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[PMID]:29480848
[Au] Autor:Yammine L; Kosten TR; Cinciripini PM; Green CE; Meininger JC; Minnix JA; Newton TF
[Ad] Endereço:University of Texas Health Science Center at Houston.
[Ti] Título:Exenatide once weekly for smoking cessation: study protocol for a randomized clinical trial.
[So] Source:Medicine (Baltimore);97(2):e9567, 2018 Jan.
[Is] ISSN:1536-5964
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Cigarette smoking is the greatest preventable cause of morbidity and premature mortality in the United States. Approved pharmacological treatments for smoking cessation are marginally effective, underscoring the need for improved pharmacotherapies. A novel approach might use glucagon-like peptide-1 (GLP-1) agonists, which reduce alcohol and drug use in preclinical studies. GLP-1 is produced in the intestinal L-cells and in the hindbrain. The peptide maintains glucose homeostasis and reduces food intake. Several GLP-1 agonists are used clinically to treat type 2 diabetes and obesity, but none have been tested in humans to reduce smoking. AIMS: We will examine whether extended-release exenatide reduces smoking, craving, and withdrawal symptoms, as well as cue-induced craving for cigarettes. METHODS: We will enroll prediabetic and/or overweight treatment seeking smokers (n = 90) into a double-blind, placebo-controlled, randomized clinical trial. Participants will be randomized in a 1:1 ratio to receive exenatide or placebo. All participants will receive transdermal nicotine replacement therapy (NRT) and behavioral counseling. Abstinence from smoking (verified via expired CO level of ≤5 ppm), craving (Questionnaire of Smoking Urges score), and withdrawal symptoms (Wisconsin Scale of Withdrawal Symptoms score) will be assessed weekly during 6 weeks of treatment and at 1 and 4 weeks posttreatment. Cue-induced craving for cigarettes will be assessed at baseline and at 3 weeks of treatment following virtual reality exposure. EXPECTED OUTCOMES: We hypothesize that exenatide will increase the number of participants able to achieve complete smoking abstinence above that achieved via standard NRT and that exenatide will reduce craving and withdrawal symptoms, as well as cue-induced craving for cigarettes.
[Mh] Termos MeSH primário: Peptídeo 1 Semelhante ao Glucagon/agonistas
Peptídeos/administração & dosagem
Abandono do Hábito de Fumar
Fumar/tratamento farmacológico
Peçonhas/administração & dosagem
[Mh] Termos MeSH secundário: Administração Cutânea
Adolescente
Adulto
Idoso
Aconselhamento
Fissura/efeitos dos fármacos
Preparações de Ação Retardada
Método Duplo-Cego
Esquema de Medicação
Seres Humanos
Meia-Idade
Abandono do Hábito de Fumar/métodos
Síndrome de Abstinência a Substâncias/tratamento farmacológico
Resultado do Tratamento
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE; RANDOMIZED CONTROLLED TRIAL
[Nm] Nome de substância:
0 (Delayed-Action Preparations); 0 (Peptides); 0 (Venoms); 89750-14-1 (Glucagon-Like Peptide 1); 9P1872D4OL (exenatide)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:180227
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000009567


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[PMID]:29260924
[Au] Autor:Molina Vega M; Muñoz-Garach A; Tinahones FJ
[Ad] Endereço:a Department of Endocrinology and Nutrition , Virgen de la Victoria Hospital, Málaga University (IBIMA). , Málaga , Spain.
[Ti] Título:Pharmacokinetic drug evaluation of exenatide for the treatment of type 2 diabetes.
[So] Source:Expert Opin Drug Metab Toxicol;14(2):207-217, 2018 02.
