Search results for "metformin"

showing 10 items of 126 documents

PCOS and infertility. Metformin administration and ovulation induction in patients with reproductive failures. Preliminary data

2014

The aim of this study is to investigate the effects of the metformin administration in patients with previous reproductive failures. Inclusion criteria: 13 patients with chronic anovulation and PCOS, age < 38 years old, sterility not less than 2 years, C.C. resistance, conception failure in previous cycles with only r-FSH and negativity to the multiple miscarriages tests, absence of others infertility factors. Metformin administration started 2 months before the ovulation induction. Alternatively a spontaneous menstruation it was induced by progestin. Ovulation was performed with r-FSH and patients were invited to have sexual intercourse during the 48h after the HCG trigger. Luteal support …

InfertilityGynecologymedicine.medical_specialtybusiness.industrymedicine.medical_treatmentPCOS InfertilityMetforminOvulation inductionPregnancy.medicine.diseaseSettore MED/40 - Ginecologia E OstetriciaMetforminmedicineOvulation inductionIn patientbusinessAdministration (government)medicine.drugGiornale Italiano di Ostetricia e Ginecologia
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Molecular basis of burn wound healing in diabetics: the effect of vitamin B17, metformin, and autologous fat stem cells

Keywords: Diabetes wound healing amygdaline (vitamin B17) inflammation Metformin adipose tissue stem cells IL-2 IL-6 IL-10 and HSP-70.
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Abstract 5476: Inhibiting lactate transporters MCT-1 and MCT-4 target hypoxic HNSCC cells and sensitize them to metformin

2018

Abstract Head and neck squamous cell carcinoma (HNSCC) is treated primarily through a combination of surgery and radiation therapy. The problem of radioresistance, however, persists and requires new approaches to overcome it. Tumor hypoxia has been shown to be a driver of radioresistance, thereby prompting the targeting of the hypoxic niche, known to be highly glycolytic. Two key components of the hypoxic metabolic profile are lactate transporters MCT-1 and MCT-4, which sustain hypoxia-driven lactate production in cells. We hypothesize that inhibition of MCT-1 and MCT-4 will selectively target the growth of hypoxic tumor cells and potentially exert a synergistic effect with the antidiabetic…

Lactate transportCancer ResearchTumor hypoxiaChemistryCell growthHypoxia (medical)medicine.diseaseHead and neck squamous-cell carcinomaMetforminOncologyCell cultureRadioresistancemedicineCancer researchmedicine.symptommedicine.drugCancer Research
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Mevalonate pathway inhibitors affect anticancer drug-induced cell death and DNA damage response of human sarcoma cells

2011

Lovastatin (Lov), bisphosphonates (BP) and metformin (Met) are widely used drugs, having in common that they interfere with the mevalonate pathway (MP). The MP generates isoprene moieties required for the function of regulatory GTPases controlling cell proliferation and survival. Here, we addressed the question whether MP inhibitors interfere with the anti-tumor efficacy of anticancer drugs. We comparatively analyzed the effect of equitoxic doses of Lov, BP and Met on cell viability, cell cycle progression, apoptosis and DNA damage response (DDR) of human osteo- and fibrosarcoma cells exposed to doxorubicin or cisplatin. We found that Lov, BP and Met modulated the anticancer drug sensitivit…

MAPK/ERK pathwayCancer ResearchDNA damageFibrosarcomaBlotting WesternMevalonic AcidAntineoplastic AgentsApoptosisBone NeoplasmsTumor Cells CulturedmedicineHumansDoxorubicinLovastatinRNA MessengerPhosphorylationCell ProliferationCisplatinOsteosarcomaDiphosphonatesbiologyReverse Transcriptase Polymerase Chain ReactionCell growthCell CycleMetforminOncologyDoxorubicinApoptosisHMG-CoA reductasebiology.proteinCancer researchMevalonate pathwayCisplatinTumor Suppressor Protein p53DNA DamageSignal Transductionmedicine.drugCancer Letters
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Roles of EGFR and KRAS and their downstream signaling pathways in pancreatic cancer and pancreatic cancer stem cells

2015

Pancreatic cancer is currently the fourth most common cancer, is increasing in incidence and soon will be the second leading cause of cancer death in the USA. This is a deadly malignancy with an incidence that approximates the mortality with 44,000 new cases and 36,000 deaths each year. Surgery, although only modestly successful, is the only curative option. However, due the locally aggressive nature and early metastasis, surgery can be performed on less than 20% of patients. Cytotoxic chemotherapy is palliative, has significant toxicity and improves survival very little. Thus new treatment paradigms are needed desperately. Due to the extremely high frequency of KRAS gene mutations (>90%) d…

