Search results for "lipogenesis"

showing 10 items of 32 documents

Lyophilized Maqui (Aristotelia chilensis) Berry Induces Browning in the Subcutaneous White Adipose Tissue and Ameliorates the Insulin Resistance in H…

2019

Maqui (Aristotelia Chilensis) berry features a unique profile of anthocyanidins that includes high amounts of delphinidin-3-O-sambubioside-5-O-glucoside and delphinidin-3-O-sambubioside and has shown positive effects on fasting glucose and insulin levels in humans and murine models of type 2 diabetes and obesity. The molecular mechanisms underlying the impact of maqui on the onset and development of the obese phenotype and insulin resistance was investigated in high fat diet-induced obese mice supplemented with a lyophilized maqui berry. Maqui-dietary supplemented animals showed better insulin response and decreased weight gain but also a differential expression of genes involved in de novo…

0301 basic medicineAnthocyaninFGF21Physiologymedicine.medical_treatmentClinical BiochemistryWhite adipose tissueWhite adipose tissueBiochemistryMaqui berryAnthocyanins0302 clinical medicinemaqui berrybiologyChemistryanthocyaninsHigh-fat diethigh-fat dietLipogenesisObesitatmedicine.medical_specialtyRatolins (Animals de laboratori)030209 endocrinology & metabolismfibroblast growth factor 21carbohydrate-responsive element binding protein bArticle03 medical and health sciencesAristotelia chilensisInsulin resistancewhite adipose tissueInternal medicinemedicineObesityCarbohydrate-responsive element-binding proteinMolecular BiologybrowningdelphinidinInsulinlcsh:RM1-950Adipose tissuesCell Biologybiology.organism_classificationmedicine.diseaseTeixit adipós030104 developmental biologyEndocrinologylcsh:Therapeutics. PharmacologyMice (Laboratory animals)AlimentsThermogenesisAntioxidants
researchProduct

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
researchProduct

Oleanolic acid improves diet-induced obesity by modulating fat preference and inflammation in mice.

2018

Obesity, triggered by high-fat diet (HFD), is associated to altered gustatory perception of dietary lipids. Oleanolic acid (OLA), a triterpene, has been reported to exert anti-obesity effects in animal models. Hence, we investigated the role of OLA in the modulation of oro-sensory perception of lipids in control and HFD-induced obese mice. As expected, OLA-treated obese mice exhibited a decrease in body, liver, and visceral adipose tissue weights. OLA treatment improved glucose tolerance, insulin level, plasma lipopolysaccharide (LPS), and hepatic cholesterol and triglyceride concentrations. OLA-treated obese mice exhibited higher fat preference compared to untreated obese mice, probably du…

0301 basic medicineCD36 AntigensLipopolysaccharidesmedicine.medical_specialtyCD36medicine.medical_treatmentInterleukin-1betaAdipose tissue030209 endocrinology & metabolismInflammationDiet High-FatDiet MediterraneanWeight GainBiochemistry03 medical and health scienceschemistry.chemical_compound0302 clinical medicineTaste receptorInternal medicinemedicineAnimalsInsulinObesityRNA MessengerOleanolic AcidCarbohydrate-responsive element-binding proteinOleanolic acidInflammationbiologyTriglycerideChemistryInterleukin-6InsulinLipogenesisGeneral MedicineGlucose Tolerance TestTaste BudsMice Inbred C57BL030104 developmental biologyEndocrinologyAdipose TissueLiverbiology.proteinCalciumFemalemedicine.symptomInflammation MediatorsBiochimie
researchProduct

Targeting cellular fatty acid synthesis limits T helper and innate lymphoid cell function during intestinal inflammation and infection

2019

CD4+ T cells contribute critically to a protective immune response during intestinal infections, but have also been implicated in the aggravation of intestinal inflammatory pathology. Previous studies suggested that T helper type (Th)1 and Th17 cells depend on de novo fatty acid (FA) synthesis for their development and effector function. Here, we report that T-cell-specific targeting of the enzyme acetyl-CoA carboxylase 1 (ACC1), a major checkpoint controlling FA synthesis, impaired intestinal Th1 and Th17 responses by limiting CD4+ T-cell expansion and infiltration into the lamina propria in murine models of colitis and infection-associated intestinal inflammation. Importantly, pharmacolog…

0301 basic medicineImmunologyBiologyMice03 medical and health scienceschemistry.chemical_compound0302 clinical medicineImmune systemRAR-related orphan receptor gammamedicineAnimalsImmunology and AllergyFatty acid synthesisBarrier functionLamina propriaEffectorFatty AcidsInnate lymphoid cellT-Lymphocytes Helper-InducerNuclear Receptor Subfamily 1 Group F Member 3ColitisInflammatory Bowel DiseasesImmunity InnateBiosynthetic PathwaysDisease Models Animal030104 developmental biologymedicine.anatomical_structurechemistryImmunologyLipogenesisBiomarkersAcetyl-CoA Carboxylase030215 immunologyMucosal Immunology
researchProduct

Resveratrol shifts energy metabolism to increase lipid oxidation in healthy old mice.

