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  1 / 202 MEDLINE  
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[PMID]:28532757
[Au] Autor:Meyskens FL; Liu-Smith F
[Ad] Endereço:Department of Medicine, Biological Chemistry, Epidemiology, and Public Health, Chao Family Comprehensive Cancer Center, University of California, Irvine, Orange, California, USA. Electronic address: flmeyske@uci.edu.
[Ti] Título:Redox-Redux and NADPH Oxidase (NOX): Even More Complicated than We Thought it Might Be.
[So] Source:J Invest Dermatol;137(6):1208-1210, 2017 Jun.
[Is] ISSN:1523-1747
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The NOX (nicotinamide adenine dinucleotide phosphate oxidase) family includes seven unique members that are involved in a multitude of physiological functions, including extensive interaction with UVR and the skin. NOX1 is uniquely present and activated by UVB radiation with biphasic expression of the enzyme immediately and then after a several-hour delay. Specific inhibition of both early and late NOX1 activation leads to evidence of decreased photocarcinogenesis in in vitro keratinocytes and in well-characterized mouse models in which antitumor efficacy has been shown; inhibiting only late NOX activation does not exhibit such effects. These results suggest a crucial function of early NOX activation in transducing a signal for cellular protection after UVB carcinogenesis provocation. We term this an intrinsic cellular ROS priming function for quenching DNA damage and promoting survival. Evolutionally, this type of priming function may be essential for addressing various types of stimuli from adverse environments.
[Mh] Termos MeSH primário: Carcinogênese/metabolismo
NADPH Oxidases/metabolismo
Estresse Oxidativo/fisiologia
Neoplasias Cutâneas/fisiopatologia
Raios Ultravioleta/efeitos adversos
[Mh] Termos MeSH secundário: Animais
Carcinogênese/patologia
Dexfenfluramina
Seres Humanos
Camundongos
Oxirredução
Espécies Reativas de Oxigênio
Sensibilidade e Especificidade
Neoplasias Cutâneas/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Reactive Oxygen Species); E35R3G56OV (Dexfenfluramine); EC 1.6.3.- (NADPH Oxidases)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170524
[St] Status:MEDLINE


  2 / 202 MEDLINE  
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[PMID]:25754908
[Au] Autor:Cambon D; Leclercq F
[Ad] Endereço:Department of Cardiology, University Hospital Montpellier, Montpellier, France. Electronic address: david.cambon@free.fr.
[Ti] Título:Clinical and echographic characteristics of patients exposed to fenfluramin or its derivatives: Results of a prospective, single-centre, observational study.
[So] Source:Arch Cardiovasc Dis;108(3):172-80, 2015 Mar.
[Is] ISSN:1875-2128
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Fenfluramine and its derivatives have been associated with significant risk of developing valvular heart disease but its exact prevalence and severity are still debated. AIM: To evaluate the clinical and echocardiographic characteristics of patients hospitalized in a cardiology centre and who had past exposure to these drugs. METHODS: Between July 2011 and February 2012, patients admitted to the hospitalization and intensive care units at the University Centre of Montpellier, France were questioned about past exposure to fenfluramine or its derivatives. In patients who reported exposure, a questionnaire assessing prescribing patterns and medical history was proposed and echocardiography performed. All of the usual echocardiographic variables were analysed. We applied criteria from a French multicentre registry for diagnosis of drug-induced valvulopathy: leaflets and subvalvular apparatus thickening and retraction, leaflets loss of coaptation, no calcification, and no stenosis. RESULTS: Ninety-five patients exposed to these drugs were included. The majority were female (n=62, 65.3%), 53.2% (n=50) had diabetes and 90.5% (n=86) were exposed to benfluorex. Mean treatment duration was 52.3months (95% confidence interval [CI] 39.0-65.6). Valvular regurgitations were observed in 64.0% of patients (n=57) while 19.8% (n=17) had pulmonary hypertension. Highly probable fenfluramine-induced regurgitations were present in 18.6% (n=16) of patients, possibly fenfluramine-induced regurgitations in 38.2% (n=34) of patients, and unlikely fenfluramine-induced regurgitations in 25.8% (n=23) of patients. Highly probable fenfluramine-induced regurgitations were mild to moderate in severity in all except three patients. CONCLUSION: Considering the frequency of probable or possible fenfluramine-induced regurgitations and in the absence of definite knowledge about the evolution of drug-induced valvular disease, systematic questioning about fenfluramine use may be advisable in hospitalized cardiac patients.