MAPK/ERK pathwayCancer ResearchmiRsEGFRmedicine.disease_causeMetastasisProto-Oncogene Proteins p21(ras)Glycogen Synthase Kinase 3GeneticCancer stem cellKRaPancreatic cancerKRasGeneticsmedicineAnimalsHumansPTENEpidermal growth factor receptorMolecular BiologyPI3K/AKT/mTOR pathwayGSK-3biologyCancer stem cellsCancer stem cellmiRCancer stem cells; Drug resistance; EGFR; GSK-3; KRas; Metformin; miRsmedicine.diseaseMetforminErbB ReceptorsPancreatic NeoplasmsDrug resistanceNeoplastic Stem Cellsbiology.proteinCancer researchMolecular MedicineKRASSignal TransductionAdvances in Biological Regulation
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Sensitivity of pancreatic cancer cells to chemotherapeutic drugs, signal transduction inhibitors and nutraceuticals can be regulated by WT-TP53

2020

Abstract Pancreatic ductal adenocarcinoma (PDAC) is a highly metastatic malignancy. Approximately 85% of pancreatic cancers are classified as PDACs. The survival of PDAC patients is very poor and only 5–10% of patients survive 5 years after diagnosis. Mutations at the KRAS and TP53 gene are frequently observed in PDAC patients. The PANC-28 cell line lacks wild-type (WT) TP53. In the following study, we have investigated the effects of restoration of WT TP53 activity on the sensitivity of PANC-28 pancreatic cancer cells to various drugs which are used to treat PDAC patients as well as other cancer patients. In addition, we have examined the effects of signal transduction inhibitors which tar…

Male0301 basic medicineDrugCancer ResearchmiRsendocrine system diseasesmedia_common.quotation_subjectSignal transduction inhibitorsTargeted therapeuticAntineoplastic AgentsMalignancymedicine.disease_causeProto-Oncogene Proteins p21(ras)03 medical and health sciences0302 clinical medicineChloroquinePancreatic cancerGeneticsmedicineHumansTP53Molecular BiologyneoplasmsSignal transduction inhibitorTargeted therapeuticsCell Proliferationmedia_commontarget therapeuticsCell growthbusiness.industryCancermedicine.diseasedigestive system diseasesMetforminPancreatic Neoplasms030104 developmental biology030220 oncology & carcinogenesisDietary SupplementsMutationCancer researchmiRs.Molecular MedicineFemaleKRASTumor Suppressor Protein p53businessSignal Transductionmedicine.drugDrug sensitivity
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The desert gerbil Psammomys obesus as a model for metformin-sensitive nutritional type 2 diabetes to protect hepatocellular metabolic damage: Impact …

2017

Introduction While metformin (MET) is the most widely prescribed antidiabetic drug worldwide, its beneficial effects in Psammomys obesus (P. obesus), a rodent model that mimics most of the metabolic features of human diabetes, have not been explored thoroughly. Here, we sought to investigate whether MET might improve insulin sensitivity, glucose homeostasis, lipid profile as well as cellular redox and energy balance in P. obesus maintained on a high energy diet (HED). Materials and methods P. obesus gerbils were randomly assigned to receive either a natural diet (ND) consisting of halophytic plants (control group) or a HED (diabetic group) for a period of 24 weeks. MET (50 mg/kg per os) was…

Male0301 basic medicinePhysiologymedicine.medical_treatment[SDV]Life Sciences [q-bio]Body-WeightRespiratory chainlcsh:MedicineMitochondria LiverBiochemistrychemistry.chemical_compoundLiver Parenchymal-CellsEndocrinologyGlucose MetabolismAnimal CellsKetogenesisMedicine and Health SciencesElectrochemistryGlucose homeostasisGut Microbiotalcsh:ScienceEnergy-Producing OrganellesComputingMilieux_MISCELLANEOUS2. Zero hungerMultidisciplinaryOrganic CompoundsMonosaccharidesFatty AcidsChemical ReactionsLipidsMetforminMitochondria3. Good healthChemistryPhysiological ParametersLiverPhysical SciencesCarbohydrate MetabolismCellular Structures and OrganellesCellular TypesAnatomyOxidation-ReductionResearch Articlemedicine.medical_specialtyIsolated Rat HepatocytesEndocrine DisordersCarbohydratesBioenergeticsBiologyCarbohydrate metabolism03 medical and health sciencesInsulin resistanceInternal medicineFood-IntakeDiabetes MellitusmedicineAnimalsHypoglycemic AgentsObesityRespiratory-Chain[ SDV ] Life Sciences [q-bio]Fatty acid metabolismInsulinBody WeightOrganic Chemistrylcsh:RChemical CompoundsGluconeogenesisBiology and Life SciencesCell Biologymedicine.diseaseGlucose-6-Phosphate HydrolysisDisease Models AnimalGlucoseMetabolism030104 developmental biologyEndocrinologyDiabetes Mellitus Type 2GluconeogenesischemistryMetabolic DisordersHepatocyteslcsh:QInsulin ResistanceGerbillinaeGlucose-ProductionFatty-Acid-MetabolismOxidation-Reduction Reactions
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Does Metformin Modulate Endoplasmic Reticulum Stress and Autophagy in Type 2 Diabetic Peripheral Blood Mononuclear Cells?

