Search results for "Fatty acid synthase"

showing 9 items of 9 documents

Pinolenic acid ameliorates oleic acid-induced lipogenesis and oxidative stress via AMPK/SIRT1 signaling pathway in HepG2 cells

2019

Pinolenic acid (PLA), a natural compound isolated from pine nut oil, has been reported to exert bioactivity against lipid anabolism. Nonetheless, the underlying mechanisms still poorly elucidated. The aim of this study is to comprehensively demonstrate the effects of PLA on oleic acid (OA)-induced non-alcoholic fatty liver disease (NAFLD) and their relationship with the lipid metabolic regulation. The results demonstrated that treatment with PLA dramatically inhibited lipid accumulation, oxidative stress as well as inflammatory responses induced by oleic acid in HepG2 cells. PLA also obviously decreased the levels of cellular triglyceride (TG), total cholesterol (TC), malondialdehyde (MDA),…

0301 basic medicineAntioxidantLinolenic Acidsmedicine.medical_treatmentPinolenic acidAMP-Activated Protein KinasesNitric Oxidemedicine.disease_causePine nut oil03 medical and health scienceschemistry.chemical_compound0302 clinical medicineSirtuin 1medicineHumansPPAR alphaPharmacologybiologyLipogenesisAMPKHep G2 CellsOxidative StressFatty acid synthaseOleic acid030104 developmental biologyGene Expression RegulationchemistryBiochemistryLipogenesisbiology.proteinlipids (amino acids peptides and proteins)030217 neurology & neurosurgeryOxidative stressOleic AcidSignal TransductionEuropean Journal of Pharmacology
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Mediterranean diet and prudent diet are both associated with low circulating esterified 3-hydroxy fatty acids, a proxy of LPS burden, among older adu…

2021

Background LPS-type endotoxins, naturally found in the gut microbiota, are recognized as triggers of inflammation and emerge as detrimental factors of healthy aging. Nutrition represents a promising strategy to reduce LPS burden, yet little is known about the relation of diet to circulating LPS concentrations. Objective The aim was to evaluate the associations between food groups, dietary patterns, and circulating 3-hydroxy fatty acids (3-OH FAs), a proxy of LPS burden. Methods In a cross-sectional study of 698 French older community-dwelling individuals, 3-OH FA concentrations were measured by LC-tandem MS. Dietary patterns were determined using food-frequency questionnaires. Adherence to …

0301 basic medicineLipopolysaccharidesMediterranean dietFetal alcohol syndromeMedicine (miscellaneous)Dietary pattern030209 endocrinology & metabolismPrincipal components analysisBiologyGut floraDiet MediterraneanFood group03 medical and health sciencesComplex carbohydrate0302 clinical medicineElderlyRisk FactorsMediterranean diet3C studymedicineHumansLipopolysaccharides (LPS)Food scienceHealthy agingAged2. Zero hungerAged 80 and over030109 nutrition & dieteticsNutrition and DieteticsFatty Acidsmedicine.diseasebiology.organism_classificationEndotoxinsFatty acid synthaseCross-Sectional Studiesbiology.proteinAlienor studyAlcohol intake[SDV.SPEE]Life Sciences [q-bio]/Santé publique et épidémiologieFranceDiet Healthy
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Pistachio Consumption Prevents and Improves Lipid Dysmetabolism by Reducing the Lipid Metabolizing Gene Expression in Diet-Induced Obese Mice.

2018

Pistachios contain beneficial substances such as unsaturated fatty acids, phytosterols, and polyphenols. In the present study, we investigated if pistachio consumption is able to prevent or to revert hyperglycemia, dyslipidemia, hepatic steatosis, and adipose tissue morphological alterations caused by high fat diet (HFD) in the mouse. Moreover, the impact of pistachio intake on the mRNA expression of peroxisome proliferator-activated receptor &gamma