[Mh] Termos MeSH primário: Depressores do Apetite/efeitos adversos
Fenfluramina/análogos & derivados
Fenfluramina/efeitos adversos
Cardiopatias/induzido quimicamente
Cardiopatias/diagnóstico
[Mh] Termos MeSH secundário: Idoso
Dexfenfluramina/efeitos adversos
Feminino
Cardiopatias/diagnóstico por imagem
Seres Humanos
Masculino
Estudos Prospectivos
Ultrassonografia
[Pt] Tipo de publicação:JOURNAL ARTICLE; OBSERVATIONAL STUDY
[Nm] Nome de substância:
0 (Appetite Depressants); 2DS058H2CF (Fenfluramine); 403FO0NQG3 (benfluorex); E35R3G56OV (Dexfenfluramine)
[Em] Mês de entrada:1602
[Cu] Atualização por classe:161125
[Lr] Data última revisão:
161125
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150311
[St] Status:MEDLINE


  3 / 202 MEDLINE  
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[PMID]:25524140
[Au] Autor:Grottick AJ; Whelan K; Sanabria EK; Behan DP; Morgan M; Sage C
[Ad] Endereço:Arena Pharmaceuticals Inc, 6154 Nancy Ridge Drive, San Diego, CA, 92121, USA, agrottick@arenapharm.com.
[Ti] Título:Investigating interactions between phentermine, dexfenfluramine, and 5-HT2C agonists, on food intake in the rat.
[So] Source:Psychopharmacology (Berl);232(11):1973-82, 2015 Jun.
[Is] ISSN:1432-2072
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:RATIONALE: Synergistic or supra-additive interactions between the anorectics (dex)fenfluramine and phentermine have been reported previously in the rat and in the clinic. Studies with 5-HT2C antagonists and 5-HT2C knockouts have demonstrated dexfenfluramine hypophagia in the rodent to be mediated by actions at the 5-HT2C receptor. Given the recent FDA approval of the selective 5-HT2C agonist lorcaserin (BELVIQ®) for weight management, we investigated the interaction between phentermine and 5-HT2C agonists on food intake. OBJECTIVES: This study aims to confirm dexfenfluramine-phentermine (dex-phen) synergy in a rat food intake assay, to extend these findings to other 5-HT2C agonists, and to determine whether pharmacokinetic interactions could explain synergistic findings with particular drug combinations. METHODS: Isobolographic analyses were performed in which phentermine was paired with either dexfenfluramine, the 5-HT2C agonist AR630, or the 5-HT2C agonist lorcaserin, and inhibition of food intake measured in the rat. Subsequent studies assessed these same phentermine-drug pair combinations spanning both the full effect range and a range of fixed ratio drug combinations. Satellite groups received single doses of each drug either alone or in combination with phentermine, and free brain concentrations were measured. RESULTS: Dex-phen synergy was confirmed in the rat and extended to the 5-HT2C agonist AR630. In contrast, although some synergistic interactions between lorcaserin and phentermine were observed, these combinations were largely additive. Synergistic interactions between phentermine and dexfenfluramine or AR630 were accompanied by combination-induced increases in brain levels of phentermine. CONCLUSIONS: Dex-phen synergy in the rat is caused by a pharmacokinetic interaction, resulting in increased central concentrations of phentermine.
[Mh] Termos MeSH primário: Depressores do Apetite/farmacologia
Dexfenfluramina/farmacologia
Ingestão de Alimentos/efeitos dos fármacos
Fenfluramina/farmacologia
Fentermina/farmacologia
Receptor 5-HT2C de Serotonina/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Depressores do Apetite/farmacocinética
Dexfenfluramina/farmacocinética
Sinergismo Farmacológico
Fenfluramina/farmacocinética
Masculino
Fentermina/farmacocinética
Ratos
Ratos Sprague-Dawley
Agonistas de Receptores 5-HT2 de Serotonina/farmacocinética
Agonistas de Receptores 5-HT2 de Serotonina/farmacologia
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Appetite Depressants); 0 (Receptor, Serotonin, 5-HT2C); 0 (Serotonin 5-HT2 Receptor Agonists); 2DS058H2CF (Fenfluramine); C045TQL4WP (Phentermine); E35R3G56OV (Dexfenfluramine)
[Em] Mês de entrada:1511
[Cu] Atualização por classe:150514
[Lr] Data última revisão:
150514
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:141220
[St] Status:MEDLINE
[do] DOI:10.1007/s00213-014-3829-2


  4 / 202 MEDLINE  
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[PMID]:23752124
[Au] Autor:Mancebo MJ; Ceballos FC; Pérez-Maceira J; Aldegunde M
[Ad] Endereço:Laboratorio de Fisiología Animal (Instituto de Acuicultura), Facultad de Biología, Universidad de Santiago de Compostela, 15782 Santiago de Compostela, Spain.