[Is] ISSN:1744-7607
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:INTRODUCTION: Glucagon-like peptide-1 (GLP-1) receptor analogs are a group of therapeutic agents which mimic endogenous GLP-1, exerting their effect by the stimulation of the GLP-1 receptor with a wide distribution. Its activation increases insulin releasing dependent on blood glucose levels, suppression of glucagon secretion and a reduction of hepatic glucose output. It delays gastric emptying and increases satiety. Exenatide is the synthetic version of exendin-4, a natural peptide with similar properties to human GLP-1. There are two pharmaceutical forms, for subcutaneous injection: twice daily and once weekly. Clinical practice guidelines recommend them because of a high efficacy reducing hyperglycemia, low risk of hypoglycemia and a significative weight loss effect. Gastrointestinal adverse events are the most common beside injection site-related. Their cost is the main limitation to use. Areas covered: We review the recent literature investigating the pharmacokinetics and pharmacodynamics and efficacy-safety studies of exenatide twice daily and once weekly in type 2 diabetes Expert opinion: GLP-1 receptor analogs are now positioned as an effective and safe drug for the treatment of type 2 diabetes. Exenatide significally reduces HbA1c and fasting plasma glucose. Additionally, it produces moderate weight loss and decreases blood pressure. One weekly formulation may improve compliance while cost is still a limitation. EXSCEL trial has shown that, despite cardiovascular safety, exenatide do not exhibits cardiovascular benefits.
[Mh] Termos MeSH primário: Diabetes Mellitus Tipo 2/tratamento farmacológico
Hipoglicemiantes/administração & dosagem
Peptídeos/administração & dosagem
Peçonhas/administração & dosagem
[Mh] Termos MeSH secundário: Animais
Glicemia/efeitos dos fármacos
Esquema de Medicação
Receptor do Peptídeo Semelhante ao Glucagon 1/agonistas
Seres Humanos
Hipoglicemia/induzido quimicamente
Hipoglicemiantes/farmacocinética
Hipoglicemiantes/farmacologia
Injeções Subcutâneas
Insulina/metabolismo
Peptídeos/farmacocinética
Peptídeos/farmacologia
Peçonhas/farmacocinética
Peçonhas/farmacologia
Perda de Peso/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Blood Glucose); 0 (Glucagon-Like Peptide-1 Receptor); 0 (Hypoglycemic Agents); 0 (Insulin); 0 (Peptides); 0 (Venoms); 9P1872D4OL (exenatide)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180222
[Lr] Data última revisão:
180222
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171221
[St] Status:MEDLINE
[do] DOI:10.1080/17425255.2018.1420160


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[PMID]:29317206
[Au] Autor:Li Z; Zhu S; Huang L; Shang M; Yu C; Zhu H; Han D; Huang H; Yu X; Li X
[Ad] Endereço:Department of Hepatopancreatobiliary Surgery, Third Xiangya Hospital, Central South University, Changsha 410013, Hunan, China.
[Ti] Título:Exendin-4 impairs the autophagic flux to induce apoptosis in pancreatic acinar AR42J cells by down-regulating LAMP-2.
[So] Source:Biochem Biophys Res Commun;496(2):294-301, 2018 02 05.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:This study aimed to explore the mechanism of impaired autophagy flux induced by exendin-4 and its role on cell apoptosis in pancreatic AR42J cells. The AR42J cells were treated with various concentration of exendin-4 for several time points to assess its cytotoxicity by MTT assay. Then the AR42J cells were treated by 10pM exendin-4 for 72 h, the cell death was analyzed by flow cytometry and caspase-3 level was examined by Western blot with or without the pretreatment of z-VAD-fmk to testify whether exendin-4 induces the cell apoptosis. The protein levels of LC3B, p62 and LAMP-2 were assessed by Western blot, the mRNA level of LAMP-2 was quantified by quantitative PCR in the absence or presence of LAMP-2 over-expression plasmid and the expression and activity of CatB and CatL were tested by ELISA or activity assay methods in AR42J cells treated by exendin-4. The normal rats and the diabetes-model rats by high-fat and high-sugar diet for two month then with streptozotocin intraperitoneally were subcutaneously injected with exendin-4 for 10 weeks to test the expression of LAMP-2 mRNA and protein in the pancreas. Cells pretreated with Bafilomycin A1 were detected for LC3B and p62 expressions by Western blot. Cells pretreated by 3-MA were used to assess whether 3-MA can protect from exendin-4 cytotoxicity. We found that exendin-4 can decrease the AR42J cell viability as well as increase the cell death and cleaved caspase-3 level, which all can be inhibited by z-VAD-fmk. Exendin-4 can downregulate the expression of LAMP-2 and then impair the autophagy flux to induce the accumulation of LC3B-II and p62, but cannot change the expression and activity of CatB and CatL. Bafilomycin A1 almostly have no impact on the change of LC3B and p62 protein levels induced by exendin-4. Both 3-MA and overexpressed LAMP-2 can reduce the cytotoxicity of exendin-4. Therefore, we considered the down-regulation of LAMP-2 which can impair the autophagy flux by inhibiting the fusion of autophagosomes with lysosomes to induce the AR42J cell apoptosis as the potential mechanism of chronic pancreatitis induced by exendin-4.
