Search results for "Methylhydrazines"

showing 10 items of 27 documents

Mitochondrial Fatty Acid β-Oxidation Inhibition Promotes Glucose Utilization and Protein Deposition through Energy Homeostasis Remodeling in Fish.

2020

BACKGROUND: Fish cannot use carbohydrate efficiently and instead utilize protein for energy supply, thus limiting dietary protein storage. Protein deposition is dependent on protein turnover balance, which correlates tightly with cellular energy homeostasis. Mitochondrial fatty acid β-oxidation (FAO) plays a crucial role in energy metabolism. However, the effect of remodeled energy homeostasis caused by inhibited mitochondrial FAO on protein deposition in fish has not been intensively studied. OBJECTIVES: This study aimed to identify the regulatory role of mitochondrial FAO in energy homeostasis maintenance and protein deposition by studying lipid, glucose, and protein metabolism in fish. M…

0301 basic medicineMaleProtein metabolismMedicine (miscellaneous)MitochondrionEnergy homeostasis03 medical and health scienceschemistry.chemical_compoundNile tilapia0302 clinical medicineAdjuvants ImmunologicmedicineAnimalsHomeostasisInsulinCarnitineProtein kinase ACells CulturedZebrafishNutrition and DieteticsbiologyCarnitine O-PalmitoyltransferaseChemistryFatty AcidsProtein turnoverProteinsMetabolismCichlidsDNACytochromes bbiology.organism_classificationMitochondria030104 developmental biologyGlucoseBiochemistryMutationHepatocytesNutrient Physiology Metabolism and Nutrient-Nutrient InteractionsEnergy MetabolismOxidation-Reduction030217 neurology & neurosurgerymedicine.drugMethylhydrazinesThe Journal of nutrition
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Inhibited fatty acid β-oxidation impairs stress resistance ability in Nile tilapia (Oreochromis niloticus)

2017

Energy metabolism plays important roles in stress resistance and immunity in mammals, however, such functions have not been established in fish. In the present study, Nile tilapia (Oreochromis niloticus) was fed with mildronate, an inhibitor of mitochondrial fatty acid (FA) β-oxidation, for six weeks subsequently challenged with Aeromonas hydrophila and ammonia nitrogen exposure. Mildronate treatment reduced significantly l-carnitine concentration and mitochondrial FA β-oxidation efficiency, while it increased lipid accumulation in liver. The fish with inhibited hepatic FA catabolism had lower survival rate when exposed to Aeromonas hydrophila and ammonia nitrogen. Moreover, fish fed mildro…

0301 basic medicineNitrogenAquatic ScienceMitochondrionFish DiseasesRandom Allocation03 medical and health sciencesNile tilapiaImmune systemAmmoniaStress PhysiologicalCarnitinemedicineAnimalsEnvironmental ChemistryCarnitinechemistry.chemical_classificationbiologyCatabolismFatty AcidsFatty acidCichlids04 agricultural and veterinary sciencesGeneral Medicinebiology.organism_classificationAnimal FeedAeromonas hydrophilaDietMitochondriaOreochromisAeromonas hydrophila030104 developmental biologychemistryBiochemistryDietary Supplements040102 fisheries0401 agriculture forestry and fisheriesGram-Negative Bacterial InfectionsOxidation-ReductionMethylhydrazinesmedicine.drugFish & Shellfish Immunology
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Anti-diabetic effects of mildronate alone or in combination with metformin in obese Zucker rats

2010

Abstract Mildronate is a cardioprotective drug, the mechanism of action of which is based on the regulation of l -carnitine concentration. We studied the metabolic effects of treatment with mildronate, metformin and a combination of the two in the Zucker rat model of obesity and impaired glucose tolerance. Zucker rats were p.o. treated daily with mildronate (200 mg/kg), metformin (300 mg/kg), and a combination of both drugs for 4 weeks. Weight gain and plasma metabolites reflecting glucose metabolism were measured. The expression of peroxisome proliferator-activated receptor (PPAR)-α and PPAR-γ and target genes was measured in rat heart and liver tissues. Each treatment decreased the blood …

Blood GlucoseMalemedicine.medical_specialtymedicine.medical_treatmentPeroxisome proliferator-activated receptorCarbohydrate metabolismImpaired glucose toleranceEatingInternal medicinemedicineAnimalsHypoglycemic AgentsInsulinPPAR alphaLactic AcidObesityRNA MessengerCarnitineCell NucleusPharmacologychemistry.chemical_classificationbusiness.industryMyocardiumInsulinBody WeightLipid Metabolismmedicine.diseaseMetforminRatsRats ZuckerMetforminPPAR gammaDrug CombinationsEndocrinologyGene Expression RegulationMechanism of actionchemistryCarnitine biosynthesismedicine.symptombusinessMethylhydrazinesmedicine.drugEuropean Journal of Pharmacology
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Correction of glycaemia and GLUT1 level by mildronate in rat streptozotocin diabetes mellitus model

