy)-2,4,9-trihydroxydibenzo-1,4-dioxin inhibits adipocyte differentiation of 3T3-L1 fibroblasts. 1968 Jul 25

Agonists of the thiazolidinedione class of peroxisome proliferator-activated receptor-gamma exhibit both insulin-sensitizing and anti-inflammatory effects. We hypothesized that pioglitazone might be able to exert its anti-inflammatory properties at a lower dose than that required for its insulin-sensitizing effect. In order to investigate this hypothesis, we evaluated the effects of pioglitazone on inflammatory as well as metabolic biomarkers in serum and white adipose tissue (WAT) at 2 different doses. Female db/db mice were treated orally with therapeutic (30 mg/kg) and subtherapeutic (3 mg/kg) doses of pioglitazone for 14 days followed by an oral glucose tolerance test. Other parameters measured were inflammatory markers such as tumor necrosis factor (TNF)-alpha, interleukin-6 (IL-6) and metabolic biomarkers in serum (insulin, glucose and adiponectin). Moreover, adiponectin, fatty acid-binding protein (aP2) and lipoprotein lipase (LPL) mRNA expression in WAT were determined by real-time PCR. A subtherapeutic dose of pioglitazone significantly suppresses the expression of TNF-alpha and IL-6 mRNA in WAT, but does not alter the serum glucose, insulin and WAT expression of adiponectin, adipocyte aP2 and LPL. A therapeutic dose of pioglitazone improves insulin sensitivity, enhances LPL, aP2 and adiponectin expression, and also suppresses TNF-alpha and IL-6 expression. In conclusion, the current study indicates that the anti-inflammatory effect of pioglitazone is produced at a subtherapeutic dose, which is considerably lower than the dose needed to produce any desired metabolic effects. Anti-inflammatory effects of pioglitazone may precede its insulin-sensitizing effects in db/db mice.
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PMID:Subtherapeutic dose of pioglitazone reduces expression of inflammatory adipokines in db/db mice. 1973 99

Insulin resistance is partly due to suppression of insulin-induced glucose uptake into adipocytes. The uptake is dependent on adipocyte differentiation, which is controlled at mRNA transcription level. The peroxisome proliferator-activated receptor (PPAR), a ligand-regulated nuclear receptor, is involved in the differentiation. Many food-derived compounds serve as ligands to activate or inactivate PPAR. In this study, we demonstrated that bixin and norbixin (annatto extracts) activate PPARgamma by luciferase reporter assay using GAL4-PPAR chimera proteins. To examine the effects of bixin on adipocytes, 3T3-L1 adipocytes were treated with bixin or norbixin. The treatment induced mRNA expression of PPARgamma target genes such as adipocyte-specific fatty acid-binding protein (aP2), lipoprotein lipase (LPL), and adiponectin in differentiated 3T3-L1 adipocytes and enhanced insulin-dependent glucose uptake. The observations indicate that bixin acts as an agonist of PPARgamma and enhances insulin sensitivity in 3T3-L1 adipocytes, suggesting that bixin is a valuable food-derived compound as a PPAR ligand to regulate lipid metabolism and to ameliorate metabolic syndrome.
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PMID:Bixin regulates mRNA expression involved in adipogenesis and enhances insulin sensitivity in 3T3-L1 adipocytes through PPARgamma activation. 1989 58

Dioxinodehydroeckol (DHE) isolated from Ecklonia cava, has previously been investigated for its inhibition of the differentiation of 3T3-L1 preadipocytes into adipocytes. Levels of lipid accumulation were measured, along with changes in the expression of genes and proteins associated with adipogenesis and lipolysis. Confluent 3T3-L1 preadipocytes in medium with or without different concentrations of DHE for 7 days were differentiated into adipocytes. Lipid accumulation was quantified by measuring direct triglyceride contents and Oil-Red O staining. The expression of genes and proteins associated with adipogenesis and lipolysis was measured using RT-PCR, quantitative real-time RT-PCR and Western blotting analysis. It was found that the presence of DHE significantly reduced lipid accumulation and down-regulated the expression of peroxisome proliferator-activated receptor-gamma (PPARgamma), sterol regulatory element-binding protein 1 (SREBP1) and CCAAT/enhancer-binding proteins (C/EBPalpha) in a dose-dependent manner. Moreover, DHE suppressed regulation of the adipocyte-specific gene promoters such as fatty acid binding protein (FABP4), fatty acid transport protein (FATP1), fatty acid synthase (FAS), lipoprotein lipase (LPL), acyl-CoA synthetase 1 (ACS1), leptin, perilipin and HSL compared to control adipocytes. The specific mechanism mediating the effects of DHE was confirmed by activation of phosphorylated AMP-activated protein kinase (pAMPK). Therefore, these results suggest that DHE exerts anti-adipogenic effect on adipocyte differentiation through the activation and modulation of the AMPK signaling pathway.
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PMID:Anti-adipogenic effect of dioxinodehydroeckol via AMPK activation in 3T3-L1 adipocytes. 2038 10

We investigated the involvement of basal sympathetic tone in brown adipose tissue (BAT) recruitment and gene expression profile induced by peroxisome proliferator-activated receptor-gamma (PPAR-gamma) activation. Innervated and surgically denervated BAT pads of rats treated or not with rosiglitazone (15 mg.kg(-1).day(-1), 7 days) were evaluated for weight, triacylglycerol (TAG) and DNA content, mitochondrial mass, and gene expression. Rosiglitazone induced BAT recruitment (increased mass, TAG and DNA content) and mRNA levels of lipolytic (adipose tissue triglyceride lipase and CGI58) and lipogenic (lipoprotein lipase, phosphoenolpyruvate carboxykinase, fatty acid binding protein 4, and diacylglycerol acyltransferase 1) proteins independently of tissue innervation status. Mitochondrial mass and mRNA levels of its regulators peroxisome proliferator-activated receptor coactivator-alpha and CCAAT/enhancer binding protein-beta were not affected by rosiglitazone, while being significantly reduced by denervation. By contrast, maximal stimulation of uncoupling protein 1 (UCP1) (thermogenesis), cell death-inducing DNA fragmentation factor-45-like effector A (inhibitor of UCP1 activity), monoacylglycerol lipase (lipolysis), small heterodimer partner (transcription), and glycerokinase (TAG synthesis) by rosiglitazone depended on the presence of intact BAT innervation. Cold exposure (5 degrees C, 24 h) significantly increased UCP1 mRNA levels in innervated BAT pads of untreated rats, without affecting the already high BAT UCP1 levels of rosiglitazone-treated animals. A similar pattern of response was found in denervated pads, but with markedly lower UCP1 expression than that in innervated BAT. In conclusion, whereas the mass (hyperplasia and hypertrophy), lipogenic, and lipolytic components of BAT recruitment induced by rosiglitazone occur independently of tissue sympathetic innervation, maximal UCP1 expression induced by PPAR-gamma in vivo depends on the presence of basal BAT adrenergic tone. The residual sympathetic tone found under rosiglitazone treatment is, therefore, involved in the modulation of a subset of major components of PPAR-gamma-mediated BAT recruitment.
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PMID:Basal adrenergic tone is required for maximal stimulation of rat brown adipose tissue UCP1 expression by chronic PPAR-gamma activation. 2039 57


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