Search results for "Lipid metabolism"

showing 10 items of 359 documents

Elucidating the molecular physiology of lantibiotic NAI-107 production in Microbispora ATCC-PTA-5024.

2016

Background The filamentous actinomycete Microbispora ATCC-PTA-5024 produces the lantibiotic NAI-107, which is an antibiotic peptide effective against multidrug-resistant Gram-positive bacteria. In actinomycetes, antibiotic production is often associated with a physiological differentiation program controlled by a complex regulatory and metabolic network that may be elucidated by the integration of genomic, proteomic and bioinformatic tools. Accordingly, an extensive evaluation of the proteomic changes associated with NAI-107 production was performed on Microbispora ATCC-PTA-5024 by combining two-dimensional difference in gel electrophoresis, mass spectrometry and gene ontology approaches. R…

0301 basic medicineProteomicsfood.ingredientMetabolic networkATP-binding cassette transporterActinomycetes Antibiotic production Differential proteomics 2D-DIGE and mass spectrometry Metabolic pathways Regulatory network Molecular and cellular functionsBiologyBioinformaticsProteomicsGram-Positive Bacteria03 medical and health sciencesfoodBacteriocinsActinomycetesGenetics2D-DIGE and mass spectrometryDifferential proteomics2. Zero hungerGel electrophoresisLipid metabolismRegulatory networkbiology.organism_classificationDrug Resistance MultipleAnti-Bacterial AgentsActinobacteriaMetabolic pathway030104 developmental biologyBiochemistryMicrobisporaMetabolic pathwaysATP-Binding Cassette TransportersAntibiotic productionPeptidesBacteriaMolecular and cellular functionsBiotechnologyResearch ArticleBMC genomics
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Impaired Kupffer Cell Self-Renewal Alters the Liver Response to Lipid Overload during Non-alcoholic Steatohepatitis

2020

International audience; Kupffer cells (KCs) are liver-resident macrophages that self-renew by proliferation in the adult independently from monocytes. However, how they are maintained during non-alcoholic steatohepatitis (NASH) remains ill defined. We found that a fraction of KCs derived from Ly-6C+ monocytes during NASH, underlying impaired KC self-renewal. Monocyte-derived KCs (MoKCs) gradually seeded the KC pool as disease progressed in a response to embryo-derived KC (EmKC) death. Those MoKCs were partly immature and exhibited a pro-inflammatory status compared to EmKCs. Yet, they engrafted the KC pool for the long term as they remained following disease regression while acquiring matur…

0301 basic medicine[SDV]Life Sciences [q-bio]OntogenyMESH: Cell Self RenewalSelf renewalMESH: MonocytesMESH: Mice KnockoutMice0302 clinical medicineNon-alcoholic Fatty Liver DiseaseImmunology and AllergyKupffer cellsMESH: AnimalsCell Self RenewalMESH: Lipid MetabolismMice KnockoutKupffer cellLipidsResearch Highlightmacrophages[SDV] Life Sciences [q-bio]Infectious Diseasesmedicine.anatomical_structureLiver030220 oncology & carcinogenesismonocytesmedicine.medical_specialtynon-alcoholic steatohepatitis (NASH)ImmunologyBiology03 medical and health sciencesMESH: Mice Inbred C57BLMESH: Cell ProliferationInternal medicinemedicineAnimalsLiver damageMESH: MiceCell ProliferationMESH: Non-alcoholic Fatty Liver DiseaseTriglyceride storageNon alcoholicLipid Metabolismmedicine.diseaseMESH: Lipidseye diseasesMice Inbred C57BLMESH: Kupffer Cells030104 developmental biologyEndocrinologySteatohepatitisHomeostasisMESH: LiverImmunity
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Mitochondrial Dysfunction, Oxidative Stress and Neuroinflammation in Neurodegeneration with Brain Iron Accumulation (NBIA)