2019

Abstract Objectives The objective of this work was to determine the specific mechanisms by which resveratrol inhibits lipogenesis and stimulates lipolysis. Methods Twelve male mice were individually introduced into a metabolic cage for 24 h to measure basal metabolic rate, prior to intervention. They were randomly divided into two groups, resveratrol (RSV) and control (C), and administered resveratrol intraperitoneally or vehicle, respectively, for two consecutive days. After 24 h, the metabolic energy expenditure was again determined for 24 h, before mice were sacrificed. Protein and gene expression of different enzymes related to metabolism in the hepatic tissue, adipose tissue and gastro…

0301 basic medicinePolyphenolMalemedicine.medical_specialtyAgingLipolysisAdipose tissueWhite adipose tissueRM1-950ResveratrolLipid catabolism03 medical and health scienceschemistry.chemical_compoundMice0302 clinical medicineInternal medicinemedicineAnimalsCarnitineBeta oxidationFatty acid synthesisRespiratory quotientPharmacologyLipogenesisFatty AcidsGeneral MedicineMice Inbred C57BL030104 developmental biologyEndocrinologyMalonyl-CoAchemistryAdipose TissueCarnitine AcyltransferasesLiverResveratrol030220 oncology & carcinogenesisLipogenesisTherapeutics. PharmacologyEnergy MetabolismOxidation-Reductionmedicine.drugAcetyl-CoA CarboxylaseBiomedicinepharmacotherapy = Biomedecinepharmacotherapie
researchProduct

The Absence of HIF-1α Increases Susceptibility to Leishmania donovani Infection via Activation of BNIP3/mTOR/SREBP-1c Axis

2020

Summary: Hypoxia-inducible factor-1 alpha (HIF-1α) is considered a global regulator of cellular metabolism and innate immune cell functions. Intracellular pathogens such as Leishmania have been reported to manipulate host cell metabolism. Herein, we demonstrate that myeloid cells from myeloid-restricted HIF-1α-deficient mice and individuals with loss-of-function HIF1A gene polymorphisms are more susceptible to L. donovani infection through increased lipogenesis. Absence of HIF-1α leads to a defect in BNIP3 expression, resulting in the activation of mTOR and nuclear translocation of SREBP-1c. We observed the induction of lipogenic gene transcripts, such as FASN, and lipid accumulation in inf…

0301 basic medicineSREBP-1cHIF1A Gene[SDV]Life Sciences [q-bio]Leishmania donovaniHIF-1αGeneral Biochemistry Genetics and Molecular BiologyMitochondrial Proteins03 medical and health sciences0302 clinical medicinevisceral leishmaniasisAnimalsHumansMyeloid Cellslcsh:QH301-705.5GenelipogenesisPI3K/AKT/mTOR pathwayDisease ResistanceMice Inbred BALB CInnate immune systembiologyIntracellular parasiteLipogenesisMacrophagesTOR Serine-Threonine KinasesGenetic VariationMembrane Proteinsbiology.organism_classificationLeishmaniaHypoxia-Inducible Factor 1 alpha SubunitFASNLipidsmacrophages3. Good healthCell biologyUp-RegulationMice Inbred C57BL030104 developmental biologylcsh:Biology (General)myeloid cellsLipogenesisLeishmaniasis VisceralDisease SusceptibilityacetateSterol Regulatory Element Binding Protein 1030217 neurology & neurosurgeryLeishmania donovaniSignal Transduction
researchProduct

Hepatic B cell leukemia-3 promotes hepatic steatosis and inflammation through insulin-sensitive metabolic transcription factors.

2016

Background & Aims The pathomechanisms underlying non-alcoholic fatty liver disease (NAFLD) and the involved molecular regulators are incompletely explored. The nuclear factor-kappa B (NF-κB)-cofactor gene B cell leukemia-3 ( Bcl-3 ) plays a critical role in altering the transcriptional capacity of NF-κB – a key inducer of inflammation – but also of genes involved in cellular energy metabolism. Methods To define the role of Bcl-3 in non-alcoholic steatohepatitis (NASH), we developed a novel transgenic mouse model with hepatocyte-specific overexpression of Bcl-3 ( Bcl-3 Hep ) and employed a high-fat, high-carbohydrate dietary feeding model. To characterize the transgenic model, deep RNA seque…

0301 basic medicinemedicine.medical_specialtyCirrhosisCarcinoma Hepatocellularmedicine.medical_treatmentBiology03 medical and health sciencesLiver diseaseMice0302 clinical medicineB-Cell Lymphoma 3 ProteinInternal medicineProto-Oncogene ProteinsmedicineAnimalsHumansInsulinInflammationHepatologyInsulinLiver cellFatty liverLiver Neoplasmsmedicine.disease030104 developmental biologyEndocrinology030220 oncology & carcinogenesisLipogenesisSteatohepatitisSteatosisTranscription FactorsJournal of hepatology
researchProduct

Diet, weight loss, and liver health in nonalcoholic fatty liver disease: Pathophysiology, evidence, and practice.