[Mh] Termos MeSH primário: Células Acinares/efeitos dos fármacos
Autofagia/efeitos dos fármacos
Diabetes Mellitus Experimental/genética
Proteína 2 de Membrana Associada ao Lisossomo/genética
Peptídeos/toxicidade
Peçonhas/toxicidade
[Mh] Termos MeSH secundário: Células Acinares/citologia
Células Acinares/metabolismo
Adenina/análogos & derivados
Adenina/farmacologia
Clorometilcetonas de Aminoácidos/farmacologia
Animais
Autofagia/genética
Caspase 3/genética
Caspase 3/metabolismo
Catepsina B/genética
Catepsina B/metabolismo
Catepsina L/genética
Catepsina L/metabolismo
Linhagem Celular
Diabetes Mellitus Experimental/induzido quimicamente
Diabetes Mellitus Experimental/metabolismo
Diabetes Mellitus Experimental/patologia
Dieta Hiperlipídica/efeitos adversos
Regulação da Expressão Gênica
Proteína 2 de Membrana Associada ao Lisossomo/antagonistas & inibidores
Proteína 2 de Membrana Associada ao Lisossomo/metabolismo
Macrolídeos/farmacologia
Masculino
Proteínas Associadas aos Microtúbulos/genética
Proteínas Associadas aos Microtúbulos/metabolismo
Pâncreas/efeitos dos fármacos
Pâncreas/metabolismo
Pâncreas/patologia
Ratos
Ratos Sprague-Dawley
Proteína Sequestossoma-1/genética
Proteína Sequestossoma-1/metabolismo
Transdução de Sinais
Estreptozocina
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Amino Acid Chloromethyl Ketones); 0 (LC3 protein, rat); 0 (Lysosomal-Associated Membrane Protein 2); 0 (Macrolides); 0 (Microtubule-Associated Proteins); 0 (Peptides); 0 (Sequestosome-1 Protein); 0 (Sqstm1 protein, rat); 0 (Venoms); 0 (benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone); 5142-23-4 (3-methyladenine); 5W494URQ81 (Streptozocin); 88899-55-2 (bafilomycin A1); 9P1872D4OL (exenatide); EC 3.4.22.- (Casp3 protein, rat); EC 3.4.22.- (Caspase 3); EC 3.4.22.1 (Cathepsin B); EC 3.4.22.1 (Ctsb protein, rat); EC 3.4.22.15 (Cathepsin L); EC 3.4.22.15 (Ctsl protein, rat); JAC85A2161 (Adenine)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180214
[Lr] Data última revisão:
180214
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180111
[St] Status:MEDLINE


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[PMID]:28454792
[Au] Autor:Mentz RJ; Bethel MA; Gustavson S; Thompson VP; Pagidipati NJ; Buse JB; Chan JC; Iqbal N; Maggioni AP; Marso SP; Ohman P; Poulter N; Ramachandran A; Zinman B; Hernandez AF; Holman RR
[Ad] Endereço:Duke Clinical Research Institute, Durham, NC. Electronic address: robert.mentz@duke.edu.
[Ti] Título:Baseline characteristics of patients enrolled in the Exenatide Study of Cardiovascular Event Lowering (EXSCEL).
[So] Source:Am Heart J;187:1-9, 2017 May.
