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[PMID]:29238190
[Au] Autor:Salade L; Wauthoz N; Deleu M; Vermeersch M; De Vriese C; Amighi K; Goole J
[Ad] Endereço:Laboratoire de Pharmacie Galénique et de Biopharmacie, Université libre de Bruxelles (ULB), Brussels.
[Ti] Título:Development of coated liposomes loaded with ghrelin for nose-to-brain delivery for the treatment of cachexia.
[So] Source:Int J Nanomedicine;12:8531-8543, 2017.
[Is] ISSN:1178-2013
[Cp] País de publicação:New Zealand
[La] Idioma:eng
[Ab] Resumo:The aim of the present study was to develop a ghrelin-containing formulation based on liposomes coated with chitosan intended for nose-brain delivery for the treatment of cachexia. Among the three types of liposomes developed, anionic liposomes provided the best results in terms of encapsulation efficiency (56%) and enzymatic protection against trypsin (20.6% vs 0% for ghrelin alone) and carboxylesterase (81.6% vs 17.2% for ghrelin alone). Ghrelin presented both electrostatic and hydrophobic interactions with the anionic lipid bilayer, as demonstrated by isothermal titration calorimetry. Then, anionic liposomes were coated with -(2-hydroxy) propyl-3-trimethyl ammonium chitosan chloride. The coating involved a size increment from 146.9±2.7 to 194±6.1 nm, for uncoated and coated liposomes, respectively. The ζ-potential was similarly increased from -0.3±1.2 mV to 6±0.4 mV before and after coating, respectively. Chitosan provided mucoadhesion, with an increase in mucin adsorption of 22.9%. Enhancement of permeation through the Calu3 epithelial monolayer was also observed with 10.8% of ghrelin recovered in the basal compartment in comparison to 0% for ghrelin alone. Finally, aerosols generated from two nasal devices (VP3 and SP270) intended for aqueous dispersion were characterized with either coated or uncoated liposomes. Contrarily to the SP270 device, VP3 device showed minor changes between coated and uncoated liposome aerosols, as shown by their median volume diameters of 38.4±5.76 and 37.6±5.74 µm, respectively. Overall, the results obtained in this study show that the developed formulation delivered by the VP3 device can be considered as a potential candidate for nose-brain delivery of ghrelin.
[Mh] Termos MeSH primário: Caquexia/tratamento farmacológico
Sistemas de Liberação de Medicamentos/métodos
Grelina/administração & dosagem
Lipossomos/administração & dosagem
Lipossomos/química
[Mh] Termos MeSH secundário: Administração Intranasal/instrumentação
Adsorção
Aerossóis/química
Encéfalo/efeitos dos fármacos
Quitosana/análogos & derivados
Quitosana/química
Estabilidade de Medicamentos
Grelina/química
Seres Humanos
Interações Hidrofóbicas e Hidrofílicas
Mucinas/metabolismo
Compostos de Amônio Quaternário/química
Eletricidade Estática
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Aerosols); 0 (Ghrelin); 0 (Liposomes); 0 (Mucins); 0 (N-(2-hydroxypropyl)-3-trimethylammonium chitosan); 0 (Quaternary Ammonium Compounds); 9012-76-4 (Chitosan)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171215
[St] Status:MEDLINE
[do] DOI:10.2147/IJN.S147650


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[PMID]:29385178
[Au] Autor:Parvaresh Rizi E; Loh TP; Baig S; Chhay V; Huang S; Caleb Quek J; Tai ES; Toh SA; Khoo CM
[Ad] Endereço:Department of Medicine, Yong Loo Lin School of Medicine, National University of Singapore, Singapore.
[Ti] Título:A high carbohydrate, but not fat or protein meal attenuates postprandial ghrelin, PYY and GLP-1 responses in Chinese men.