2011

Anti-ischaemic drug mildronate suppresses fatty acid metabolism and increases glucose utilization in myocardium. It was proposed that it could produce a favourable effect on metabolic parameters and glucose transport in diabetic animals. Rats with streptozotocin diabetes mellitus were treated with mildronate (100 mg/kg daily, per os, 6 weeks). Therapeutic effect of mildronate was monitored by measuring animal weight, concentrations of blood glucose, insulin, blood triglycerides, free fatty acids, blood ketone bodies and cholesterol, glycated haemoglobin per cent (HbA1c%) and glucose tolerance. GLUT1 mRNA and protein expression in kidneys, heart, liver and muscles were studied by means of re…

Blood Glucosemedicine.medical_specialtyendocrine system diseasesmedicine.medical_treatmentClinical BiochemistryBiochemistryStreptozocinDiabetes Mellitus Experimentalchemistry.chemical_compoundInternal medicineDiabetes mellitusDiabetes MellitusmedicineAnimalsBody SizeHypoglycemic AgentsInsulinRNA MessengerRats WistarTriglyceridesGlycated HemoglobinGlucose Transporter Type 1Glucose tolerance testmedicine.diagnostic_testFatty acid metabolismbiologyCholesterolbusiness.industryInsulinFatty AcidsGlucose transporternutritional and metabolic diseasesCell BiologyGeneral MedicineGlucose Tolerance Testmedicine.diseaseRatsEndocrinologychemistrybiology.proteinKetone bodiesGLUT1businessMethylhydrazinesCell Biochemistry and Function
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Mildronate treatment improves functional recovery following middle cerebral artery occlusion in rats

2011

Mildronate (3-(2,2,2-trimethylhydrazinium) propionate) is an inhibitor of l-carnitine biosynthesis and an anti-ischemic drug. In the present study, we investigated the effects of mildronate in rats following focal cerebral ischemia. Male Wistar rats were subjected to transient occlusion of the middle cerebral artery (MCAO) for 90min, followed by the intraperitoneal administration of mildronate at doses of 100 and 200mg/kg 2h after reperfusion and then daily for an additional 14days. The beam-walking, rota-rod and cylinder tests were used to assess sensorimotor function, and vibrissae-evoked forelimb-placing and limb-placing tests examined responses to tactile and proprioceptive stimulation.…

Brain InfarctionMaleIschemiaStimulationPharmacologyRotarod performance testBrain ischemiaBehavioral NeuroscienceAdjuvants ImmunologicTandem Mass SpectrometryCarnitinemedicine.arterymedicineAnimalsRats WistarStrokeChromatography High Pressure LiquidAnalysis of VarianceDose-Response Relationship Drugbusiness.industryExtremitiesInfarction Middle Cerebral ArteryRecovery of Functionmedicine.diseaseRatsBetaineDose–response relationshipRotarod Performance TestVibrissaeMiddle cerebral arterySystemic administrationbusinessNeuroscienceLocomotionPsychomotor PerformanceMethylhydrazinesBehavioural Brain Research
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Mechanisms of tumor invasion: evidence from in vivo observations.

1985

The major mechanisms of tumor invasion in vivo are discussed in the present review. A special emphasis is placed on tumor dedifferentiation which has proved to be of paramount importance for the invasion process. Based on in vivo observations obtained from various human and animal tumors a concept for the mechanism of tumor invasion is proposed which mainly comprises the following basic events: the first and essential step in tumor invasion is the tumor dedifferentiation and dissociation at the invasion front. This apparently temporary and reversible process mobilizes the tumor cells out of the main tumor bulk and enables them to invade the host tissue by active locomotion. This mechanism i…

Cancer ResearchPathologymedicine.medical_specialtyCell divisionColonCellular differentiationBiologyHost tissueBasement MembraneExtracellular matrixIn vivoCell MovementmedicineAnimalsEdemaHumansNeoplasm InvasivenessProcess (anatomy)Cells CulturedDimethylhydrazinesCell DifferentiationMuscle SmoothCell biology12-DimethylhydrazineExtracellular MatrixNeoplasm ProteinsRatsOxygenInterstitial edemaIntercellular JunctionsOncologyColonic NeoplasmsAtrophyIntracellularCell DivisionPeptide HydrolasesCancer metastasis reviews
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Effect of Experimental and Sample Factors on Dehydration Kinetics of Mildronate Dihydrate: Mechanism of Dehydration and Determination of Kinetic Para…