2015

Fatty liver accumulation results from an imbalance between lipid deposition and removal, driven by the hepatic synthesis of triglycerides and de novo lipogenesis. The habitual diet plays a relevant role in the pathogenesis of nonalcoholic fatty liver disease (NAFLD), and both risky (e.g., fructose) and protective foods (Mediterranean diet) have been described, but the contribution of excess calories remains pivotal. Accordingly, weight loss is the most effective way to promote liver fat removal. Several controlled studies have confirmed that an intense approach to lifestyle changes, carried on along the lines of cognitive-behavior treatment, is able to attain the desired 7%-10% weight loss,…

0301 basic medicinemedicine.medical_specialtyMediterranean diet03 medical and health sciences0302 clinical medicineFibrosisWeight lossNon-alcoholic Fatty Liver DiseaseRisk FactorsInternal medicineNonalcoholic fatty liver diseaseWeight LossmedicineHumansExerciseHepatologybusiness.industryFatty liverLipid metabolismHepatologymedicine.diseaseLipid MetabolismDiet030104 developmental biologyEndocrinologyLiverLipogenesis030211 gastroenterology & hepatologymedicine.symptomSedentary BehaviorbusinessHepatology (Baltimore, Md.)
researchProduct

Palmitic Acid: Physiological Role, Metabolism and Nutritional Implications

2017

Palmitic acid (PA) has been for long time negatively depicted for its putative detrimental health effects, shadowing its multiple crucial physiological activities. PA is the most common saturated fatty acid accounting for 20–30% of total fatty acids in the human body and can be provided in the diet or synthesized endogenously via de novo lipogenesis (DNL). PA tissue content seems to be controlled around a well-defined concentration, and changes in its intake do not influence significantly its tissue concentration because the exogenous source is counterbalanced by PA endogenous biosynthesis. Particular physiopathological conditions and nutritional factors may strongly induce DNL, resulting i…

0301 basic medicinemedicine.medical_specialtyPhysiologyReviewBiologyprotein palmitoylationlcsh:PhysiologyPalmitic acidlung surfactant03 medical and health scienceschemistry.chemical_compoundPhysiology (medical)Internal medicinemedicinepalmitic acidProtein palmitoylationpalmitoylethanolamidechemistry.chemical_classificationPalmitoylethanolamidelcsh:QP1-981Metabolism030104 developmental biologyEndocrinologyde novo lipogenesischemistryLipogenesisSaturated fatty acidHomeostasisPolyunsaturated fatty acidFrontiers in Physiology
researchProduct

Insulin Dissociates the Effects of Liver X Receptor on Lipogenesis, Endoplasmic Reticulum Stress, and Inflammation

2016

IF 4.258; International audience; Diabetes is characterized by increased lipogenesis as well as increased endoplasmic reticulum (ER) stress and inflammation. The nuclear hormone receptor liver X receptor (LXR) is induced by insulin and is a key regulator of lipid metabolism. It promotes lipogenesis and cholesterol efflux, but suppresses endoplasmic reticulum stress and inflammation. The goal of these studies was to dissect the effects of insulin on LXR action. We used antisense oligonucleotides to knock down Lxr alpha in mice with hepatocytespecific deletion of the insulin receptor and their controls. We found, surprisingly, that knock-out of the insulin receptor and knockdown of Lxr alpha …

0301 basic medicinemedicine.medical_treatmentLipid-metabolismResistanceBiochemistryHepatitisMESH: HepatitisMESH: Endoplasmic Reticulum Stresspolycyclic compoundsInsulinGene-expressionPhospholipidsLiver X ReceptorsMice KnockoutbiologyMESH : Gene Expression RegulationFatty-acid synthesisfood and beveragesEndoplasmic Reticulum StressOrphan Nuclear ReceptorsCultured-cellsLipidsMESH: Gene Expression RegulationMESH : Endoplasmic Reticulum StressMessenger-rnaLiverMESH: Orphan Nuclear ReceptorsGene Knockdown TechniquesLipogenesisFemalelipids (amino acids peptides and proteins)Signal Transductionliver X receptormedicine.medical_specialtyLxr-alphaMice Transgenicdigestive systemPhospholipid transfer proteinGene Expression Regulation Enzymologic03 medical and health sciencesInsulin resistanceMESH : HepatitisLysophosphatidylcholine acyltransferaseInternal medicinemedicineAnimals[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyLiver X receptorMolecular Biology[ SDV.BBM ] Life Sciences [q-bio]/Biochemistry Molecular BiologyCrosses GeneticLipogenesisEndoplasmic reticulumInsulinElement-binding protein-1cMESH : LiverCell Biologymedicine.diseaseMESH : Orphan Nuclear ReceptorsReceptor InsulinMice Inbred C57BLInsulin receptor030104 developmental biologyEndocrinologyDiabetes Mellitus Type 2Gene Expression RegulationNuclear receptorbiology.proteinUnfolded protein responseInsulin ResistanceMESH: Liver
researchProduct