[So] Source:PLoS One;13(1):e0191609, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:It is known that the macronutrient content of a meal has different impacts on the postprandial satiety and appetite hormonal responses. Whether obesity interacts with such nutrient-dependent responses is not well characterized. We examined the postprandial appetite and satiety hormonal responses after a high-protein (HP), high-carbohydrate (HC), or high-fat (HF) mixed meal. This was a randomized cross-over study of 9 lean insulin-sensitive (mean±SEM HOMA-IR 0.83±0.10) and 9 obese insulin-resistant (HOMA-IR 4.34±0.41) young (age 21-40 years), normoglycaemic Chinese men. We measured fasting and postprandial plasma concentration of glucose, insulin, active glucagon-like peptide-1 (GLP-1), total peptide-YY (PYY), and acyl-ghrelin in response to HP, HF, or HC meals. Overall postprandial plasma insulin response was more robust in the lean compared to obese subjects. The postprandial GLP-1 response after HF or HP meal was higher than HC meal in both lean and obese subjects. In obese subjects, HF meal induced higher response in postprandial PYY compared to HC meal. HP and HF meals also suppressed ghrelin greater compared to HC meal in the obese than lean subjects. In conclusion, a high-protein or high-fat meal induces a more favorable postprandial satiety and appetite hormonal response than a high-carbohydrate meal in obese insulin-resistant subjects.
[Mh] Termos MeSH primário: Carboidratos da Dieta/administração & dosagem
Gorduras na Dieta/administração & dosagem
Proteínas na Dieta/administração & dosagem
Grelina/sangue
Peptídeo 1 Semelhante ao Glucagon/sangue
Peptídeo YY/sangue
[Mh] Termos MeSH secundário: Adulto
Grupo com Ancestrais do Continente Asiático
Glicemia/metabolismo
Estudos Cross-Over
Dieta Hiperlipídica
Dieta Rica em Proteínas
Seres Humanos
Insulina/sangue
Resistência à Insulina
Masculino
Obesidade/sangue
Obesidade/dietoterapia
Período Pós-Prandial/fisiologia
Resposta de Saciedade/fisiologia
Singapura
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE; RANDOMIZED CONTROLLED TRIAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Blood Glucose); 0 (Dietary Carbohydrates); 0 (Dietary Fats); 0 (Dietary Proteins); 0 (Ghrelin); 0 (Insulin); 106388-42-5 (Peptide YY); 89750-14-1 (Glucagon-Like Peptide 1)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180302
[Lr] Data última revisão:
180302
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180201
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0191609


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[PMID]:29366747
[Au] Autor:Camargo-Silva G; Turones LC; da Cruz KR; Gomes KP; Mendonça MM; Nunes A; de Jesus IG; Colugnati DB; Pansani AP; Pobbe RLH; Santos R; Fontes MAP; Guatimosim S; de Castro CH; Ianzer D; Ferreira RN; Xavier CH
[Ad] Endereço:Laboratory of Cardiovascular Physiology and Therapeutics, Department of Physiological Sciences, Institute of Biological Sciences, Federal University of Goiás, Goiania, GO, Brazil.
[Ti] Título:Ghrelin potentiates cardiac reactivity to stress by modulating sympathetic control and beta-adrenergic response.
[So] Source:Life Sci;196:84-92, 2018 Mar 01.
[Is] ISSN:1879-0631
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Prior evidence indicates that ghrelin is involved in the integration of cardiovascular functions and behavioral responses. Ghrelin actions are mediated by the growth hormone secretagogue receptor subtype 1a (GHS-R1a), which is expressed in peripheral tissues and central areas involved in the control of cardiovascular responses to stress. AIMS: In the present study, we assessed the role of ghrelin - GHS-R1a axis in the cardiovascular reactivity to acute emotional stress in rats. MAIN METHODS AND KEY FINDINGS: Ghrelin potentiated the tachycardia evoked by restraint and air jet stresses, which was reverted by GHS-R1a blockade. Evaluation of the autonomic balance revealed that the sympathetic branch modulates the ghrelin-evoked positive chronotropy. In isolated hearts, the perfusion with ghrelin potentiated the contractile responses caused by stimulation of the beta-adrenergic receptor, without altering the amplitude of the responses evoked by acetylcholine. Experiments in isolated cardiomyocytes revealed that ghrelin amplified the increases in calcium transient changes evoked by isoproterenol. SIGNIFICANCE: Taken together, our results indicate that the Ghrelin-GHS-R1a axis potentiates the magnitude of stress-evoked tachycardia by modulating the autonomic nervous system and peripheral mechanisms, strongly relying on the activation of cardiac calcium transient and beta-adrenergic receptors.