2018

Since type 2 diabetes (T2D) is associated with oxidative stress and metformin has been shown to exert a protective role against the said stress, we wondered whether metformin treatment might also modulate endoplasmic reticulum (ER) stress and autophagy in leukocytes of T2D patients. We studied 53 T2D patients (37 of whom had been treated with metformin 1700 mg for at least 1 year) and 30 healthy volunteers. Leukocytes from both groups of T2D patients exhibited increased protein levels of 78-kDa glucose-regulated protein (GRP78) with respect to controls, whereas activating transcription factor 6 (ATF6) was enhanced specifically in nonmetformin-treated T2D, and (s-xbp1) and phosphorylated euk…

Male0301 basic medicinemedicine.medical_specialtyendocrine system diseasesPhysiologyClinical BiochemistryAdministration OralType 2 diabetesBiologymedicine.disease_causeBiochemistry03 medical and health sciencesInternal medicineAutophagymedicineHumansEndoplasmic Reticulum Chaperone BiPMolecular BiologyGeneral Environmental ScienceDose-Response Relationship DrugATF6Endoplasmic reticulumAutophagynutritional and metabolic diseasesCell BiologyBECN1Middle AgedEndoplasmic Reticulum Stressmedicine.diseaseMetforminMetforminOxidative StressCross-Sectional Studies030104 developmental biologyEndocrinologyDiabetes Mellitus Type 2Leukocytes MononuclearUnfolded protein responseGeneral Earth and Planetary SciencesFemaleOxidative stressmedicine.drugAntioxidants &amp; Redox Signaling
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Investigating the Vascular Toxicity Outcomes of the Irreversible Proteasome Inhibitor Carfilzomib

2020

Background: Carfilzomib&rsquo

Male0301 basic medicinevasculature030204 cardiovascular system & hematologyPharmacologyDinoprostEndoplasmic Reticulumlcsh:ChemistryMicechemistry.chemical_compound0302 clinical medicineAMP-Activated Protein Kinase Kinasesvascular smooth muscle cellsCytotoxicitylcsh:QH301-705.5endoplasmatic-reticulum stressSpectroscopychemistry.chemical_classificationcarfilzomibCobaltGeneral MedicineMetforminComputer Science ApplicationsRespiratory burstMetforminDrug Therapy CombinationGlycolysisOligopeptidesProteasome Inhibitorsmedicine.drugProteasome Endopeptidase ComplexautophagyCell SurvivalMyocytes Smooth MuscleAntineoplastic AgentsNitric OxideArticleCatalysisInorganic Chemistry03 medical and health sciencesmedicineAnimalsHumansPhysical and Theoretical ChemistryMolecular BiologyReactive oxygen speciesbusiness.industryOrganic ChemistryAutophagyCarfilzomibActinsVasoprotectiveMice Inbred C57BLGlucose030104 developmental biologychemistrylcsh:Biology (General)lcsh:QD1-999Proteasome inhibitorTumor Suppressor Protein p53Reactive Oxygen SpeciesbusinessProtein KinasesInternational Journal of Molecular Sciences
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Metformin induces an agonist-specific increase in albumin production by primary cultured rat hepatocytes

1995

Abstract Metformin (MET) is known to increase several biological effects of insulin (INS), but there is no information concerning its direct effects on protein synthesis. We studied the action of MET on albumin production by primary cultures of freshly isolated rat hepatocytes, alone or in combination with various agonists: INS, IGF-1, EGF, thyroxin, and dexamethasone. While having no effect alone, MET in vitro potentiates the effects of INS, IGF-1, and EGF. When this increasing effect toward INS was studied over a broad concentration range, MET appeared to improve low-acting INS levels and to intensify the maximal INS effects. In contrast, MET did not change the production of albumin stimu…

MaleAgonistmedicine.medical_specialtyTime FactorsCell Survivalmedicine.drug_classBiologyBiochemistryIn vivoCell surface receptorAlbuminsInternal medicinemedicineAnimalsInsulinInsulin-Like Growth Factor IRats WistarCells CulturedPharmacologyEpidermal Growth FactorBody WeightAlbuminMetforminIn vitroRatsMetforminmedicine.anatomical_structureEndocrinologyLiverCell cultureHepatocytemedicine.drugBiochemical Pharmacology
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