2014

The dehydration kinetics of mildronate dihydrate [3-(1,1,1-trimethylhydrazin-1-ium-2-yl)propionate dihydrate] was analyzed in isothermal and nonisothermal modes. The particle size, sample preparation and storage, sample weight, nitrogen flow rate, relative humidity, and sample history were varied in order to evaluate the effect of these factors and to more accurately interpret the data obtained from such analysis. It was determined that comparable kinetic parameters can be obtained in both isothermal and nonisothermal mode. However, dehydration activation energy values obtained in nonisothermal mode showed variation with conversion degree because of different rate-limiting step energy at hi…

ChemistrySAMPLE historyKineticsWaterPharmaceutical ScienceThermodynamicsCardiovascular AgentsActivation energyKinetic energymedicine.diseaseIsothermal processKineticsmedicineSample preparationParticle sizeDehydrationParticle SizeMethylhydrazinesJournal of Pharmaceutical Sciences
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Protection of Azidothymidine-Induced Cardiopathology in Mice by Mildronate, a Mitochondria-Targeted Drug

2006

Azidothymidine, a nucleoside-analogue reverse transcriptase inhibitor (NRTI), is a commonly used antiretroviral drug in AIDS treatment, however its use is limited by severe toxic side effects due to its influence on mitochondria that result in myopathy, particularly affecting the cardiac muscle. We suggest that effective protection of azidothymidine- induced cardiopathology can be expected from drugs that are capable of targeting mitochondria. Therefore the present study in mice was carried out with mildronate, a cardioprotective drug of the aza-butyrobetaine class, which previously has been shown to act as a highly potent protector of mitochondrial processes. In our study, saline (control)…

DrugHeart Diseasesmedia_common.quotation_subjectInflammationMitochondrionPharmacologyToxicologymedicine.disease_causeMiceZidovudinemedicineAnimalsmedia_commonPharmacologyMice Inbred ICRbiologyReverse-transcriptase inhibitorCardiovascular AgentsGeneral MedicineVirologyMitochondriaDisease Models AnimalEnzyme inhibitorbiology.proteinmedicine.symptomZidovudineNucleosideOxidative stressMethylhydrazinesmedicine.drugBasic <html_ent glyph="@amp;" ascii="&"/> Clinical Pharmacology <html_ent glyph="@amp;" ascii="&"/> Toxicology
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Hypolipidaemic effects of fenofibrate are not altered by mildronate-mediated normalization of carnitine concentration in rat liver.

1999

The five-fold higher carnitine content in the liver of fenofibrate-treated rats addresses the question about the possible role of this enhancement in the hypolipidaemic effect of the drug and the underlying mechanisms. When fenofibrate was administered with mildronate (a gamma-butyrobetaine hydroxylase inhibitor) in suitable amount, the content in carnitine was found to be normalized in liver. However, triglyceride contents of liver and serum were then at least as low as in rats treated by fenofibrate only. When carnitine concentration was lowered by mildronate to the third of the normal value, a marked increase in triglycerides occurred both in liver and serum, while the five-fold increase…

DrugMalemedicine.medical_specialtymedia_common.quotation_subjectBlood lipidsKetone BodiesBiochemistrychemistry.chemical_compoundFenofibrateInternal medicineCarnitinemedicineAnimalsCarnitineRats WistarMuscle SkeletalBeta oxidationPhospholipidsTriglyceridesmedia_commonHypolipidemic AgentsFenofibrateTriglycerideChemistryMyocardiumGeneral MedicinePeroxisomeRatsEndocrinologyCholesterolBiochemistryLiverKetone bodiesmedicine.drugMethylhydrazinesBiochimie
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Mildronate: An Antiischemic Drug for Neurological Indications

2005

Mildronate (3-(2,2,2-trimethylhydrazinium)propionate; MET-88; meldonium, quaterine) is an antiischemic drug developed at the Latvian Institute of Organic Synthesis. Mildronate was designed to inhibit carnitine biosynthesis in order to prevent accumulation of cytotoxic intermediate products of fatty acid beta-oxidation in ischemic tissues and to block this highly oxygen-consuming process. Mildronate is efficient in the treatment of heart ischemia and its consequences. Extensive evaluation of pharmacological activities of mildronate revealed its beneficial effect on cerebral circulation disorders and central nervous system (CNS) functions. The drug is used in neurological clinics for the trea…

Drugmedia_common.quotation_subjectCentral nervous systemIschemiaStimulationKetone BodiesPharmacologyNitric OxideToxicologyModels BiologicalArticleNitric oxidechemistry.chemical_compoundNeuropharmacologyIschemiamedicineAnimalsHumansReceptormedia_commonPharmacologyMeldoniumbusiness.industryCardiovascular Agentsmedicine.diseaseNeuropsychology and Physiological Psychologymedicine.anatomical_structurechemistryMechanism of actionDrug Evaluationmedicine.symptombusinessmedicine.drugMethylhydrazines
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