0301 basic medicineMaleAdipose tissueMice ObeseSettore BIO/09 - Fisiologiachemistry.chemical_compoundAdipocytelipid metabolizing gene expressionNutsHypertriglyceridemiaNutrition and Dieteticsbiologyfood and beveragesPhytosterolsFatty acid synthaseCholesterolAdipose TissueLiverPistacialipids (amino acids peptides and proteins)Sterol Regulatory Element Binding Protein 1lcsh:Nutrition. Foods and food supplyStearoyl-CoA Desaturasemedicine.medical_specialtyobesity-related dysfunctionslcsh:TX341-641pistachio consumptionDiet High-FatArticle03 medical and health sciencesInternal medicineobesity-related dysfunctionmedicineAnimalsObesityRNA MessengerDyslipidemias030109 nutrition & dieteticsFatty Acid Transport ProteinsPlant ExtractsHypertriglyceridemianutritional and metabolic diseasesPolyphenolsLipid metabolismmedicine.diseaseLipid MetabolismDietFatty LiverMice Inbred C57BLPPAR gammaEndocrinologychemistrybiology.proteinSteatosisFatty Acid SynthasesDiet-induced obeseFood ScienceNutrients
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Hepatic and very low-density lipoprotein fatty acids in obese offspring of overfed dams.

2010

The combined effects of developmental programming and high-fat feeding at weaning on fatty acid metabolism of the offspring are not well known. In the present study, we aim at characterizing the influence of maternal and offspring's own diets on liver and very low-density lipoprotein (VLDL) lipids; fatty acid profiles of VLDL and liver phospholipids, triglycerides, and cholesteryl esters; and hepatic enzyme activities. Twenty obese male rats born to cafeteria diet-fed dams and 20 control rats born to control diet-fed dams were selected. At weaning, 10 rats of each group were fed control or cafeteria diet. Obese rats had a significant increase in serum glucose, insulin, leptin, VLDL apolipop…

Blood GlucoseLeptinMalemedicine.medical_specialtyVery low-density lipoproteinOffspringEndocrinology Diabetes and MetabolismLinoleic acidFatty Acids NonesterifiedLipoproteins VLDLchemistry.chemical_compoundEndocrinologyPregnancyInternal medicinemedicineAnimalsInsulinObesityRats Wistarchemistry.chemical_classificationbiologyFatty acid metabolismBody WeightFatty acidOrgan Sizemedicine.diseaseRatsFatty acid synthaseEndocrinologychemistryLiverMaternal Exposurebiology.proteinlipids (amino acids peptides and proteins)FemaleSteatosisEnergy IntakeEnergy MetabolismPolyunsaturated fatty acidMetabolism: clinical and experimental
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ERK1 and ERK2 activation modulates diet-induced obesity in mice

2017

IF 3.112; International audience; Obesity is a worldwide problem, and dietary lipids play an important role in its pathogenesis. Recently, Erk1 knock-out (ERK1(-/-)) mice have been shown to exhibit low preference for dietary fatty acids. Hence, we maintained Erk1(-/-) mice on a high-fat diet (HFD) to assess the implication of this mitogen-activated protein (MAP) kinase in obesity. The Erk1(-/-) mice, fed the HFD, were more obese than wild-type (WT) animals, fed the same diet. Erk1(-/-) obese mice gained more fat and liver mass than WT obese animals. No difference was observed in daily food and energy intake in HFD-fed both group of animals. However, feed efficiency was higher in Erk1(-/-) t…

Blood GlucoseMale0301 basic medicinemedicine.medical_treatmentMice ObeseBiochemistryMicechemistry.chemical_compoundPhosphorylationBeta oxidationCells CulturedMice KnockoutMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Reverse Transcriptase Polymerase Chain ReactionGeneral MedicineLipidsFatty acid synthaseLiverLipogenesisHomeostatic model assessmentmedicine.medical_specialtyBlotting WesternBiologyDiet High-FatReal-Time Polymerase Chain Reaction03 medical and health sciencesInsulin resistanceInternal medicinemedicineAnimals[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyRNA MessengerObesity[ SDV.BBM ] Life Sciences [q-bio]/Biochemistry Molecular BiologyInflammationTriglycerideLipogenesisInsulinBody WeightLipid Metabolismmedicine.diseaseObesityMice Inbred C57BL030104 developmental biologyEndocrinologychemistrybiology.proteinMAP kinaseInsulin ResistanceBiochimie
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Transcriptional induction of the fatty acid binding protein gene in mouse liver by bezafibrate

1993

AbstractThe mechanism by which hypolipidemic peroxisome proliferators of the fibrate family induce the liver fatty acid binding protein in liver of rodents is unknown. In order to delineate the level at which this protein is induced, the transcriptional activity of the specific gene encoding for liver fatty acid binding protein was measured in isolated hepatocyte nuclei obtained from male Swiss mice daily force-fed during 7 days with 400 mg/kg body weight bezafibrate. This treatment induced a 4-fold increase in the liver fatty acid binding protein transcription rate. Liver fatty acid binding protein mRNA level, measured by Northern blot analysis and cytosolic content of this protein, analyz…