2020

The syndromes of neurodegeneration with brain iron accumulation (NBIA) encompass a group of invalidating and progressive rare diseases that share the abnormal accumulation of iron in the basal ganglia. The onset of NBIA disorders ranges from infancy to adulthood. Main clinical signs are related to extrapyramidal features (dystonia, parkinsonism and choreoathetosis), and neuropsychiatric abnormalities. Ten NBIA forms are widely accepted to be caused by mutations in the genes PANK2, PLA2G6, WDR45, C19ORF12, FA2H, ATP13A2, COASY, FTL1, CP, and DCAF17. Nonetheless, many patients remain without a conclusive genetic diagnosis, which shows that there must be additional as yet undiscovered NBIA gen…

0301 basic medicineautophagybrain iron accumulationPhysiologyNeurodegeneration with brain iron accumulationClinical BiochemistryChoreoathetosisrare diseaseReviewmedicine.disease_causeBiochemistryneuroinflammation03 medical and health sciences0302 clinical medicineWDR45lipid metabolismmitochondrial dysfunctionMedicineoxidative stressiron metabolismMolecular BiologyNeuroinflammationDystoniabusiness.industryParkinsonismlcsh:RM1-950Cell Biologymedicine.diseasePANK2030104 developmental biologylcsh:Therapeutics. Pharmacologymembrane remodellingmedicine.symptombusinessneurodegenerative disorderNeuroscience030217 neurology & neurosurgeryOxidative stressAntioxidants
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Age‐related ultrastructural changes of the basement membrane in the mouse blood‐brain barrier

2018

Abstract The blood‐brain barrier (BBB) is essential for a functional neurovascular unit. Most studies focused on the cells forming the BBB, but very few studied the basement membrane (BM) of brain capillaries in ageing. We used transmission electron microscopy and electron tomography to investigate the BM of the BBB in ageing C57BL/6J mice. The thickness of the BM of the BBB from 24‐month‐old mice was double as compared with that of 6‐month‐old mice (107 nm vs 56 nm). The aged BBB showed lipid droplets gathering within the BM which further increased its thickness (up to 572 nm) and altered its structure. The lipids appeared to accumulate toward the glial side of the BM. Electron tomography …

0301 basic medicineblood‐brain barrierAgingElectron Microscope TomographyMyocytes Smooth Muscleelectron tomographyBlood–brain barrierMuscle Smooth Vascular03 medical and health sciencesMice0302 clinical medicineMicroscopy Electron TransmissionLipid dropletmedicineAnimalsBasement membraneChemistryNeurodegenerationBrainLipid metabolismBiological TransportCell BiologyOriginal ArticlesLipid Dropletsmedicine.diseaseLipid Metabolismbasement membraneCell biologyCapillariesMice Inbred C57BL030104 developmental biologymedicine.anatomical_structureElectron tomographyAgeingageingBlood-Brain Barrier030220 oncology & carcinogenesisAstrocytesUltrastructureMolecular MedicineOriginal ArticleNeuroglia
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Arabidopsis Serine Decarboxylase 1 (SDC1) in Phospholipid and Amino Acid Metabolism

2018

Arabidopsis thaliana serine decarboxylase 1 (SDC1) catalyzes conversion of serine to ethanolamine, the first reaction step of phosphatidylcholine and phosphatidylethanolamine biosynthesis. However, an involvement of SDC1 in amino acid metabolism remains elusive despite that serine is the substrate of SDC1. Here, we showed that SDC1 localizes in mitochondria although phosphatidylcholine and phosphatidylethanolamine are known to be produced in the endoplasmic reticulum (ER). Moreover, we found that overexpression of SDC1 decreased levels of amino acid compounds derived from mitochondrial tricarboxylic acid cycle. These results suggest that mitochondria-localized SDC1 plays an important role i…