[Ti] Título:Hypothalamic neuropeptide Y (NPY) gene expression is not affected by central serotonin in the rainbow trout (Oncorhynchus mykiss).
[So] Source:Comp Biochem Physiol A Mol Integr Physiol;166(1):186-90, 2013 Sep.
[Is] ISSN:1531-4332
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Mammalian studies have shown a link between serotonin (5-HT) and neuropeptide Y (NPY) in the acute regulation of feeding and energy homeostasis. Taking into account that the actions of 5-HT and NPY on food intake in fish are similar to those observed in mammals, the objective of this study was to characterize a possible short-term interaction between hypothalamic 5-HT and NPY, by examining whether 5-HT regulates NPY gene expression, to help clarify the mechanism underlying the observed anorexigenic action of central 5-HT in the rainbow trout. We used qRT-PCR to determine the levels of NPY mRNA in the hypothalamus-preoptic area (HPA) of rainbow trout after intraperitoneal (i.p.) injection of a single dose of dexfenfluramine (dFF, 3mgkg(-1); 24h-fasted and fed fish) or intracerebroventricular (i.c.v.) administration of 5-HT (100µgkg(-1); 24h-fasted fish). Significant suppression of food intake was observed after administration of 5-HT and dFF. No significant changes in NPY gene expression were obtained 150min after administration of 5-HT or dFF. However, administration of the 5HT1B receptor agonist anpirtoline did not have any significant effect on food intake in rainbow trout. The results suggest that in fish, unlike in mammals, neither the NPY neurons of the HPA nor the 5-HT1B receptor subtype participate in the neural circuitry involved in the inhibition of food intake induced by central serotoninergic activation.
[Mh] Termos MeSH primário: Hipotálamo/metabolismo
Neuropeptídeo Y/genética
Oncorhynchus mykiss/genética
Serotonina/farmacologia
[Mh] Termos MeSH secundário: Animais
Dexfenfluramina/administração & dosagem
Dexfenfluramina/farmacologia
Comportamento Alimentar/efeitos dos fármacos
Regulação da Expressão Gênica/efeitos dos fármacos
Hipotálamo/efeitos dos fármacos
Injeções Intraperitoneais
Neuropeptídeo Y/metabolismo
Piperidinas/administração & dosagem
Piperidinas/farmacologia
Piridinas/administração & dosagem
Piridinas/farmacologia
RNA Mensageiro/genética
RNA Mensageiro/metabolismo
Serotonina/administração & dosagem
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Neuropeptide Y); 0 (Piperidines); 0 (Pyridines); 0 (RNA, Messenger); 32K9S228IK (anpirtoline); 333DO1RDJY (Serotonin); E35R3G56OV (Dexfenfluramine)
[Em] Mês de entrada:1401
[Cu] Atualização por classe:130708
[Lr] Data última revisão:
130708
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:130612
[St] Status:MEDLINE


  5 / 202 MEDLINE  
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[PMID]:23519266
[Au] Autor:Dempsie Y; MacRitchie NA; White K; Morecroft I; Wright AF; Nilsen M; Loughlin L; Mair KM; MacLean MR
[Ad] Endereço:Institute of Cardiovascular and Medical Sciences, College of Medical, Veterinary and Life Sciences, Glasgow University, West Medical Building, Glasgow G12 8QQ, UK.
[Ti] Título:Dexfenfluramine and the oestrogen-metabolizing enzyme CYP1B1 in the development of pulmonary arterial hypertension.
[So] Source:Cardiovasc Res;99(1):24-34, 2013 Jul 01.
