Search results for "High-Fat"

showing 10 items of 107 documents

Fibroblast Growth Factor 21 (FGF21) Protects against High Fat Diet Induced Inflammation and Islet Hyperplasia in Pancreas

2015

Fibroblast growth factor 21 (FGF21) is an important endocrine metabolic regulator expressed in multiple tissues including liver and adipose tissue. Although highest levels of expression are in pancreas, little is known about the function of FGF21 in this tissue. In order to understand the physiology of FGF21 in the pancreas, we analyzed its expression and regulation in both acinar and islet tissues. We found that acinar tissue express 20-fold higher levels than that observed in islets. We also observed that pancreatic FGF21 is nutritionally regulated; a marked reduction in FGF21 expression was noted with fasting while obesity is associated with 3–4 fold higher expression. Acinar and islet c…

Male0301 basic medicineFGF21Fibroblast Growth FactorPhysiologyReceptors Antigen T-Cell alpha-betaPeptide Hormoneslcsh:MedicineAdipose tissueAcinar CellsPathology and Laboratory MedicineBiochemistryFatsMiceEndocrinologyMedicine and Health SciencesInsulinlcsh:ScienceImmune ResponseMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Multidisciplinarygeography.geographical_feature_categoryFOXP3Forkhead Transcription FactorsFastingHyperplasiaIsletLipidsmedicine.anatomical_structurePhysiological ParametersOrgan SpecificityTumor necrosis factor alphaAnatomymedicine.symptomPancreasSignal TransductionResearch Articlemedicine.medical_specialtyImmunologyEndocrine SystemInflammationBiologyDiet High-FatInterferon-gammaIslets of Langerhans03 medical and health sciencesExocrine GlandsSigns and SymptomsGrowth FactorsInternal medicinemedicineAnimalsObesityPancreasNutritionInflammationDiabetic EndocrinologygeographyHyperplasiaEndocrine PhysiologyTumor Necrosis Factor-alphaBody Weightlcsh:RBiology and Life SciencesGlucagonmedicine.diseaseDietary FatsHormonesDietFibroblast Growth FactorsMice Inbred C57BL030104 developmental biologyEndocrinologyGene Expression RegulationPancreatitisThy-1 Antigenslcsh:QPLOS ONE
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An Experimental Model of Diet-Induced Metabolic Syndrome in Rabbit: Methodological Considerations, Development, and Assessment

2018

In recent years, obesity and metabolic syndrome (MetS) have become a growing problem for public health and clinical practice, given their increased prevalence due to the rise of sedentary lifestyles and unhealthy eating habits. Thanks to animal models, basic research can investigate the mechanisms underlying pathological processes such as MetS. Here, we describe the methods used to develop an experimental rabbit model of diet-induced MetS and its assessment. After a period of acclimation, animals are fed a high-fat (10% hydrogenated coconut oil and 5% lard), high-sucrose (15% sucrose dissolved in water) diet for 28 weeks. During this period, several experimental procedures were performed to…

Male0301 basic medicineGeneral Chemical EngineeringPhysiologyDisease030204 cardiovascular system & hematologyDiet High-FatGeneral Biochemistry Genetics and Molecular Biology03 medical and health scienceschemistry.chemical_compound0302 clinical medicinemedicineAnimalsPathologicalMetabolic Syndrome030109 nutrition & dieteticsGeneral Immunology and MicrobiologyTriglyceridebusiness.industryExperimental modelGeneral NeuroscienceModels Theoreticalmedicine.diseaseObesityDisease Models AnimalBlood pressurechemistryMedicineRabbitsMetabolic syndromebusinessDyslipidemiaJournal of Visualized Experiments
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Obesogen effects after perinatal exposure of 4,4′-sulfonyldiphenol (Bisphenol S) in C57BL/6 mice

2016

International audience; Bisphenol A were removed from consumer products and replaced by chemical substitutes such as Bisphenol S (BPS). Based on their structural similarity, BPS may be obesogen like Bisphenol A in mice. Our objective was to determine the impact of BPS on lipid homeostasis in C57B1/6 mice after perinatal and chronic exposure. Pregnant mice were exposed to BPS via the drinking water (0.2; 1.5; 50 mu g/kg bw/d). Treatment began at gestational day 0 and continued in offspring up to 23-weeks old. Then, offspring mice were fed with a standard or high fat diet. The body weight, food consumption, fat mass and energy expenditure were measured. A lipid load test was performed to chec…