[Mh] Termos MeSH primário: Grelina/farmacologia
Coração/efeitos dos fármacos
Receptores Adrenérgicos beta/efeitos dos fármacos
Estresse Psicológico/fisiopatologia
Sistema Nervoso Simpático/efeitos dos fármacos
[Mh] Termos MeSH secundário: Agonistas Adrenérgicos beta/farmacologia
Animais
Pressão Arterial/efeitos dos fármacos
Canais de Cálcio/efeitos dos fármacos
Coração/inervação
Frequência Cardíaca/efeitos dos fármacos
Técnicas In Vitro
Masculino
Agonistas Muscarínicos/farmacologia
Ratos
Ratos Wistar
Receptores de Grelina/efeitos dos fármacos
Restrição Física
Taquicardia/induzido quimicamente
Taquicardia/fisiopatologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Adrenergic beta-Agonists); 0 (Calcium Channels); 0 (Ghrelin); 0 (Muscarinic Agonists); 0 (Receptors, Adrenergic, beta); 0 (Receptors, Ghrelin)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180226
[Lr] Data última revisão:
180226
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180126
[St] Status:MEDLINE


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[PMID]:29208260
[Au] Autor:Fu T; Wang L; Zeng Q; Zhang Y; Sheng B; Han L
[Ad] Endereço:Department of Respiration, the 1st People's Hospital of Jining, Jining, China.
[Ti] Título:Ghrelin Ameliorates Asthma by Inhibiting Endoplasmic Reticulum Stress.
[So] Source:Am J Med Sci;354(6):617-625, 2017 12.
[Is] ISSN:1538-2990
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: This study aimed to confirm the ameliorative effect of ghrelin on asthma and investigate its mechanism. MATERIALS AND METHODS: The murine model of asthma was induced by ovalbumin (OVA) treatment and assessed by histological pathology and airway responsiveness to methacholine. The total and differential leukocytes were counted. Tumor necrosis factor α, interferon γ, interleukin-5 and interleukin-13 levels in bronchoalveolar lavage fluid were quantified by commercial kits. The protein levels in pulmonary tissues were measured by Western blot analysis. RESULTS: Ghrelin ameliorated the histological pathology and airway hyperresponsiveness in the OVA-induced asthmatic mouse model. Consistently, OVA-increased total and differential leukocytes and levels of tumor necrosis factor α, interferon γ, interleukin-5 and interleukin-13 in bronchoalveolar lavage fluid were significantly attenuated by ghrelin. Ghrelin prevented the increased protein levels of the endoplasmic reticulum stress markers glucose regulated protein 78 and CCAAT/enhancer binding protein homologous protein and reversed the reduced levels of p-Akt in asthmatic mice. CONCLUSIONS: Ghrelin might prevent endoplasmic reticulum stress activation by stimulating the Akt signaling pathway, which attenuated inflammation and ameliorated asthma in mice. Ghrelin might be a new target for asthma therapy.