MalePeroxisome proliferator activated receptorTranscription GeneticImmunoblottingBiophysicsPeroxisome proliferator-activated receptorNerve Tissue ProteinsFatty Acid-Binding ProteinsPeroxisome proliferator hypolipidemic drugBiochemistryFatty acid-binding proteinMiceStructural BiologyGeneticsmedicineAnimalsRNA Messengeradipocyte protein 2Molecular Biologychemistry.chemical_classificationLiver fatty acid binding proteinBezafibratebiologyBinding proteinBody WeightCell BiologyOrgan SizePeroxisomeBlotting NorthernMolecular biologyLipidsNeoplasm ProteinsGene regulationFatty acid synthasechemistryBiochemistryGene Expression RegulationLiverbiology.proteinElectrophoresis Polyacrylamide GelPeroxisome proliferator-activated receptor alphaBezafibrateCarrier ProteinsDNA ProbesFatty Acid-Binding Protein 7medicine.drugFEBS Letters
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Paracrine Activation of Hepatic CB1 Receptors by Stellate Cell-Derived Endocannabinoids Mediates Alcoholic Fatty Liver

2008

SummaryAlcohol-induced fatty liver, a major cause of morbidity, has been attributed to enhanced hepatic lipogenesis and decreased fat clearance of unknown mechanism. Here we report that the steatosis induced in mice by a low-fat, liquid ethanol diet is attenuated by concurrent blockade of cannabinoid CB1 receptors. Global or hepatocyte-specific CB1 knockout mice are resistant to ethanol-induced steatosis and increases in lipogenic gene expression and have increased carnitine palmitoyltransferase 1 activity, which, unlike in controls, is not reduced by ethanol treatment. Ethanol feeding increases the hepatic expression of CB1 receptors and upregulates the endocannabinoid 2-arachidonoylglycer…

Malemedicine.medical_specialtyPhysiologyHUMDISEASEArachidonic AcidsGlyceridesMiceCarnitine palmitoyltransferase 1PiperidinesReceptor Cannabinoid CB1Internal medicineCannabinoid Receptor ModulatorsParacrine CommunicationmedicineAnimalsReceptorDiet Fat-RestrictedMolecular BiologyCells CulturedMice KnockoutCarnitine O-PalmitoyltransferaseEthanolChemistryLipogenesisFatty AcidsFatty liverCell Biologymedicine.diseaseEndocannabinoid systemCoculture TechniquesUp-RegulationMice Inbred C57BLDisease Models AnimalLipoprotein LipaseEndocrinologyLiverLipogenesisHepatocytesHepatic stellate cellPyrazoleslipids (amino acids peptides and proteins)Alcoholic fatty liverFatty Acid SynthasesRimonabantSteatosisSterol Regulatory Element Binding Protein 1Oxidation-ReductionEndocannabinoidsFatty Liver AlcoholicCell Metabolism
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Interferons increase cell resistance to Staphylococcal alpha-toxin.

2007

ABSTRACTMany bacterial pathogens, includingStaphylococcus aureus, use a variety of pore-forming toxins as important virulence factors. Staphylococcal alpha-toxin, a prototype β-barrel pore-forming toxin, triggers the release of proinflammatory mediators and induces primarily necrotic death in susceptible cells. However, whether host factors released in response to staphylococcal infections may increase cell resistance to alpha-toxin is not known. Here we show that prior exposure to interferons (IFNs) prevents alpha-toxin-induced membrane permeabilization, the depletion of ATP, and cell death. Moreover, pretreatment with IFN-α decreases alpha-toxin-induced secretion of interleukin 1β (IL-1β)…

Programmed cell deathStaphylococcus aureusCell Membrane Permeabilitymedicine.medical_treatmentImmunologyBacterial ToxinsInterleukin-1betaBiologyStaphylococcal infectionsMicrobiologyProinflammatory cytokineMicrobiologyCell LineHemolysin ProteinsAdenosine TriphosphateInterferonmedicineHumansSecretionCell DeathKinaseEpithelial CellsBacterial Infectionsmedicine.diseaseInfectious DiseasesCytokineProtein BiosynthesisParasitologyTumor necrosis factor alphaInterferonsFatty Acid Synthasesmedicine.drugInfection and immunity
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Mboat7 down-regulation by hyper-insulinemia induces fat accumulation in hepatocytes.