[Is] ISSN:1755-3245
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:AIMS: Pulmonary arterial hypertension (PAH) occurs more frequently in women than men. Oestrogen and the oestrogen-metabolising enzyme cytochrome P450 1B1 (CYP1B1) play a role in the development of PAH. Anorectic drugs such as dexfenfluramine (Dfen) have been associated with the development of PAH. Dfen mediates PAH via a serotonergic mechanism and we have shown serotonin to up-regulate expression of CYP1B1 in human pulmonary artery smooth muscle cells (PASMCs). Thus here we assess the role of CYP1B1 in the development of Dfen-induced PAH. METHODS AND RESULTS: Dfen (5 mg kg(-1) day(-1) PO for 28 days) increased right ventricular pressure and pulmonary vascular remodelling in female mice only. Mice dosed with Dfen showed increased whole lung expression of CYP1B1 and Dfen-induced PAH was ablated in CYP1B1(-/-) mice. In line with this, Dfen up-regulated expression of CYP1B1 in PASMCs from PAH patients (PAH-PASMCs) and Dfen-mediated proliferation of PAH-PASMCs was ablated by pharmacological inhibition of CYP1B1. Dfen increased expression of tryptophan hydroxylase 1 (Tph1; the rate-limiting enzyme in the synthesis of serotonin) in PAH-PASMCs and both Dfen-induced proliferation and Dfen-induced up-regulation of CYP1B1 were ablated by inhibition of Tph1. 17ß-Oestradiol increased expression of both Tph1 and CYP1B1 in PAH-PASMCs, and Dfen and 17ß-oestradiol had synergistic effects on proliferation of PAH-PASMCs. Finally, ovariectomy protected against Dfen-induced PAH in female mice. CONCLUSION: CYP1B1 is critical in the development of Dfen-induced PAH in mice in vivo and proliferation of PAH-PASMCs in vitro. CYP1B1 may provide a novel therapeutic target for PAH.
[Mh] Termos MeSH primário: Hidrocarboneto de Aril Hidroxilases/metabolismo
Dexfenfluramina
Hipertensão Pulmonar/enzimologia
Músculo Liso Vascular/enzimologia
Miócitos de Músculo Liso/enzimologia
[Mh] Termos MeSH secundário: Animais
Pressão Arterial
Hidrocarboneto de Aril Hidroxilases/antagonistas & inibidores
Hidrocarboneto de Aril Hidroxilases/deficiência
Hidrocarboneto de Aril Hidroxilases/genética
Proliferação Celular
Células Cultivadas
Citocromo P-450 CYP1B1
Modelos Animais de Doenças
Relação Dose-Resposta a Droga
Inibidores Enzimáticos/farmacologia
Estradiol/farmacologia
Hipertensão Pulmonar Primária Familiar
Feminino
Hipertensão Pulmonar/induzido quimicamente
Hipertensão Pulmonar/genética
Hipertensão Pulmonar/patologia
Hipertensão Pulmonar/fisiopatologia
Hipertensão Pulmonar/prevenção & controle
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Músculo Liso Vascular/efeitos dos fármacos
Músculo Liso Vascular/patologia
Músculo Liso Vascular/fisiopatologia
Miócitos de Músculo Liso/efeitos dos fármacos
Miócitos de Músculo Liso/patologia
Norfenfluramina/toxicidade
Ovariectomia
Artéria Pulmonar/enzimologia
Artéria Pulmonar/fisiopatologia
Serotonina/metabolismo
Fatores Sexuais
Triptofano Hidroxilase/metabolismo
Função Ventricular Direita
Pressão Ventricular
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Enzyme Inhibitors); 1886-26-6 (Norfenfluramine); 333DO1RDJY (Serotonin); 4TI98Z838E (Estradiol); E35R3G56OV (Dexfenfluramine); EC 1.14.14.1 (Aryl Hydrocarbon Hydroxylases); EC 1.14.14.1 (CYP1B1 protein, human); EC 1.14.14.1 (Cyp1b1 protein, mouse); EC 1.14.14.1 (Cytochrome P-450 CYP1B1); EC 1.14.16.4 (Tph1 protein, mouse); EC 1.14.16.4 (Tryptophan Hydroxylase)
[Em] Mês de entrada:1401
[Cu] Atualização por classe:170322
[Lr] Data última revisão:
170322
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:130323
[St] Status:MEDLINE
[do] DOI:10.1093/cvr/cvt064


  6 / 202 MEDLINE  
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[PMID]:22370224
[Au] Autor:Simonyi G; Pados G; Medvegy M; Bedros JR
[Ad] Endereço:Pest Megyei Flór Ferenc Kórház, Kardiometabolikus Centrum V. Belgyógyászat-Lipidológiai Osztály, Regionális Zsíranyagcsere-központ és Hypertonia Decentrum, Budapest. bmbel3@gmail.com
[Ti] Título:[The pharmacological treatment of obesity: past, present and future].