0301 basic medicinechemistry.chemical_classificationPhosphatidylethanolamineArabidopsis thalianaEndoplasmic reticulumPhospholipidPlant ScienceMetabolismlcsh:Plant cultureAmino acidSerineCitric acid cycle03 medical and health scienceschemistry.chemical_compound030104 developmental biologychemistryBiochemistryBiosynthesislcsh:SB1-1110phospholipid biosynthesisserine decarboxylaseglycerolipid metabolismphospholipidOriginal ResearchFrontiers in Plant Science
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Activation of Mevalonate Pathway Via LKB1 is Essential for Stability of Treg Cells

2019

Summary: The function of regulatory T (Treg) cells depends on lipid oxidation. However, the molecular mechanism by which Treg cells maintain lipid metabolism after activation remains elusive. Liver kinase B1 (LKB1) acts as a coordinator by linking cellular metabolism to substrate AMP-activated protein kinase (AMPK). We show that deletion of LKB1 in Treg cells exhibited reduced suppressive activity and developed fatal autoimmune inflammation. Mechanistically, LKB1 induced activation of the mevalonate pathway by upregulating mevalonate genes, which was essential for Treg cell functional competency and stability by inducing Treg cell proliferation and suppressing interferon-gamma and interleuk…

0301 basic medicinecongenital hereditary and neonatal diseases and abnormalitiesGeranylgeranyl pyrophosphateKinaseAMPKFOXP3hemic and immune systemschemical and pharmacologic phenomenaLipid metabolismGeneral Biochemistry Genetics and Molecular BiologyCell biology03 medical and health scienceschemistry.chemical_compound030104 developmental biology0302 clinical medicinelcsh:Biology (General)chemistryLipid oxidationMevalonate pathwayskin and connective tissue diseasesProtein kinase Alcsh:QH301-705.5030217 neurology & neurosurgeryHomeostasisSSRN Electronic Journal
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Potential Role of ANGPTL4 in the Cross Talk between Metabolism and Cancer through PPAR Signaling Pathway

2017

The angiopoietin-like 4 (ANGPTL4) protein belongs to a superfamily of secreted proteins structurally related to factors modulating angiogenesis known as angiopoietins. At first, ANGPTL4 has been identified as an adipokine exclusively involved in lipid metabolism, because of its prevalent expression in liver and adipose tissue. This protein regulates lipid metabolism by inhibiting lipoprotein lipase (LPL) activity and stimulating lipolysis of white adipose tissue (WAT), resulting in increased levels of plasma triglycerides (TG) and fatty acids. Subsequently, ANGPTL4 has been shown to be involved in several nonmetabolic and metabolic conditions, both physiological and pathological, including …

0301 basic medicinemedicine.medical_specialtyAdipose tissueAdipokinePeroxisome proliferator-activated receptorWhite adipose tissueReview ArticleBiologyPPARANGPTL4; PPAR; Cancer03 medical and health sciencesANGPTL4ANGPTL4Internal medicineDrug DiscoverymedicineLipolysisPharmacology (medical)lcsh:QH301-705.5Cancerchemistry.chemical_classificationLipoprotein lipaseLipid metabolism030104 developmental biologyEndocrinologychemistrylcsh:Biology (General)lipids (amino acids peptides and proteins)metabolism
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Loss of c-Met signaling sensitizes hepatocytes to lipotoxicity and induces cholestatic liver damage by aggravating oxidative stress.

2016

Recent studies confirmed a critical importance of c-Met signaling for liver regeneration by modulating redox balance. Here we used liver-specific conditional knockout mice (MetKO) and a nutritional model of hepatic steatosis to address the role of c-Met in cholesterol-mediated liver toxicity. Liver injury was assessed by histopathology and plasma enzymes levels. Global transcriptomic changes were examined by gene expression microarray, and key molecules involved in liver damage and lipid homeostasis were evaluated by Western blotting. Loss of c-Met signaling amplified the extent of liver injury in MetKO mice fed with high-cholesterol diet for 30days as evidenced by upregulation of liver enz…