[Mh] Termos MeSH primário: Antiasmáticos/uso terapêutico
Asma/tratamento farmacológico
Retículo Endoplasmático/efeitos dos fármacos
Grelina/uso terapêutico
[Mh] Termos MeSH secundário: Animais
Antiasmáticos/farmacologia
Asma/patologia
Asma/fisiopatologia
Western Blotting
Líquido da Lavagem Broncoalveolar/química
Líquido da Lavagem Broncoalveolar/citologia
Modelos Animais de Doenças
Grelina/farmacologia
Queratinas/análise
Pulmão/efeitos dos fármacos
Pulmão/patologia
Masculino
Cloreto de Metacolina/farmacologia
Camundongos
Camundongos Endogâmicos C57BL
Estresse Fisiológico/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Anti-Asthmatic Agents); 0 (Ghrelin); 0W5ETF9M2K (Methacholine Chloride); 68238-35-7 (Keratins)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:180223
[Lr] Data última revisão:
180223
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:171207
[St] Status:MEDLINE


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[PMID]:29181895
[Au] Autor:Shiina Y; Murakami T; Matsumoto N; Okamura D; Takahashi Y; Nishihata Y; Komiyama N; Niwa K
[Ad] Endereço:Department of Cardiology, Cardiovascular Center, St. Luke's International Hospital, Tokyo, Japan.
[Ti] Título:Body composition, appetite-related hormones, adipocytokines, and heart failure in adult patients with congenital heart disease: A preliminary study.
[So] Source:Congenit Heart Dis;13(1):79-84, 2018 Jan.
[Is] ISSN:1747-0803
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVES: To assess body composition and relationships among body composition, appetite-related hormones, adipocytokines, and heart failure (HF) in adult patients with congenital heart disease (CHD). PATIENTS: This prospective study enrolled 46 consecutive adult patients with CHD and 12 age-matched healthy controls. The patients and control subjects were divided into four groups: 13 patients with Fontan circulation (group A), 16 patients with cyanosis (group B), 17 patients who previously underwent biventricular repair (group C), and 12 age-matched healthy controls. DESIGN: Body composition was measured using InBody730, and levels of appetite-related hormones (ghrelin and leptin) and adipocytokines (leptin, interleukin-6, and tumor necrosis factor-α) were determined. Relationships of these measurements between severe HF, defined as New York Heart Association functional class III-IV and/or recent repeated unscheduled hospitalizations due to HF, were examined using univariate logistic analysis. RESULTS: Mean patient age was 32.1 ± 7.4 years. The skeletal muscle mass was significantly decreased in groups A and B compared with that in controls. Interestingly, ghrelin levels in groups A and B were also significantly lower than those in controls. Univariate logistic analysis revealed that ghrelin level, percent body fat, and pulse oximetric oxygen saturation were significantly associated with severe HF. CONCLUSIONS: Patients with Fontan circulation and those with cyanosis might be at a risk of sarcopenia. Despite the decreased skeletal muscle mass and increased body fat, ghrelin levels in these patients were decreased. These changes might have a negative impact on HF in these patients.
[Mh] Termos MeSH primário: Adipocinas/metabolismo
Composição Corporal
Grelina/metabolismo
Cardiopatias Congênitas/complicações
Insuficiência Cardíaca/fisiopatologia
Músculo Esquelético/metabolismo
Sarcopenia/etiologia
[Mh] Termos MeSH secundário: Adulto
Biomarcadores/metabolismo
Feminino
Cardiopatias Congênitas/metabolismo
Cardiopatias Congênitas/fisiopatologia
Insuficiência Cardíaca/complicações
Insuficiência Cardíaca/metabolismo
Seres Humanos
Masculino
Estudos Prospectivos
Sarcopenia/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Adipokines); 0 (Biomarkers); 0 (Ghrelin)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180219
[Lr] Data última revisão:
180219
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171129
[St] Status:MEDLINE
[do] DOI:10.1111/chd.12555


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[PMID]:29300858
[Au] Autor:Fernandez G; Cabral A; Andreoli MF; Labarthe A; M'Kadmi C; Ramos JG; Marie J; Fehrentz JA; Epelbaum J; Tolle V; Perello M
[Ad] Endereço:Laboratory of Neurophysiology of the Multidisciplinary Institute of Cell Biology (Argentine Research Council, Scientific Research Commission of the Province of Buenos Aires and National University of La Plata), La Plata, Buenos Aires, Argentina.
[Ti] Título:Evidence Supporting a Role for Constitutive Ghrelin Receptor Signaling in Fasting-Induced Hyperphagia in Male Mice.
[So] Source:Endocrinology;159(2):1021-1034, 2018 02 01.