[Ti] Título:Az elhízás gyógyszeres kezelése: múlt, jelen, jövo.
[So] Source:Orv Hetil;153(10):363-73, 2012 Mar 11.
[Is] ISSN:0030-6002
[Cp] País de publicação:Hungary
[La] Idioma:hun
[Ab] Resumo:Currently, obesity presents one of the biggest health problems. Management strategies for weight reduction in obese individuals include changes in life style such as exercise and diet, behavioral therapy, and pharmacological treatment, and in certain cases surgical intervention. Diet and exercise are best for both prevention and treatment, but both require much discipline and are difficult to maintain. Drug treatment of obesity offer a possible adjunct, but it may only have modest results, limited by side effects; furthermore, the weight lowering effects last only as long as the drug is being taken and, unfortunately, as soon as the administration is stopped, the weight is regained. These strategies should be used in a combination for higher efficacy. Drugs used to induce weight loss have various effects: they increase satiety, reduce the absorption of nutrients or make metabolism faster; but their effect is usually moderate. In the past, several drugs were used in the pharmacological therapy of weight reduction including thyroid hormone, dinitrophenol, amphetamines and their analogues, e.g. fenfluramine, At present, only orlistat is available in the long term treatment (≥ 24 weeks) of obesity as sibutramine and rimonabant were withdrawn form the market. Several new anti-obesity drugs are being tested at present, and liraglutide, a GLP-1 analogue (incretin mimetic), is the most promising one.
[Mh] Termos MeSH primário: Fármacos Antiobesidade/uso terapêutico
Obesidade/tratamento farmacológico
[Mh] Termos MeSH secundário: Amidas/uso terapêutico
Fármacos Antiobesidade/administração & dosagem
Fármacos Antiobesidade/efeitos adversos
Fármacos Antiobesidade/farmacologia
Anticonvulsivantes/uso terapêutico
Antidepressivos/uso terapêutico
Metabolismo Basal/efeitos dos fármacos
Benzazepinas/uso terapêutico
Benzoxazinas/uso terapêutico
Índice de Massa Corporal
Compostos Bicíclicos Heterocíclicos com Pontes/uso terapêutico
Fator Neurotrófico Ciliar/uso terapêutico
Ensaios Clínicos como Assunto
Terapia Combinada
Ciclobutanos/uso terapêutico
Dexfenfluramina/uso terapêutico
Ácidos Graxos/uso terapêutico
Feminino
Fenfluramina/uso terapêutico
Peptídeo 1 Semelhante ao Glucagon/análogos & derivados
Peptídeo 1 Semelhante ao Glucagon/farmacologia
Hormônio do Crescimento Humano/uso terapêutico
Seres Humanos
Absorção Intestinal/efeitos dos fármacos
Lactonas/uso terapêutico
Leptina/uso terapêutico
Estilo de Vida
Liraglutida
Masculino
Norepinefrina/análogos & derivados
Obesidade/prevenção & controle
Obesidade/terapia
Obesidade Mórbida/tratamento farmacológico
Piperidinas/uso terapêutico
Pirazóis/uso terapêutico
Piridinas/uso terapêutico
Receptor Tipo 4 de Melanocortina/antagonistas & inibidores
Saciação/efeitos dos fármacos
Serotonina/análogos & derivados
Proteínas de Transporte de Sódio-Glucose/antagonistas & inibidores
Sacarose/análogos & derivados
Sacarose/uso terapêutico
Hormônios Tireóideos/uso terapêutico
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Amides); 0 (Anti-Obesity Agents); 0 (Anticonvulsants); 0 (Antidepressive Agents); 0 (Benzazepines); 0 (Benzoxazines); 0 (Bridged Bicyclo Compounds, Heterocyclic); 0 (Ciliary Neurotrophic Factor); 0 (Cyclobutanes); 0 (Fatty Acids); 0 (Lactones); 0 (Leptin); 0 (Piperidines); 0 (Pyrazoles); 0 (Pyridines); 0 (Receptor, Melanocortin, Type 4); 0 (Sodium-Glucose Transport Proteins); 0 (Thyroid Hormones); 12629-01-5 (Human Growth Hormone); 2DS058H2CF (Fenfluramine); 333DO1RDJY (Serotonin); 57-50-1 (Sucrose); 637E494O0Z (lorcaserin); 6742Y30KGK (sucrose polyester); 839I73S42A (Liraglutide); 89750-14-1 (Glucagon-Like Peptide 1); 95M8R751W8 (orlistat); BLH9UKX9V1 (Tesofensine); E35R3G56OV (Dexfenfluramine); LC5G1JUA39 (cetilistat); RML78EN3XE (rimonabant); WV5EC51866 (sibutramine); X4W3ENH1CV (Norepinephrine); X9U622S114 (N-(3-(4-chlorophenyl)-2-(3-cyanophenyl)-1-methylpropyl)-2-methyl-2-((5-(trifluoromethyl)pyridin-2-yl)oxy)propanamide)
[Em] Mês de entrada:1204
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:120229
[St] Status:MEDLINE
[do] DOI:10.1556/OH.2012.29317


  7 / 202 MEDLINE  
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[PMID]:22209745
[Au] Autor:Papazoglou I; Berthou F; Vicaire N; Rouch C; Markaki EM; Bailbe D; Portha B; Taouis M; Gerozissis K
[Ad] Endereço:CNRS, Center of Neurosciences Paris-Sud, UMR 8195, Orsay F-91405, France.