0301 basic medicinemedicine.medical_specialtyCell SurvivalCholestasis IntrahepaticBiologyToxicologymedicine.disease_causeArticleCholesterol Dietary03 medical and health sciencesMice0302 clinical medicineLiver Function TestsInternal medicinemedicineAnimalsLiver X receptorLiver injuryMice Knockoutmedicine.diagnostic_testLipid metabolismProto-Oncogene Proteins c-metmedicine.diseaseLipid MetabolismGlutathioneLipidsLiver regenerationOxidative Stress030104 developmental biologyEndocrinologyLipotoxicity030220 oncology & carcinogenesisHepatocytesLipid PeroxidationSteatosisLiver function testsOxidative stressSignal TransductionToxicology
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Assessing the Contribution of Relative Macrophage Frequencies to Subcutaneous Adipose Tissue

2021

Background: Macrophages play an important role in regulating adipose tissue function, while their frequencies in adipose tissue vary between individuals. Adipose tissue infiltration by high frequencies of macrophages has been linked to changes in adipokine levels and low-grade inflammation, frequently associated with the progression of obesity. The objective of this project was to assess the contribution of relative macrophage frequencies to the overall subcutaneous adipose tissue gene expression using publicly available datasets.Methods: Seven publicly available microarray gene expression datasets from human subcutaneous adipose tissue biopsies (n = 519) were used together with TissueDecod…

0301 basic medicinemedicine.medical_specialtyDOWN-REGULATIONsubcutaneous adipose tissueEndocrinology Diabetes and MetabolismAdipose tissueAdipokine030209 endocrinology & metabolismInflammationBiologycell-type composition03 medical and health scienceschemistry.chemical_compound0302 clinical medicineDownregulation and upregulationINFLAMMATIONInternal medicineGene expressionlipid metabolismmedicinelow-grade inflammationpublicly available dataMacrophagecomputational deconvolutionTX341-641OXIDATIVE STRESSPHOSPHORYLATIONFatty acid synthesisGENE-EXPRESSIONNutritionOriginal ResearchINSULIN-RESISTANCENutrition and DieteticsNutrition. Foods and food supplyWOMENLipid metabolismmacrophages030104 developmental biologyEndocrinologychemistryOBESITYmedicine.symptomSTEM-CELLSFood ScienceACID-METABOLISMFrontiers in Nutrition
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Protective effect of quercetin on high-fat diet-induced non-alcoholic fatty liver disease in mice is mediated by modulating intestinal microbiota imb…

2016

Gut microbiota is involved in obesity, metabolic syndrome and the progression of nonalcoholic fatty liver disease (NAFLD). It has been recently suggested that the flavonoid quercetin may have the ability to modulate the intestinal microbiota composition, suggesting a prebiotic capacity which highlights a great therapeutic potential in NAFLD. The present study aims to investigate benefits of experimental treatment with quercetin on gut microbial balance and related gut-liver axis activation in a nutritional animal model of NAFLD associated to obesity. C57BL/6J mice were challenged with high fat diet (HFD) supplemented or not with quercetin for 16 weeks. HFD induced obesity, metabolic syndrom…

0301 basic medicinemedicine.medical_specialtyGut floraDiet High-FatBiochemistryMice03 medical and health sciencesNon-alcoholic Fatty Liver DiseasePhysiology (medical)Internal medicineNonalcoholic fatty liver diseasemedicineAnimalsHumansObesityMetabolic SyndromebiologyFatty liverLipid metabolismLipid Metabolismmedicine.diseasebiology.organism_classificationGastrointestinal MicrobiomeIntestinesToll-Like Receptor 4Disease Models Animal030104 developmental biologyEndocrinologyLiverLipotoxicityImmunologyQuercetinInsulin ResistanceSteatosisMetabolic syndromeDysbiosisSignal TransductionFree Radical Biology and Medicine
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