2020

Background: Naturally occurring variation in Membrane-bound O-acyltransferase domain-containing 7 (MBOAT7), encoding for an enzyme involved in phosphatidylinositol acyl-chain remodelling, has been associated with fatty liver and hepatic disorders. Here, we examined the relationship between hepatic Mboat7 down-regulation and fat accumulation. Methods: Hepatic MBOAT7 expression was surveyed in 119 obese individuals and in experimental models. MBOAT7 was acutely silenced by antisense oligonucleotides in C57Bl/6 mice, and by CRISPR/Cas9 in HepG2 hepatocytes. Findings: In obese individuals, hepatic MBOAT7 mRNA decreased from normal liver to steatohepatitis, independently of diabetes, inflammatio…

Research paperTGFβ Transforming Growth Factor BetaIntracellular SpaceCRISPR Clustered Regularly Interspaced Short Palindromic RepeatshHEPS Human HepatocytesMice0302 clinical medicineLPIAT1DAG Diacylglyceroli.p. Intraperitonealmedia_commonFatty AcidsGeneral Medicine3. Good health030220 oncology & carcinogenesisHOMA-IR homeostasis Model Assessment of Insulin ResistanceMPO morpholinolcsh:Medicine (General)medicine.medical_specialtyPE Phosphatidyl-EthanolamineNashGeneral Biochemistry Genetics and Molecular Biology03 medical and health sciencesTNFα tumor Necrosis Factor AlphaLDL Low Density LipoproteinsHyperinsulinismNAFLDSD Standard Dietmedia_common.cataloged_instanceHumansCPT1 Carnitine Palmitoyltransferase IPhosphatidylinositolGene SilencingEuropean unionVLDL Very Low Density Lipoproteinlcsh:RhHSC Human Hepatic Stellate Cellsmedicine.diseaseLipid MetabolismOA Oleic AcidCI Confidence IntervalMboat7 Membrane bound O-acyltransferase domain containing 7MCD methionine choline deficient diet030104 developmental biologyEndocrinologychemistryCDP Cytidine-DiphosphateFOXO1 Forkhead Box protein O1NAFLD nonalcoholic fatty liver diseaseSteatohepatitisBMI Body Mass IndexCL CardiolipinAcyltransferases0301 basic medicineAlcoholic liver diseaseCXCL10 C-X-C Motif Chemokine 10lcsh:Medicinechemistry.chemical_compoundNon-alcoholic Fatty Liver DiseaseIFG Impaired Fasting GlucoseAPOB Apolipoprotein BNonalcoholic fatty liver diseasePIP Phosphatidyl-Inositol-PhosphateSteatohepatitisqRT-PCR quantitative Real Time Polymerase Chain ReactionMice Knockoutlcsh:R5-920ORO Oil Red O StainingPI PhosphatidylinositolFatty liverTM6SF2 Transmembrane 6 Superfamily Member 2PhospholipidTAG TriglyceridesNASH Nonalcoholic SteatohepatitisLipogenesisLPA Lyso-Phosphatidic AcidPhosphatidylinositolSignal TransductionPS Phosphatidyl-SerinePA Palmitic AcidALD alcoholic liver diseasePC Phosphatidylcholinei.v. IntravenousFATP1 Fatty Acid Transport Protein 1Models BiologicalInternal medicinemedicineAnimalsNonalcoholic fatty liver diseasePPARα Peroxisome Proliferator-Activated Receptor alphaObesityG3P Glyceraldehyde-3-PhosphateSREBP1c Sterol Regulatory Element-Binding Protein 1HDL High Density Lipoproteinsbusiness.industryPI3K Phosphatidylinositol 3 KinaseMembrane ProteinsNHEJ Non-Homologues End JoiningPNPLA3 Patatin-like Phospholipase Domain-containing-3MTTP Microsomal Triglyceride Transfer ProteinLPIAT1 Lysophosphatidylinositol Acyltransferase 1TMC4 Transmembrane Channel-Like 4Disease Models AnimalGene Expression RegulationHepatocytesFOXA2 Forkhead Box A2mTOR mammalian target of RapamycinSteatosisInsulin ResistancebusinessPG Phosphatidyl-GlycerolFABP1 Fatty Acid-Binding Protein 1 FAS Fatty Acid SynthaseT2DM Type 2 Diabetes MellitusEBioMedicine
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