[Ti] Título:Hypothalamic serotonin-insulin signaling cross-talk and alterations in a type 2 diabetic model.
[So] Source:Mol Cell Endocrinol;350(1):136-44, 2012 Mar 05.
[Is] ISSN:1872-8057
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:Serotonin and insulin are key regulators of homeostatic mechanisms in the hypothalamus. However, in type 2 diabetes, the hypothalamic responsiveness to serotonin is not clearly established. We used a diabetic model, the Goto Kakizaki (GK) rats, to explore insulin receptor expression, insulin and serotonin efficiency in the hypothalamus and liver by means of Akt phosphorylation. Insulin or dexfenfluramine (stimulator of serotonin) treatment induced Akt phosphorylation in Wistar rats but not in GK rats that exhibit down-regulated insulin receptor. Studies in a neuroblastoma cell line showed that serotonin-induced Akt phosphorylation is PI3-kinase dependent. Finally, in response to food intake, hypothalamic serotonin release was reduced in GK rats, indicating impaired responsiveness of this neurotransmitter. In conclusion, hypothalamic serotonin as insulin efficiency is impaired in diabetic GK rats. The insulin-serotonin cross-talk and impairment observed is one potential key modification in the brain during the onset of diabetes.
[Mh] Termos MeSH primário: Diabetes Mellitus Tipo 2/sangue
Insulina/sangue
Receptor Cross-Talk
Serotonina/sangue
[Mh] Termos MeSH secundário: Animais
Glicemia
Linhagem Celular Tumoral
Dexfenfluramina/farmacologia
Diabetes Mellitus Tipo 2/metabolismo
Modelos Animais de Doenças
Ingestão de Alimentos
Seres Humanos
Hipotálamo/enzimologia
Hipotálamo/metabolismo
Insulina/farmacologia
Insulina/fisiologia
Leptina/sangue
Fígado/enzimologia
Fígado/metabolismo
Masculino
Fosfatidilinositol 3-Quinases/metabolismo
Fosforilação
Período Pós-Prandial
Proteínas Proto-Oncogênicas c-akt/metabolismo
Ratos
Ratos Wistar
Receptor de Insulina/metabolismo
Serotonina/farmacologia
Serotonina/fisiologia
Agonistas de Receptores de Serotonina/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Blood Glucose); 0 (Insulin); 0 (Leptin); 0 (Serotonin Receptor Agonists); 333DO1RDJY (Serotonin); E35R3G56OV (Dexfenfluramine); EC 2.7.1.- (Phosphatidylinositol 3-Kinases); EC 2.7.10.1 (Receptor, Insulin); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
[Em] Mês de entrada:1205
[Cu] Atualização por classe:131121
[Lr] Data última revisão:
131121
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:120103
[St] Status:MEDLINE
[do] DOI:10.1016/j.mce.2011.12.007


  8 / 202 MEDLINE  
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[PMID]:21996132
[Au] Autor:Quednow BB; Treyer V; Hasler F; Dörig N; Wyss MT; Burger C; Rentsch KM; Westera G; Schubiger PA; Buck A; Vollenweider FX
[Ad] Endereço:Clinic of Affective Disorders and General Psychiatry, University Hospital of Psychiatry, Zurich, Switzerland. quednow@bli.uzh.ch
[Ti] Título:Assessment of serotonin release capacity in the human brain using dexfenfluramine challenge and [18F]altanserin positron emission tomography.