Male0301 basic medicineLeptinBisphenol S[ SDV.TOX ] Life Sciences [q-bio]/ToxicologyAdipose tissue010501 environmental sciencesToxicologyurologic and male genital diseases01 natural sciencesPolyethylene GlycolsMicechemistry.chemical_compoundPregnancyInduced ObesityHyperinsulinemiapériode perinataleObesogenSulfones2. Zero hungerLeptinHigh-Fat Dietsanté humaineLipidsEnergy-Balance3. Good healthSafe AlternativesobésitéAdipose TissuePrenatal Exposure Delayed Effects[SDV.TOX]Life Sciences [q-bio]/Toxicologybisphénol sFemalehormones hormone substitutes and hormone antagonistsmedicine.medical_specialtyOffspringDiet High-Fat03 medical and health sciencesInsulin resistancePhenolsInternal medicinemedicineAnimalshoméostasie lipidiqueObesityRNA MessengerTriglycerides0105 earth and related environmental sciencesDose-Response Relationship DrugAdiponectinTriglycerideInsulin-ResistanceBody WeightOverweightmedicine.diseasebisphenol S;food contaminant;perinatal exposure;low dose;obesogenPerinatal exposureMice Inbred C57BLFood contaminant030104 developmental biologyEndocrinologycontaminant chimiqueLow doseGlucoseMetabolismGene Expression RegulationchemistryIn-VitroObesogenAnalogs
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The LepR-mediated leptin transport across brain barriers controls food reward

2018

Objective Leptin is a key hormone in the control of appetite and body weight. Predominantly produced by white adipose tissue, it acts on the brain to inhibit homeostatic feeding and food reward. Leptin has free access to circumventricular organs, such as the median eminence, but entry into other brain centers is restricted by the blood–brain and blood–CSF barriers. So far, it is unknown for which of its central effects leptin has to penetrate brain barriers. In addition, the mechanisms mediating the transport across barriers are unclear although high expression in brain barriers suggests an important role of the leptin receptor (LepR). Methods We selectively deleted LepR in brain endothelia…

Male0301 basic medicineLeptinHFD high-fat dietEndothelial cellsWhite adipose tissueCSF cerebrospinal fluidMice0302 clinical medicineCPP conditioned place preferenceBBB blood–brain barrierCells Culturedmedia_commonLeptindigestive oral and skin physiologyi.p. intraperitonealmedicine.anatomical_structureLepRBlood-Brain BarrierBlood–brain barrier; Endothelial cells; LepR; Leptin; Obesity; RewardMedian eminenceqPCR quantitative polymerase chain reactionReceptors LeptinOriginal ArticleChoroid plexusmedicine.medical_specialtylcsh:Internal medicinemedia_common.quotation_subjectHyperphagiaBiologyBlood–brain barrierVTA ventral tegmental areaBC bottle choice testCapillary PermeabilityBlood–brain barrierARC arcuate nucleus03 medical and health sciencesPBS phosphate buffered salineRewardInternal medicinemedicineAnimalsObesitylcsh:RC31-1245Molecular BiologyCircumventricular organsBlood-Nerve BarrierLeptin receptorNCD normal chow dietAppetiteCell Biology030104 developmental biologyEndocrinologyLepR leptin receptorChoroid PlexusBSA bovine serum albuminPFA paraformaldehyde030217 neurology & neurosurgeryDAPI 4′6-diamidino-2-phenylindoleMolecular Metabolism
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Short-term moderate diet restriction in adulthood can reverse oxidative, cardiovascular and metabolic alterations induced by postnatal overfeeding in…

2016

AbstractWe aimed to determine whether moderate diet restriction could restore cardiac, oxidative and metabolic alterations induced by postnatal overfeeding (PNOF). Litters of C57BL/6 male mice were either maintained at 9 (normal litter, NL), or reduced to 3 (small litter, SL) in order to induce PNOF. At 6 months, half of the NL and SL mice were subjected to 20% calorie-restriction (CR: NLCR, SLCR) for one month, while the other half continued to eat ad libitum (AL: NLAL, SLAL). Six-month old SL mice presented overweight, fat accumulation, hyperleptinemia, glucose intolerance, insulin resistance, increased cardiac ROS production and decreased left ventricular ejection fraction (LVEF). After …

