6533b830fe1ef96bd1297d2e
RESEARCH PRODUCT
Apelin treatment increases complete Fatty Acid oxidation, mitochondrial oxidative capacity, and biogenesis in muscle of insulin-resistant mice.
Philippe ValetJosef M. PenningerLuc PénicaudCédric DrayKeiji KubaMariano Ruiz-gayoThierry LevadeCamille FoussalRocío Guzmán-ruizIsabelle Castan-laurellDanièle DaviaudCamille AttanéEstelle WanecqAlexandre BenaniSophie Le GonidecRémy BurcelinChloé RancouleVeronic Bezairesubject
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 Nutritiondescription
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 had a better use of lipids. The complete FAO, the oxidative capacity, and mitochondrial biogenesis were increased in soleus of apelin-treated mice. The action of apelin was AMP-activated protein kinase (AMPK) dependent since all the effects studied were abrogated in HFD apelin-treated mice with muscle-specific inactive AMPK. Finally, the apelin-stimulated improvement of oxidative capacity led to decreased levels of acylcarnitines and enhanced insulin-stimulated glucose uptake in soleus. Thus, by promoting complete lipid use in muscle of insulin-resistant mice through mitochondrial biogenesis and tighter matching between FAO and the tricarboxylic acid cycle, apelin treatment could contribute to insulin sensitivity improvement.
| year | journal | country | edition | language |
|---|---|---|---|---|
| 2012-02-01 |