[Is] ISSN:1097-6744
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: EXSCEL is a randomized, double-blind, placebo-controlled trial examining the effect of exenatide once-weekly (EQW) versus placebo on time to the primary composite outcome (cardiovascular death, nonfatal myocardial infarction or nonfatal stroke) in patients with type 2 diabetes mellitus (DM) and a wide range of cardiovascular (CV) risk. METHODS: Patients were enrolled at 688 sites in 35 countries. We describe their baseline characteristics according to prior CV event status and compare patients with those enrolled in prior glucagon-like peptide-1 receptor agonist (GLP-1RA) outcomes trials. RESULTS: Of a total of 14,752 participants randomized between June 2010 and September 2015, 6,788 (46.0%) patients were enrolled in Europe; 3,708 (25.1%), North America; 2,727 (18.5%), Latin America; and 1,529 (10.4%), Asia Pacific. Overall, 73% had at least one prior CV event (70% coronary artery disease, 24% peripheral arterial disease, 22% cerebrovascular disease). The median (IQR) age was 63 years (56, 69), 38% were female, median baseline HbA1c was 8.0% (7.3, 8.9) and 16% had a prior history of heart failure. Those without a prior CV event were younger with a shorter duration of diabetes and better renal function than those with at least one prior CV event. Compared with prior GLP-1RA trials, EXSCEL has a larger percentage of patients without a prior CV event and a notable percentage who were taking a dipeptidyl peptidase-4 inhibitor at baseline (15%). CONCLUSIONS: EXSCEL is one of the largest global GLP-1RA trials, evaluating the safety and efficacy of EQW with a broad patient population that may extend generalizability compared to prior GLP-1RA trials (ClinicalTrials.gov number, NCT01144338).
[Mh] Termos MeSH primário: Doenças Cardiovasculares/prevenção & controle
Diabetes Mellitus Tipo 2/tratamento farmacológico
Receptor do Peptídeo Semelhante ao Glucagon 1/antagonistas & inibidores
Hipoglicemiantes/administração & dosagem
Peptídeos/administração & dosagem
Peçonhas/administração & dosagem
[Mh] Termos MeSH secundário: Idoso
Doenças Cardiovasculares/mortalidade
Método Duplo-Cego
Feminino
Seres Humanos
Hipoglicemiantes/efeitos adversos
Masculino
Meia-Idade
Infarto do Miocárdio/prevenção & controle
Peptídeos/efeitos adversos
Fatores de Risco
Acidente Vascular Cerebral/prevenção & controle
Peçonhas/efeitos adversos
[Pt] Tipo de publicação:JOURNAL ARTICLE; MULTICENTER STUDY; RANDOMIZED CONTROLLED TRIAL
[Nm] Nome de substância:
0 (Glucagon-Like Peptide-1 Receptor); 0 (Hypoglycemic Agents); 0 (Peptides); 0 (Venoms); 9P1872D4OL (exenatide)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:180121
[Lr] Data última revisão:
180121
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170430
[Cl] Clinical Trial:ClinicalTrial
[St] Status:MEDLINE


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[PMID]:29262286
[Au] Autor:Holman RR; Bethel MA; Hernandez AF
[Ad] Endereço:University of Oxford, Oxford, United Kingdom
[Ti] Título:Once-Weekly Exenatide and Cardiovascular Outcomes in Type 2 Diabetes.
[So] Source:N Engl J Med;377(25):2502, 2017 12 21.
[Is] ISSN:1533-4406
[Cp] País de publicação:United States
[La] Idioma:eng
[Mh] Termos MeSH primário: Diabetes Mellitus Tipo 2
Peçonhas
[Mh] Termos MeSH secundário: Esquema de Medicação
Hemoglobina A Glicada/análise
Seres Humanos
Hipoglicemiantes
Peptídeos
[Pt] Tipo de publicação:LETTER; COMMENT
[Nm] Nome de substância:
0 (Glycated Hemoglobin A); 0 (Hypoglycemic Agents); 0 (Peptides); 0 (Venoms); 9P1872D4OL (exenatide)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180109
[Lr] Data última revisão:
180109
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:171221
[St] Status:MEDLINE
[do] DOI:10.1056/NEJMc1714163


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[PMID]:29265780
[Au] Autor:Imprialos KP; Stavropoulos K; Doumas M
[Ad] Endereço:Aristotle University of Thessaloniki, Thessaloniki, Greece
[Ti] Título:Once-Weekly Exenatide and Cardiovascular Outcomes in Type 2 Diabetes.
[So] Source:N Engl J Med;377(25):2502, 2017 12 21.