Male0301 basic medicineLitter Size[ SDV.AEN ] Life Sciences [q-bio]/Food and NutritionAdipose tissueMitochondria HeartMice0302 clinical medicine[SDV.MHEP.EM] Life Sciences [q-bio]/Human health and pathology/Endocrinology and metabolismMultidisciplinaryEjection fractionHigh-Fat Diet[ SDV.MHEP.CSC ] Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular system[ SDV.MHEP.EM ] Life Sciences [q-bio]/Human health and pathology/Endocrinology and metabolism[SDV.MHEP.EM]Life Sciences [q-bio]/Human health and pathology/Endocrinology and metabolism[SDV.MHEP.CSC] Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular systemAdipose-Tissuecoronary-heart-disease;adipose-tissue;insulin-resistance;blood-pressure;weight-gain;rats;obesity;high-fat diet;caloric restriction;glucocorticoid metabolismAlimentation et NutritionBlood-PressureBody Compositionmedicine.symptommedicine.medical_specialtyRespiratory rate030209 endocrinology & metabolismOxidative phosphorylationCarbohydrate metabolismBiologyArticle03 medical and health sciencesInsulin resistanceMetabolic Diseases[SDV.MHEP.CSC]Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular systemInternal medicinemedicineFood and NutritionAnimalsObesityGlucocorticoid MetabolismCaloric RestrictionWeight-GainInsulin-ResistanceBody Weightmedicine.diseaseRatsMice Inbred C57BL[SDV.AEN] Life Sciences [q-bio]/Food and NutritionOxidative Stress030104 developmental biologyEndocrinologyBlood pressureAnimals NewbornInsulin ResistanceCoronary-Heart-Disease[SDV.AEN]Life Sciences [q-bio]/Food and NutritionWeight gainScientific Reports
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CD40L controls obesity-associated vascular inflammation, oxidative stress, and endothelial dysfunction in high fat diet-treated and db/db mice

2018

Abstract Aims CD40 ligand (CD40L) signaling controls vascular oxidative stress and related dysfunction in angiotensin-II-induced arterial hypertension by regulating vascular immune cell recruitment and platelet activation. Here we investigated the role of CD40L in experimental hyperlipidemia. Methods and results Male wild type and CD40L−/− mice (C57BL/6 background) were subjected to high fat diet for sixteen weeks. Weight, cholesterol, HDL, and LDL levels, endothelial function (isometric tension recording), oxidative stress (NADPH oxidase expression, dihydroethidium fluorescence) and inflammatory parameters (inducible nitric oxide synthase, interleukin-6 expression) were assessed. CD40L exp…

Male0301 basic medicinePhysiologyAnti-Inflammatory AgentsNitric Oxide Synthase Type II030204 cardiovascular system & hematologyWeight Gainmedicine.disease_causeAntioxidantschemistry.chemical_compound0302 clinical medicineHyperlipidemiaEndothelial dysfunctionMice KnockoutbiologyLeptinLipidsVasodilationNitric oxide synthaseInflammation Mediatorsmedicine.symptomCardiology and Cardiovascular Medicinemedicine.medical_specialtyCD40 LigandHyperlipidemiasInflammationDiet High-Fat03 medical and health sciencesPhysiology (medical)Internal medicinemedicineAnimalsHumansObesityPlatelet activationInflammationTNF Receptor-Associated Factor 6Interleukin-6Cholesterolbusiness.industryMyocardiumNADPH OxidasesPlatelet Activationmedicine.diseaseMice Inbred C57BLDisease Models AnimalOxidative Stress030104 developmental biologyEndocrinologyDiabetes Mellitus Type 2chemistrybiology.proteinEndothelium VascularbusinessBiomarkersOxidative stressCardiovascular Research
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Glucagon-like peptide-2 treatment improves glucose dysmetabolism in mice fed a high fat diet

2016

Previous studies suggested that endogenous glucagon-like peptide 2 (GLP-2) is dispensable for the regulation of glucose homeostasis under normal conditions, while it can play a beneficial role in obesity conditions. The purpose of the present study was to investigate whether chronic treatment with Gly2-GLP-2, a stable analogue of GLP-2, can have an impact on glycaemic and lipid control in mice fed a high-fat diet (HFD), an animal model of human obesity and insulin resistance. HFD mice were treated once a day with Gly2-GLP-2 for 4 weeks. Body weight, food intake, fasting glucose, intraperitoneal glucose tolerance, insulin-induced glucose clearance, glucose-stimulated insulin secretion, β-cel…

Male0301 basic medicinemedicine.medical_specialtyEndocrinology Diabetes and MetabolismDrug Evaluation PreclinicalMicrovesicular SteatosisCarbohydrate metabolismDiet High-FatSettore BIO/09 - FisiologiaRandom Allocation03 medical and health sciencesEndocrinologyInsulin resistanceInternal medicineDiabetes mellitusGlucagon-Like Peptide 2medicineAnimalsGlucose homeostasisObesityPancreasPancreatic islets.Glucose Metabolism Disordersbusiness.industrydigestive oral and skin physiologyInsulin resistancemedicine.diseaseGlucagon-like peptide-2LipidsObesityMice Inbred C57BL030104 developmental biologyEndocrinologyLiverPeptidesbusinessGLP-2Dyslipidemia
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Uncoupling of Endothelial Nitric Oxide Synthase in Perivascular Adipose Tissue of Diet-Induced Obese Mice