[So] Source:Neuroimage;59(4):3922-32, 2012 Feb 15.
[Is] ISSN:1095-9572
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Although alterations of serotonin (5-HT) system functioning have been proposed for a variety of psychiatric disorders, a direct method quantitatively assessing 5-HT release capacity in the living human brain is still lacking. Therefore, we evaluated a novel method to assess 5-HT release capacity in vivo using dexfenfluramine challenge and [(18)F]altanserin positron emission tomography (PET). Thirteen healthy male subjects received placebo and single oral doses of 40 mg (n = 6) or 60 mg (n = 7) of the potent 5-HT releaser dexfenfluramine separated by an interval of 14 days. Three further subjects received placebo on both days. Two hours after placebo/drug administration, 250 MBq of the 5-HT(2A) receptor selective PET-radiotracer [(18)F]altanserin was administered intravenously as a 30s bolus. Dynamic PET data were subsequently acquired over 90 min. Moreover, arterial blood samples were drawn for measurement of total activity and metabolite correction of the input function. Dexfenfluramine as well as cortisol and prolactin plasma concentration-time profiles was quantitatively determined. Tracer distribution volumes for five volumes-of-interest (prefrontal and occipital cortex, insula, thalamus, caudatum) were calculated by the Logan plot and a 2-tissue compartment model. Dexfenfluramine dose-dependently decreased the total distribution volume of [(18)F]altanserin in cortical regions independent of the PET modeling approach. Cortisol and prolactin plasma concentrations were dose-dependently increased by dexfenfluramine. The decrease in cortical [(18)F]altanserin receptor binding under dexfenfluramine was correlated with the increase of plasma prolactin. These data suggest that the combination of a dexfenfluramine-induced 5-HT release and subsequent assessment of 5-HT(2A) receptor availability with [(18)F]altanserin PET is suitable to measure cortical 5-HT release capacity in the human brain.
[Mh] Termos MeSH primário: Encéfalo/diagnóstico por imagem
Encéfalo/fisiologia
Dexfenfluramina
Radioisótopos de Flúor
Ketanserina/análogos & derivados
Tomografia por Emissão de Pósitrons
Agonistas de Receptores de Serotonina
Serotonina/secreção
[Mh] Termos MeSH secundário: Adulto
Método Duplo-Cego
Seres Humanos
Masculino
Tomografia por Emissão de Pósitrons/métodos
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE; RANDOMIZED CONTROLLED TRIAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Fluorine Radioisotopes); 0 (Serotonin Receptor Agonists); 333DO1RDJY (Serotonin); 5015H744JQ (altanserin); 97F9DE4CT4 (Ketanserin); E35R3G56OV (Dexfenfluramine)
[Em] Mês de entrada:1207
[Cu] Atualização por classe:161125
[Lr] Data última revisão:
161125
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:111015
[St] Status:MEDLINE
[do] DOI:10.1016/j.neuroimage.2011.09.045


  9 / 202 MEDLINE  
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[PMID]:21972386
[Au] Autor:Natali D; Girerd B; Montani D; Soubrier F; Simonneau G; Humbert M; Sitbon O
[Ad] Endereço:Faculté de Médecine, Université Paris-Sud, Kremlin-Bicêtre, France; Service de Pneumologie et Réanimation, Centre de Référence de l'Hypertension Pulmonaire Sévère, Hôpital Antoine Béclère, Assistance Publique-Hôpitaux de Paris, Clamart, France; INSERM U999, Hypertension Artérielle Pulmonaire: Physio
[Ti] Título:Pulmonary arterial hypertension in a patient with Cowden syndrome and anorexigen exposure.
[So] Source:Chest;140(4):1066-1068, 2011 Oct.
[Is] ISSN:1931-3543
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:We report a case of pulmonary arterial hypertension (PAH) occurring in a patient with Cowden syndrome with a mutation in the phosphatase and tensin (PTEN) tumor suppressor gene, in the context of exposure to the appetite suppressant dexfenfluramine. Anorexigen exposure is known to be a risk factor for PAH. However, the role of PTEN in cell function and the development of pulmonary vascular remodeling and histopathologic signs of PAH in mice with a Pten depletion in smooth muscle cells suggest that the association of PAH and Cowden syndrome may be relevant. In this case report, we hypothesize that PTEN mutations may be a predisposing factor for the development of PAH, with anorexigen exposure as a potential trigger.
