0000000000599961

AUTHOR

Rémy Burcelin

showing 4 related works from this author

Cytoskeletal transgelin 2 contributes to gender-dependent adipose tissue expandability and immune function

2019

During adipogenesis, preadipocytes' cytoskeleton reorganizes in parallel with lipid accumulation. Failure to do so may impact the ability of adipose tissue (AT) to shift between lipid storage and mobilization. Here, we identify cytoskeletal transgelin 2 (TAGLN2) as a protein expressed in AT and associated with obesity and inflammation, being normalized upon weight loss. TAGLN2 was primarily found in the adipose stromovascular cell fraction, but inflammation, TGF-β, and estradiol also prompted increased expression in human adipocytes. Tagln2 knockdown revealed a key functional role, being required for proliferation and differentiation of fat cells, whereas transgenic mice overexpressing Tagl…

0301 basic medicineGenetically modified mouseMalemedicine.medical_specialtyTHP-1 CellsBlotting WesternAdipose tissueMuscle ProteinsInflammationMice TransgenicDiet High-FatBiochemistry03 medical and health sciencesMice0302 clinical medicineImmune systemSex FactorsInternal medicineGeneticsmedicineAdipocytesAnimalsHumansObesityadipocyte protein 2CytoskeletonMolecular BiologyCytoskeletonInflammationbiologyMicrofilament ProteinsPhenotypeImmunohistochemistryMice Inbred C57BL030104 developmental biologyEndocrinologyAdipose TissueAdipogenesisbiology.proteinFemalemedicine.symptom030217 neurology & neurosurgeryBiotechnology
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Apelin treatment increases complete Fatty Acid oxidation, mitochondrial oxidative capacity, and biogenesis in muscle of insulin-resistant mice.

2012

Both acute and chronic apelin treatment have been shown to improve insulin sensitivity in mice. However, the effects of apelin on fatty acid oxidation (FAO) during obesity-related insulin resistance have not yet been addressed. Thus, the aim of the current study was to determine the impact of chronic treatment on lipid use, especially in skeletal muscles. High-fat diet (HFD)-induced obese and insulin-resistant mice treated by an apelin injection (0.1 μmol/kg/day i.p.) during 4 weeks had decreased fat mass, glycemia, and plasma levels of triglycerides and were protected from hyperinsulinemia compared with HFD PBS-treated mice. Indirect calorimetry experiments showed that apelin-treated mice…

MESH: Oxidation-Reduction[ SDV.AEN ] Life Sciences [q-bio]/Food and NutritionEndocrinology Diabetes and MetabolismGlucose uptakeAMP-Activated Protein KinasesInbred C57BLMice0302 clinical medicineAMP-activated protein kinaseMESH : Lipid MetabolismHyperinsulinemiaMESH: AnimalsMESH: AMP-Activated Protein KinasesMESH : Muscle SkeletalMESH : Fatty AcidsBeta oxidationMESH: Lipid Metabolism0303 health sciencesMESH: Muscle SkeletalbiologyMESH : Diet High-FatFatty AcidsMESH: Energy MetabolismMESH : AMP-Activated Protein KinasesMESH: Mitochondria MuscleSkeletal3. Good healthApelinMitochondriaMESH: Fatty AcidsMESH : Cyclic AMP-Dependent Protein KinasesMESH: Insulin ResistanceAlimentation et NutritionApelinIntercellular Signaling Peptides and ProteinsMuscleMESH : Insulin ResistanceOxidation-Reductionmedicine.medical_specialtyMESH : Mitochondria Muscle030209 endocrinology & metabolismMESH : Mice Inbred C57BLMESH: Cyclic AMP-Dependent Protein KinasesDiet High-Fat03 medical and health sciencesInsulin resistanceAdipokinesMESH: Mice Inbred C57BLInternal medicineMESH : MiceInternal MedicinemedicineFood and NutritionAnimalsMuscle SkeletalMESH: Intercellular Signaling Peptides and ProteinsMESH: MiceMESH : Intercellular Signaling Peptides and Proteins030304 developmental biologyMESH : Oxidation-ReductionAMPKmedicine.diseaseLipid MetabolismCyclic AMP-Dependent Protein KinasesMitochondria MuscleDietMice Inbred C57BLMESH : Energy Metabolism[SDV.AEN] Life Sciences [q-bio]/Food and NutritionAMP-Activated Protein Kinases;Animals;Cyclic AMP-Dependent Protein Kinases;Diet;High-Fat;Energy Metabolism;Fatty Acids;Insulin Resistance;Intercellular Signaling Peptides and Proteins;Lipid Metabolism;Mice;Inbred C57BL;Mitochondria;Muscle;Skeletal;Oxidation-ReductionHigh-FatMESH: Diet High-FatMetabolismEndocrinologyMitochondrial biogenesisbiology.proteinMESH : AnimalsInsulin ResistanceEnergy Metabolism[SDV.AEN]Life Sciences [q-bio]/Food and Nutrition
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ITCH E3 ubiquitin ligase downregulation compromises hepatic degradation of branched-chain amino acids

2022

Objective: Metabolic syndrome, obesity, and steatosis are characterized by a range of dysregulations including defects in ubiquitin ligase tagging proteins for degradation. The identification of novel hepatic genes associated with fatty liver disease and metabolic dysregulation may be relevant to unravelling new mechanisms involved in liver disease progression Methods: Through integrative analysis of liver transcriptomic and metabolomic obtained from obese subjects with steatosis, we identified itchy E ubiquitin protein ligase (ITCH) as a gene downregulated in human hepatic tissue in relation to steatosis grade. Wild-type or ITCH knockout mouse models of non-alcoholic fatty liver disease (N…

Mice KnockoutBCAAm Metabolomic NAFLD TranscriptomicsUbiquitin-Protein Ligases[SDV]Life Sciences [q-bio]Liver NeoplasmsDown-RegulationBCAA; Metabolomics; NAFLD; Transcriptomics.Settore MED/09Cell BiologyMiceNon-alcoholic Fatty Liver DiseaseNAFLDotorhinolaryngologic diseasesAnimalsHumansMetabolomicsFemaleObesityBCAAskin and connective tissue diseasesTranscriptomicsMolecular BiologyAmino Acids Branched-Chain
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40(th) EASD Annual Meeting of the European Association for the Study of Diabetes : Munich, Germany, 5-9 September 2004

2004

0303 health sciencesmedicine.medical_specialtybusiness.industryEASDEndocrinology Diabetes and MetabolismHuman physiologymedicine.disease03 medical and health sciences0302 clinical medicineDiabetes mellitusFamily medicineInternal MedicineMedicinebusiness030217 neurology & neurosurgery030304 developmental biology
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