[Is] ISSN:1945-7170
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Ghrelin is a potent orexigenic peptide hormone that acts through the growth hormone secretagogue receptor (GHSR), a G protein-coupled receptor highly expressed in the hypothalamus. In vitro studies have shown that GHSR displays a high constitutive activity, whose physiological relevance is uncertain. As GHSR gene expression in the hypothalamus is known to increase in fasting conditions, we tested the hypothesis that constitutive GHSR activity at the hypothalamic level drives the fasting-induced hyperphagia. We found that refed wild-type (WT) mice displayed a robust hyperphagia that continued for 5 days after refeeding and changed their food intake daily pattern. Fasted WT mice showed an increase in plasma ghrelin levels, as well as in GHSR expression levels and ghrelin binding sites in the hypothalamic arcuate nucleus. When fasting-refeeding responses were evaluated in ghrelin- or GHSR-deficient mice, only the latter displayed an ∼15% smaller hyperphagia, compared with WT mice. Finally, fasting-induced hyperphagia of WT mice was significantly smaller in mice centrally treated with the GHSR inverse agonist K-(D-1-Nal)-FwLL-NH2, compared with mice treated with vehicle, whereas it was unaffected in mice centrally treated with the GHSR antagonists D-Lys3-growth hormone-releasing peptide 6 or JMV2959. Taken together, genetic models and pharmacological results support the notion that constitutive GHSR activity modulates the magnitude of the compensatory hyperphagia triggered by fasting. Thus, the hypothalamic GHSR signaling system could affect the set point of daily food intake, independently of plasma ghrelin levels, in situations of negative energy balance.
[Mh] Termos MeSH primário: Jejum/fisiologia
Grelina/fisiologia
Hiperfagia/etiologia
Receptores de Grelina/fisiologia
[Mh] Termos MeSH secundário: Animais
Ingestão de Alimentos/fisiologia
Grelina/metabolismo
Hiperfagia/genética
Hiperfagia/metabolismo
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Receptores de Grelina/genética
Receptores de Grelina/metabolismo
Transdução de Sinais/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Ghrelin); 0 (Receptors, Ghrelin)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180215
[Lr] Data última revisão:
180215
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:180105
[St] Status:MEDLINE
[do] DOI:10.1210/en.2017-03101


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[PMID]:29320575
[Au] Autor:Allas S; Caixàs A; Poitou C; Coupaye M; Thuilleaux D; Lorenzini F; Diene G; Crinò A; Illouz F; Grugni G; Potvin D; Bocchini S; Delale T; Abribat T; Tauber M
[Ad] Endereço:Alizé Pharma, Ecully, France.
[Ti] Título:AZP-531, an unacylated ghrelin analog, improves food-related behavior in patients with Prader-Willi syndrome: A randomized placebo-controlled trial.
[So] Source:PLoS One;13(1):e0190849, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:CONTEXT AND OBJECTIVE: Prader-Willi syndrome (PWS) is characterized by early-onset hyperphagia and increased circulating levels of the orexigenic Acylated Ghrelin (AG) hormone with a relative deficit of Unacylated Ghrelin (UAG). AZP-531, a first-in-class UAG analog, was shown to inhibit the orexigenic effect of AG in animals, to improve glycemic control and decrease body weight in humans. We aimed to investigate the safety and efficacy of AZP-531 in patients with PWS for whom no approved treatment for hyperphagia is currently available. METHODS AND DESIGN: Multi-center, randomized, double-blind, placebo-controlled trial. Forty-seven patients with genetically confirmed PWS and evidence of hyperphagia received daily subcutaneous injections of AZP-531 (3 and 4 mg for 50-70 kg and >70 kg body weight, respectively) or matching placebo for 14 days. Assessments included adverse events, vital signs, safety laboratory tests, the Hyperphagia Questionnaire (HQ), patient-reported appetite, body composition and glycemic measures. RESULTS: AZP-531 was well tolerated. There was a significant improvement with AZP-531 versus placebo in the mean total score, the 9-item score and the severity domain score of the HQ (p < .05). The highest reduction in the total and 9-item scores was observed in AZP-531 subjects with the highest hyperphagia score at baseline. Findings were supported by a reduction in appetite scores observed with AZP-531 only. Body weight did not change in both groups while a significant reduction in waist circumference and fat mass was observed only with AZP-531. AZP-531 significantly decreased post-prandial glucose levels in a baseline glucose dependent fashion. CONCLUSIONS: AZP-531 may constitute a new treatment strategy to improve hyperphagia and metabolic issues in patients with PWS. These findings support further investigation in longer-term clinical trials.