[Mh] Termos MeSH primário: Depressores do Apetite/efeitos adversos
Síndrome do Hamartoma Múltiplo/epidemiologia
Síndrome do Hamartoma Múltiplo/genética
Hipertensão Pulmonar/epidemiologia
Hipertensão Pulmonar/genética
[Mh] Termos MeSH secundário: Comorbidade
Dexfenfluramina/efeitos adversos
Hipertensão Pulmonar Primária Familiar
Feminino
Seres Humanos
Meia-Idade
Mutação/genética
PTEN Fosfo-Hidrolase/genética
Linhagem
Fatores de Risco
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Appetite Depressants); E35R3G56OV (Dexfenfluramine); EC 3.1.3.67 (PTEN Phosphohydrolase)
[Em] Mês de entrada:1112
[Cu] Atualização por classe:170528
[Lr] Data última revisão:
170528
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:111006
[St] Status:MEDLINE


  10 / 202 MEDLINE  
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[PMID]:21510964
[Au] Autor:Foltin RW
[Ad] Endereço:Division on Substance Abuse, New York State Psychiatric Institute and Department of Psychiatry, College of Physicians and Surgeons of Columbia University, 1051 Riverside Drive, Unit 120, New York, NY 10032, USA. rwf2@columbia.edu
[Ti] Título:Consumption of palatable food decreases the anorectic effects of serotonergic, but not dopaminergic drugs in baboons.
[So] Source:Physiol Behav;103(5):493-500, 2011 Jul 06.
[Is] ISSN:1873-507X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:We examined the effects of periodic access to a palatable, high sugar content food (candy) in 8 male baboons on the anorectic response to d-amphetamine, which increases dopamine, and dexfenfluramine, which increases serotonin. During candy access, up to 200 candies containing 75% of energy as sugar were available during the morning on Mondays, Wednesdays and Fridays; food pellets (19% of energy as sugar) were available in the afternoon and throughout the remaining days of the week. During candy access, baboons consumed a mean of 177 pieces of candy containing 696 kcal (2.91 MJ) in the morning compared to 44 food pellets and 150 kcal (0.63 MJ) in the morning on non-candy days. Food pellet intake was lower during candy access. Complete dose-response functions for the effects of the drugs on food pellet intake on days that candy was not available were determined before, during, and after the period of access to candy. Dexfenfluramine and amphetamine produced dose-dependent decreases in food pellet intake and increases in latency to eat food pellets before, during, and after candy access. During access to candy, the dose-response function for dexfenfluramine was shifted to the right indicating the development of tolerance, while that for amphetamine was shifted to the left indicating sensitization. Only the dose-response function for dexfenfluramine returned to baseline after candy access suggesting that the difference was specific to concurrent palatable food consumption. We hypothesize that tolerance to the effects of dexfenfluramine reflects a decrease in the satiating effect of serotonin release due to repeatedly eating large amounts of palatable food.
[Mh] Termos MeSH primário: Anfetamina/farmacologia
Anorexia/dietoterapia
Dexfenfluramina/farmacologia
Sacarose na Dieta/uso terapêutico
[Mh] Termos MeSH secundário: Anfetamina/antagonistas & inibidores
Animais
Anorexia/induzido quimicamente
Dexfenfluramina/antagonistas & inibidores
Sacarose na Dieta/farmacologia
Modelos Animais de Doenças
Inibidores da Captação de Dopamina/antagonistas & inibidores
Inibidores da Captação de Dopamina/farmacologia
Relação Dose-Resposta a Droga
Interações Medicamentosas
Tolerância a Medicamentos
Ingestão de Alimentos/efeitos dos fármacos
Comportamento Alimentar/efeitos dos fármacos
Masculino
Papio
Agonistas de Receptores de Serotonina/farmacologia
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Dietary Sucrose); 0 (Dopamine Uptake Inhibitors); 0 (Serotonin Receptor Agonists); CK833KGX7E (Amphetamine); E35R3G56OV (Dexfenfluramine)
[Em] Mês de entrada:1109
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:110423
[St] Status:MEDLINE
[do] DOI:10.1016/j.physbeh.2011.04.004



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