2015

Objective— The present study was conducted to investigate the contribution of perivascular adipose tissue (PVAT) to vascular dysfunction in a mouse model of diet-induced obesity. Approach and Results— Obesity was induced in male C57BL/6J mice with a high-fat diet for 20 weeks, and vascular function was studied with myograph. In PVAT-free aortas isolated from obese mice, the endothelium-dependent, nitric oxide–mediated vasodilator response to acetylcholine remained normal. In contrast, a clear reduction in the vasodilator response to acetylcholine was observed in aortas from obese mice when PVAT was left in place. Adipocytes in PVAT were clearly positive in endothelial nitric oxide synthase…

Male0301 basic medicinemedicine.medical_specialtyNitric Oxide Synthase Type IIIVasodilator AgentsAdipose tissueAorta ThoracicVasodilation030204 cardiovascular system & hematologyArginineDiet High-FatNitric OxideNitric oxide03 medical and health scienceschemistry.chemical_compound0302 clinical medicineAdipokinesSuperoxidesEnosInternal medicineParacrine CommunicationAdipocytesmedicineAnimalsObesityEnzyme InhibitorsPhosphorylationAdiposityArginaseDose-Response Relationship DrugbiologyNitric Oxide Synthase Type IIIbiology.organism_classificationMice Inbred C57BLVasodilationArginaseDisease Models Animal030104 developmental biologyEndocrinologyAdipose TissuechemistryCytokinesInflammation MediatorsCardiology and Cardiovascular MedicineDiet-induced obeseSignal TransductionMyographArteriosclerosis, Thrombosis, and Vascular Biology
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Impact of diet-induced obesity on the mouse brain phosphoproteome

2018

Obesity is closely associated to several diseases such as type 2 diabetes, cardiovascular disease, hepatic steatosis, airway disease, neurodegeneration, biliary diseases and certain cancers. It is, therefore, of importance to assess the role of nutrition in disease prevention as well as its effect in the course of such pathologies. In the present study, we addressed the impact of the exposure to different obesogenic diets in the mice brains phosphoproteome. To analyze if the obesity could be able to modify the protein pattern expression of brain neurons, obesity was induced in two different groups of mice. One group of mice was fed with hyperglycemic diet (HGD) and the other one was fed wit…

Male0301 basic medicinemedicine.medical_specialtyPhosphoproteomicsEndocrinology Diabetes and MetabolismClinical BiochemistryHyperglycemic dietType 2 diabetesDiseaseBiologyDiet High-FatBiochemistry03 medical and health sciences0302 clinical medicineInternal medicinemedicineAnimalsProtein phosphorylationObesityPhosphorylationMolecular BiologyGSK3BNutritionNeuronal impairmentNutrition and DieteticsNeurodegenerationta1182BrainObesity; Nutrition; High-fat diet; Hyperglycemic diet; Neuronal impairment; PhosphoproteomicsPhosphoproteinsmedicine.diseaseObesityMice Inbred C57BLHigh-fat dietGene Ontology030104 developmental biologyEndocrinologyHyperglycemiaPhosphorylationCalcium ChannelsSteatosis030217 neurology & neurosurgeryThe Journal of Nutritional Biochemistry
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Cholesterol burden in the liver induces mitochondrial dynamic changes and resistance to apoptosis

2018

Non-alcoholic fatty liver disease (NAFLD) encompasses a broad spectrum of histopathological changes ranging from non-inflammatory intracellular fat deposition to non-alcoholic steatohepatitis (NASH), which may progress into hepatic fibrosis, cirrhosis, or hepatocellular carcinoma. Recent data suggest that impaired hepatic cholesterol homeostasis and its accumulation are relevant to the pathogenesis of NAFLD/NASH. Despite a vital physiological function of cholesterol, mitochondrial dysfunction is an important consequence of dietary-induced hypercholesterolemia and was, subsequently, linked to many pathophysiological conditions. The aim in the current study was to evaluate the morphological a…

Male0301 basic medicinemedicine.medical_specialtyTime FactorsCirrhosisPhysiologyClinical BiochemistryApoptosisMitochondria LiverMitochondrionDiet High-Fatmedicine.disease_causeMitochondrial DynamicsCholesterol Dietary03 medical and health scienceschemistry.chemical_compound0302 clinical medicineNon-alcoholic Fatty Liver DiseaseInternal medicinemedicineAnimalsCells CulturedCell ProliferationCholesterolbusiness.industryFatty liverCell Biologymedicine.diseaseMice Inbred C57BLDisease Models AnimalOxidative Stress030104 developmental biologymedicine.anatomical_structureEndocrinologyGene Expression RegulationLiverchemistry030220 oncology & carcinogenesisHepatocyteHepatocytesSteatohepatitisTranscriptomeHepatic fibrosisbusinessOxidative stressJournal of Cellular Physiology
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