[Mh] Termos MeSH primário: Comportamento Alimentar/efeitos dos fármacos
Grelina/uso terapêutico
Hiperfagia/tratamento farmacológico
Hipoglicemiantes/uso terapêutico
Fragmentos de Peptídeos/uso terapêutico
Peptídeos Cíclicos/uso terapêutico
Síndrome de Prader-Willi/tratamento farmacológico
[Mh] Termos MeSH secundário: Adolescente
Adulto
Fármacos Antiobesidade/efeitos adversos
Fármacos Antiobesidade/uso terapêutico
Apetite/efeitos dos fármacos
Apetite/fisiologia
Glicemia/efeitos dos fármacos
Composição Corporal/efeitos dos fármacos
Peso Corporal/efeitos dos fármacos
Método Duplo-Cego
Comportamento Alimentar/fisiologia
Feminino
Seguimentos
Grelina/efeitos adversos
Seres Humanos
Hiperfagia/sangue
Hiperfagia/genética
Hipoglicemiantes/efeitos adversos
Masculino
Meia-Idade
Fragmentos de Peptídeos/efeitos adversos
Peptídeos Cíclicos/efeitos adversos
Síndrome de Prader-Willi/sangue
Síndrome de Prader-Willi/genética
Resultado do Tratamento
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE; MULTICENTER STUDY; RANDOMIZED CONTROLLED TRIAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Anti-Obesity Agents); 0 (Blood Glucose); 0 (Ghrelin); 0 (Hypoglycemic Agents); 0 (Peptide Fragments); 0 (Peptides, Cyclic); 0 (cyclic des-acyl ghrelin (6-13))
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180205
[Lr] Data última revisão:
180205
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180111
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0190849


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[PMID]:28468316
[Au] Autor:Bonior J; Ceranowicz P; Gajdosz R; Kusnierz-Cabala B; Pierzchalski P; Warzecha Z; Dembinski A; Pedziwiatr M; Kot M; Leja-Szpak A; Nawrot-Porabka K; Link-Lenczowski P; Olszanecki R; Bartus K; Jaworek J
[Ad] Endereço:Department of Medical Physiology, Faculty of Health Sciences, Jagiellonian University Medical College, 12 Michalowskiego St., 31-126 Krakow, Poland. joanna.bonior@uj.edu.pl.
[Ti] Título:Molecular Ghrelin System in the Pancreatic Acinar Cells: The Role of the Polypeptide, Caerulein and Sensory Nerves.
[So] Source:Int J Mol Sci;18(5), 2017 May 02.
[Is] ISSN:1422-0067
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:Ghrelin (GHRL) is an endogenous ligand for the growth hormone secretagogue receptor (GHS-R). Experimental studies showed that GHRL protects the stomach and pancreas against acute damage, but the effect of GHRL on pancreatic acinar cells was still undetermined. AIM: To investigate the effect of GHRL and caerulein on the functional ghrelin system in pancreatic acinar cells taking into account the role of sensory nerves (SN). METHODS: Experiments were carried out on isolated pancreatic acinar cells and AR42J cells. Before acinar cells isolation, GHRL was administered intraperitoneally at a dose of 50 µg/kg to rats with intact SN or with capsaicin deactivation of SN (CDSN). After isolation, pancreatic acinar cells were incubated in caerulein-free or caerulein containing solution. AR42J cells were incubated under basal conditions and stimulated with caerulein, GHRL or a combination of the above. RESULTS: Incubation of isolated acinar cells with caerulein inhibited GHS-R and GHRL expression at the level of mRNA and protein in those cells. Either in rats with intact SN or with CDSN, administration of GHRL before isolation of acinar cells increased expression of GHRL and GHS-R in those cells and reversed the caerulein-induced reduction in expression of those parameters. Similar upregulation of GHS-R and GHRL was observed after administration of GHRL in AR42J cells. CONCLUSIONS: GHRL stimulates its own expression and expression of its receptor in isolated pancreatic acinar cells and AR42J cells on the positive feedback pathway. This mechanism seems to participate in the pancreatoprotective effect of GHRL in the course of acute pancreatitis.