[Is] ISSN:1533-4406
[Cp] País de publicação:United States
[La] Idioma:eng
[Mh] Termos MeSH primário: Diabetes Mellitus Tipo 2
Peçonhas
[Mh] Termos MeSH secundário: Seres Humanos
Peptídeos
[Pt] Tipo de publicação:LETTER; COMMENT
[Nm] Nome de substância:
0 (Peptides); 0 (Venoms); 9P1872D4OL (exenatide)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171227
[Lr] Data última revisão:
171227
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:171222
[St] Status:MEDLINE
[do] DOI:10.1056/NEJMc1714163


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[PMID]:29040320
[Au] Autor:Song I; Roels S; Martens GA; Bouwens L
[Ad] Endereço:Cell Differentiation Lab, Vrije Universiteit Brussel (VUB), Brussels, Belgium.
[Ti] Título:Circulating microRNA-375 as biomarker of pancreatic beta cell death and protection of beta cell mass by cytoprotective compounds.
[So] Source:PLoS One;12(10):e0186480, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: Previous studies demonstrated that circulating microRNA-375 (miR-375) is a suitable plasma biomarker for real-time detection of beta cell death. The present study evaluated the use of this biomarker to assess the beta cytoprotective effect of phenylpropenoic acid glucoside (PPAG), which was previously demonstrated to protect beta cells against various types of injury, and of exendin-4, which is an established antidiabetic drug. METHODS: PPAG or exendin-4 were administered in mice treated with streptozotocin (STZ) to acutely induce beta cell death. Beta cell mass and apoptotic death were measured in pancreatic tissue sections. Circulating miR-375 was measured in blood plasma by RT-qPCR. The release of miR-375 was also measured in vitro by MIN-6 beta cells. RESULTS: Administration of STZ resulted in measurable circulating levels of miR-375, a decrease in beta cell mass and increase in frequency of apoptotic beta cells. In vitro, there was a good correlation between miR-375 release and the extent of beta cell death. Treatment of mice with PPAG or exendin-4 significantly attenuated STZ-induced loss of beta cell mass and beta cell apoptosis, and normalized the blood level of miR-375. CONCLUSIONS: These findings show the potential use of serological miR-375 measurements to evaluate the beta cytoprotective effect of (potential) antidiabetic drugs in vivo.
[Mh] Termos MeSH primário: Diabetes Mellitus Experimental/sangue
Diabetes Mellitus Experimental/tratamento farmacológico
Glucosídeos/farmacologia
Hipoglicemiantes/farmacologia
Células Secretoras de Insulina/metabolismo
MicroRNAs/genética
Fenilpropionatos/farmacologia
[Mh] Termos MeSH secundário: Animais
Apoptose/genética
Biomarcadores/sangue
Glicemia/efeitos dos fármacos
Glicemia/metabolismo
Linhagem Celular
Diabetes Mellitus Experimental/induzido quimicamente
Diabetes Mellitus Experimental/genética
Células Secretoras de Insulina/efeitos dos fármacos
Células Secretoras de Insulina/patologia
Masculino
Camundongos
Camundongos Endogâmicos BALB C
MicroRNAs/sangue
Pâncreas/efeitos dos fármacos
Pâncreas/metabolismo
Pâncreas/patologia
Peptídeos/farmacologia
Substâncias Protetoras/farmacologia
Estreptozocina
Peçonhas/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (2-(glucopyranosyloxy)-3-phenylpropenoic acid); 0 (Biomarkers); 0 (Blood Glucose); 0 (Glucosides); 0 (Hypoglycemic Agents); 0 (MicroRNAs); 0 (Mirn375 microRNA, mouse); 0 (Peptides); 0 (Phenylpropionates); 0 (Protective Agents); 0 (Venoms); 5W494URQ81 (Streptozocin); 9P1872D4OL (exenatide)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171031
[Lr] Data última revisão:
171031
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171018
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0186480


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[PMID]:28991932
[Au] Autor:Edelman SV
[Ad] Endereço:Professor of Medicine, University of California San Diego, Veterans Affairs Medical Center, San Diego, California, USA.
[Ti] Título:Addressing Unmet Needs With Injectable Medications in Type 2 Diabetes Treatment: Glucagon-Like Peptide-1 Receptor Agonists.