[Mh] Termos MeSH primário: Células Acinares/metabolismo
Ceruletídeo/farmacologia
Grelina/metabolismo
Receptores de Grelina/metabolismo
Células Receptoras Sensoriais/fisiologia
[Mh] Termos MeSH secundário: Células Acinares/efeitos dos fármacos
Animais
Linhagem Celular
Células Cultivadas
Retroalimentação Fisiológica
Grelina/genética
Masculino
Pâncreas/citologia
Pâncreas/inervação
Ratos
Ratos Wistar
Receptores de Grelina/genética
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Ghrelin); 0 (Receptors, Ghrelin); 888Y08971B (Ceruletide)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180202
[Lr] Data última revisão:
180202
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170505
[St] Status:MEDLINE


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[PMID]:29216250
[Au] Autor:Choi YY; Noh SH; An JY
[Ad] Endereço:Department of Surgery, Yonsei University College of Medicine, Seoul, Korea.
[Ti] Título:A randomized controlled trial of Roux-en-Y gastrojejunostomy vs. gastroduodenostomy with respect to the improvement of type 2 diabetes mellitus after distal gastrectomy in gastric cancer patients.
[So] Source:PLoS One;12(12):e0188904, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The purpose of this study is to compare the effect of diabetes control induced by Roux-en-Y gastrojejunostomy(RY) vs Billroth-I reconstruction(BI) after distal gastrectomy in patients with early gastric cancer(EGC) and type 2 diabetes(T2DM). Forty EGC patients with T2DM, aged 20-80 years, who were expected to undergo curative distal gastrectomy were randomized 1:1 to RY(n = 20) or BI(n = 20). Diabetes medication status, biochemical and hormonal data including blood glucose, HbA1c, insulin, C-peptide, HOMA-IR, ghrelin, leptin, GLP-1, PYY, and GIP were evaluated for 12 months after surgery. Although pre- and postoperative 12-month fasting and postprandial glucose levels did not show a significant difference, HbA1c, C-peptide, and HOMA-IR levels were significantly improved at 12 months after surgery in both BI and RY groups. Sixty percent of RY patients and 20% of BI patients decreased their medication satisfying FBS<126 mg/dL and HbA1c<6.5% and 5% of BI patients stopped their medication satisfying the criteria of FBS<126 mg/dL and HbA1c<6.0%. The improvement patterns were more sustainable with less fluctuation in RY than in BI. On hormonal analysis, ghrelin and leptin levels were decreased and PYY and GIP levels were increased at 12 months after surgery in both groups without significant difference according to the reconstruction type and diabetic improvement status except ghrelin. In gastric cancer surgery, RY reconstruction showed better and more durable diabetes control compared to BI during the first year after surgery. Gastric cancer surgery led to decreased ghrelin and leptin and increased PYY and GIP, which might have a role in improving insulin resistance and glucose homeostasis.
[Mh] Termos MeSH primário: Diabetes Mellitus Tipo 2/cirurgia
Duodeno/cirurgia
Derivação Gástrica/métodos
Neoplasias Gástricas/cirurgia
Estômago/cirurgia
[Mh] Termos MeSH secundário: Idoso
Diabetes Mellitus Tipo 2/complicações
Feminino
Polipeptídeo Inibidor Gástrico/sangue
Grelina/sangue
Peptídeo 1 Semelhante ao Glucagon/sangue
Seres Humanos
Leptina/sangue
Masculino
Meia-Idade
Peptídeo YY/sangue
Estudos Prospectivos
Neoplasias Gástricas/complicações
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE; RANDOMIZED CONTROLLED TRIAL
[Nm] Nome de substância:
0 (Ghrelin); 0 (Leptin); 106388-42-5 (Peptide YY); 59392-49-3 (Gastric Inhibitory Polypeptide); 89750-14-1 (Glucagon-Like Peptide 1)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171226
[Lr] Data última revisão:
171226
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171208
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0188904


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[PMID]:29222553
[Au] Autor:Zhu K; Zhang ML; Liu ST; Li XY; Zhong SM; Li F; Xu GZ; Wang Z; Miao Y
[Ad] Endereço:Institutes of Brain Science, State Key Laboratory of Medical Neurobiology, Collaborative Innovation Center for Brain Science, Fudan University, Shanghai, China.
[Ti] Título:Ghrelin Attenuates Retinal Neuronal Autophagy and Apoptosis in an Experimental Rat Glaucoma Model.
[So] Source:Invest Ophthalmol Vis Sci;58(14):6113-6122, 2017 Dec 01.
[Is] ISSN:1552-5783
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Purpose: Ghrelin, a natural ligand for the growth hormone secretagogue receptor type 1a (GHSR-1a), may protect retinal neurons against glaucomatous injury. We therefore characterized the underlying mechanism of the ghrelin/GHSR-1a-mediated neuroprotection with a rat chronic intraocular hypertension (COH) model. Methods: The rat COH model was produced by blocking episcleral veins. A combination of immunohistochemistry, Western blot, TUNEL assay, and retrograde labeling of retinal ganglion cells (RGCs) was used. Results: Elevation of intraocular pressure induced a significant increase in ghrelin and GHSR-1a expression in retinal cells, including RGCs and Müller cells. Western blot confirmed that the protein levels of ghrelin exhibited a transient upregulation at week 2 after surgery (G2w), while the GHSR-1a protein levels were maintained at high levels from G2w to G4w. In COH retinas, the ratio of LC3-II/LC-I and beclin1, two autophagy-related proteins, were increased from G1w to G4w, and the cleavage product of caspase3, an apoptotic executioner, was detected from G2w to G4w. Intraperitoneal injection of ghrelin significantly increased the number of surviving RGCs; inhibited the changes of LC3-II/LC-I, beclin1, and the cleavage products of caspase3; and reduced the number of TUNEL-positive cells in COH retinas. Ghrelin treatment also reversed the decreased levels of p-Akt and p-mTOR, upregulated GHSR-1a protein levels, and attenuated glial fibrillary acidic protein levels in COH retinas. Conclusions: All these results suggest that ghrelin may provide neuroprotective effect in COH retinas through activating ghrelin/GHSR-1a system, which was mediated by inhibiting retinal autophagy, ganglion cell apoptosis, and Müller cell gliosis.
[Mh] Termos MeSH primário: Apoptose
Autofagia
Regulação da Expressão Gênica
Grelina/genética
Glaucoma/genética
Receptores de Grelina/genética
Células Ganglionares da Retina/patologia
[Mh] Termos MeSH secundário: Animais
Western Blotting
Modelos Animais de Doenças
Grelina/biossíntese
Glaucoma/metabolismo
Glaucoma/patologia
Imuno-Histoquímica
Marcação In Situ das Extremidades Cortadas
Pressão Intraocular
Masculino
RNA/genética
Ratos
Ratos Sprague-Dawley
Receptores de Grelina/biossíntese
Células Ganglionares da Retina/metabolismo
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Ghrelin); 0 (Ghsr1a protein, rat); 0 (Receptors, Ghrelin); 63231-63-0 (RNA)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171215
[Lr] Data última revisão:
171215
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171210
[St] Status:MEDLINE
[do] DOI:10.1167/iovs.17-22465



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