[So] Source:J Fam Pract;66(10 Suppl):S12-S16, 2017 Oct.
[Is] ISSN:1533-7294
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Since 2005, four new GLP-1RAs (liraglutide, albiglutide, dulaglutide, and lixisenatide) and a once-weekly formulation of exenatide were approved for the treatment of persons with T2DM. Another GLP-1RA, semaglutide, is under review by the FDA, as is exenatide administered via an osmotic mini-pump.
[Mh] Termos MeSH primário: Diabetes Mellitus Tipo 2/tratamento farmacológico
Receptor do Peptídeo Semelhante ao Glucagon 1/agonistas
Hipoglicemiantes/uso terapêutico
[Mh] Termos MeSH secundário: Peptídeos Semelhantes ao Glucagon/análogos & derivados
Peptídeos Semelhantes ao Glucagon/uso terapêutico
Seres Humanos
Hipoglicemiantes/farmacologia
Fragmentos Fc das Imunoglobulinas/uso terapêutico
Liraglutida/uso terapêutico
Peptídeos/uso terapêutico
Proteínas Recombinantes de Fusão/uso terapêutico
Peçonhas/uso terapêutico
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Glucagon-Like Peptide-1 Receptor); 0 (Hypoglycemic Agents); 0 (Immunoglobulin Fc Fragments); 0 (Peptides); 0 (Recombinant Fusion Proteins); 0 (Venoms); 62340-29-8 (Glucagon-Like Peptides); 74O62BB01U (lixisenatide); 839I73S42A (Liraglutide); 9P1872D4OL (exenatide); WTT295HSY5 (dulaglutide)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171013
[Lr] Data última revisão:
171013
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:171010
[St] Status:MEDLINE


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[PMID]:28920919
[Au] Autor:Dai C; Hang Y; Shostak A; Poffenberger G; Hart N; Prasad N; Phillips N; Levy SE; Greiner DL; Shultz LD; Bottino R; Kim SK; Powers AC
[Ad] Endereço:Division of Diabetes, Endocrinology and Metabolism, Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee, USA.
[Ti] Título:Age-dependent human ß cell proliferation induced by glucagon-like peptide 1 and calcineurin signaling.
[So] Source:J Clin Invest;127(10):3835-3844, 2017 Oct 02.
[Is] ISSN:1558-8238
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Inadequate pancreatic ß cell function underlies type 1 and type 2 diabetes mellitus. Strategies to expand functional cells have focused on discovering and controlling mechanisms that limit the proliferation of human ß cells. Here, we developed an engraftment strategy to examine age-associated human islet cell replication competence and reveal mechanisms underlying age-dependent decline of ß cell proliferation in human islets. We found that exendin-4 (Ex-4), an agonist of the glucagon-like peptide 1 receptor (GLP-1R), stimulates human ß cell proliferation in juvenile but not adult islets. This age-dependent responsiveness does not reflect loss of GLP-1R signaling in adult islets, since Ex-4 treatment stimulated insulin secretion by both juvenile and adult human ß cells. We show that the mitogenic effect of Ex-4 requires calcineurin/nuclear factor of activated T cells (NFAT) signaling. In juvenile islets, Ex-4 induced expression of calcineurin/NFAT signaling components as well as target genes for proliferation-promoting factors, including NFATC1, FOXM1, and CCNA1. By contrast, expression of these factors in adult islet ß cells was not affected by Ex-4 exposure. These studies reveal age-dependent signaling mechanisms regulating human ß cell proliferation, and identify elements that could be adapted for therapeutic expansion of human ß cells.
[Mh] Termos MeSH primário: Envelhecimento/metabolismo
Calcineurina/metabolismo
Peptídeo 1 Semelhante ao Glucagon/metabolismo
Células Secretoras de Insulina/metabolismo
Transdução de Sinais
[Mh] Termos MeSH secundário: Adulto
Animais
Ciclina A1/metabolismo
Feminino
Proteína Forkhead Box M1/metabolismo
Receptor do Peptídeo Semelhante ao Glucagon 1/agonistas
Receptor do Peptídeo Semelhante ao Glucagon 1/metabolismo
Seres Humanos
Insulina/secreção
Masculino
Camundongos Endogâmicos NOD
Meia-Idade
Fatores de Transcrição NFATC/metabolismo
Peptídeos/farmacologia
Peçonhas/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CCNA1 protein, human); 0 (Cyclin A1); 0 (FOXM1 protein, human); 0 (Forkhead Box Protein M1); 0 (GLP1R protein, human); 0 (Glucagon-Like Peptide-1 Receptor); 0 (Insulin); 0 (NFATC Transcription Factors); 0 (NFATC1 protein, human); 0 (Peptides); 0 (Venoms); 89750-14-1 (Glucagon-Like Peptide 1); 9P1872D4OL (exenatide); EC 3.1.3.16 (Calcineurin)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171019
[Lr] Data última revisão:
171019
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170919
[St] Status:MEDLINE


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[PMID]:28918840
[Au] Autor:Aksoy D; Solmaz V; Çavusoglu T; Meral A; Ates U; Erbas O
[Ad] Endereço:Department of Neurology, Gaziosmanpasa University Faculty of Medicine, Tokat, Turkey. Electronic address: dbekar@yahoo.com.
[Ti] Título:Neuroprotective Effects of Eexenatide in a Rotenone-Induced Rat Model of Parkinson's Disease.
[So] Source:Am J Med Sci;354(3):319-324, 2017 Sep.
[Is] ISSN:1538-2990
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKROUND: Several studies suggest an association between Parkinson's disease (PD) and type 2 diabetes mellitus; these 2 diseases are both known to affect the common molecular pathways. As a synthetic agonist for the glucagon-like peptide 1 receptor, exenatide has been evaluated as a neuroprotective agent in multiple animal models. Rotenone models of PD have great potential for the investigation of PD pathology and motor and nonmotor symptoms, as well as the role of gene-environment interactions in PD causation and pathogenesis. Therefore, in this study, the neurochemical, behavioral and histologic effects of exenatide on a rotenone-induced rat model of PD were examined. MATERIALS AND METHODS: Eighteen adult male rats were randomly divided into the following 3 groups (n = 6): 1 group received stereotaxical infusion of dimethyl sulfoxide (vehicle, group 1) and the others received stereotaxical infusion of rotenone (groups 2 and 3). Apomorphine-induced rotation test was applied to the rats after 10 days. Thereafter, group 2 was administered isotonic saline, whereas group 3 was administered exenatide for 28 days. RESULTS: Malondialdehyde and tumor necrosis factor alpha levels increased in the rats with PD induced by rotenone, whereas malondialdehyde and tumor necrosis factor alpha levels markedly decreased in the rats treated with exenatide. The apomorphine-induced rotation test scores of exenatide-treated rats were determined to be lower compared with the untreated group. Additionally, treatment with exenatide significantly reduced the loss of dopaminergic neurons in striatum. CONCLUSIONS: These results have shown that exenatide has neuroprotective, anti-inflammatory and antioxidant effects in a rotenone-induced rat model of PD.
[Mh] Termos MeSH primário: Encéfalo/efeitos dos fármacos
Fármacos Neuroprotetores/uso terapêutico
Transtornos Parkinsonianos/tratamento farmacológico
Peptídeos/uso terapêutico
Rotenona/farmacologia
Peçonhas/uso terapêutico
[Mh] Termos MeSH secundário: Animais
Comportamento Animal/efeitos dos fármacos
Encéfalo/metabolismo
Encéfalo/patologia
Neurônios Dopaminérgicos/efeitos dos fármacos
Neurônios Dopaminérgicos/patologia
Peroxidação de Lipídeos/efeitos dos fármacos
Masculino
Fármacos Neuroprotetores/administração & dosagem
Transtornos Parkinsonianos/induzido quimicamente
Transtornos Parkinsonianos/patologia
Peptídeos/administração & dosagem
Ratos
Ratos Sprague-Dawley
Fator de Necrose Tumoral alfa/metabolismo
Peçonhas/administração & dosagem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Neuroprotective Agents); 0 (Peptides); 0 (Tumor Necrosis Factor-alpha); 0 (Venoms); 03L9OT429T (Rotenone); 9P1872D4OL (exenatide)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170925
[Lr] Data última revisão:
170925
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170919
[St] Status:MEDLINE



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