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  1 / 1183 MEDLINE  
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[PMID]:27973438
[Au] Autor:Petta S; Gastaldelli A; Rebelos E; Bugianesi E; Messa P; Miele L; Svegliati-Baroni G; Valenti L; Bonino F
[Ad] Endereço:Gastroenterology, Di.Bi.M.I.S Policlinic Paolo Giaccone Hospital, University of Palermo, PC 90127, Palermo, Italy. petsa@inwind.it.
[Ti] Título:Pathophysiology of Non Alcoholic Fatty Liver Disease.
[So] Source:Int J Mol Sci;17(12), 2016 Dec 11.
[Is] ISSN:1422-0067
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:The physiopathology of fatty liver and metabolic syndrome are influenced by diet, life style and inflammation, which have a major impact on the severity of the clinicopathologic outcome of non-alcoholic fatty liver disease. A short comprehensive review is provided on current knowledge of the pathophysiological interplay among major circulating effectors/mediators of fatty liver, such as circulating lipids, mediators released by adipose, muscle and liver tissues and pancreatic and gut hormones in relation to diet, exercise and inflammation.
[Mh] Termos MeSH primário: Hepatopatia Gordurosa não Alcoólica/fisiopatologia
[Mh] Termos MeSH secundário: Tecido Adiposo/metabolismo
Hormônios Gastrointestinais/metabolismo
Seres Humanos
Lipídeos/sangue
Músculos/metabolismo
Hepatopatia Gordurosa não Alcoólica/sangue
Hormônios Pancreáticos/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Gastrointestinal Hormones); 0 (Lipids); 0 (Pancreatic Hormones)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170403
[Lr] Data última revisão:
170403
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161216
[St] Status:MEDLINE


  2 / 1183 MEDLINE  
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[PMID]:27632150
[Au] Autor:Iessi IL; Sinzato YK; Gallego FQ; Nielsen JH; Damasceno DC
[Ad] Endereço:Laboratory of Experimental Research in Gynecology and Obstetrics, Program of Gynecology, Obstetrics and Mastology Graduate Course, Botucatu Medical School, Unesp Univ Estadual Paulista, Botucatu, São Paulo State, Brazil.
[Ti] Título:Effect of Diabetes on Circulating Pancreatic Hormones in Pregnant Rats and Their Offspring.
[So] Source:Horm Metab Res;48(10):682-686, 2016 Sep.
[Is] ISSN:1439-4286
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:The aim of the study was to investigate the role of diabetic intrauterine environment on circulating insulin, glucagon, and somatostatin levels in pregnant rats, fetuses, and offspring. Diabetes was induced in female Wistar rats by streptozotocin at birth or as adult and the animals were assigned into: control (C); mildly diabetic (MD); and severely diabetic (SD). The rats were mated and distributed into 2 subgroups: euthanasia at day 21 of pregnancy and at day 10 postpartum. Both MD and SD dams showed impaired oral glucose tolerance. SD dams had lower body weight and insulin levels compared to C and MD dams. SD fetuses presented hyperglycemia and reduction of insulin and glucagon levels compared to C and MD fetuses. SD newborns had diminished total pancreatic insulin and plasma somatostatin compared to the other groups. MD dams and fetuses had lower glucagon and somatostatin levels compared to C dams. MD offspring had maintained lower somatostatin levels to neonatal period. Diabetes causes alterations in circulating levels of pancreatic hormones in the mother and offspring.
[Mh] Termos MeSH primário: Biomarcadores/sangue
Diabetes Mellitus Experimental/fisiopatologia
Glucagon/sangue
Insulina/sangue
Hormônios Pancreáticos/sangue
Somatostatina/sangue
[Mh] Termos MeSH secundário: Animais
Animais Recém-Nascidos
Feminino
Gravidez
Ratos
Ratos Wistar
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (Insulin); 0 (Pancreatic Hormones); 51110-01-1 (Somatostatin); 9007-92-5 (Glucagon)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:170314
[Lr] Data última revisão:
170314
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160916
[St] Status:MEDLINE


  3 / 1183 MEDLINE  
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[PMID]:27404266
[Au] Autor:Parbhu SK; Adler DG
[Ad] Endereço:a Department of Internal Medicine, Division of Gastroenterology and Hepatology , University of Utah School of Medicine, Huntsman Cancer Center , Salt Lake City , Utah , USA.
[Ti] Título:Pancreatic neuroendocrine tumors: contemporary diagnosis and management.
[So] Source:Hosp Pract (1995);44(3):109-19, 2016 Aug.
[Is] ISSN:2154-8331
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Pancreatic neuroendocrine tumors (PNETs) are neoplasms that arise from the hormone producing cells of the islets of Langerhans, also known as pancreatic islet cells. PNETs are considered a subgroup of neuroendocrine tumors, and have unique biology, natural history and clinical management. These tumors are classified as 'functional' or 'non-functional' depending on whether they release peptide hormones that produce specific hormone- related symptoms, usually in established patterns based on tumor subtype. This manuscript will review pancreatic neuroendocrine tumor subtypes, syndromes, diagnosis, and clinical management.
[Mh] Termos MeSH primário: Tumores Neuroendócrinos/diagnóstico
Tumores Neuroendócrinos/terapia
Neoplasias Pancreáticas/diagnóstico
Neoplasias Pancreáticas/terapia
[Mh] Termos MeSH secundário: Carcinoma de Células das Ilhotas Pancreáticas/fisiopatologia
Carcinoma de Células das Ilhotas Pancreáticas/terapia
Grupos de Populações Continentais
Seres Humanos
Insulinoma/fisiopatologia
Insulinoma/terapia
Ilhotas Pancreáticas
Neoplasia Endócrina Múltipla Tipo 1/fisiopatologia
Neoplasia Endócrina Múltipla Tipo 1/terapia
Gradação de Tumores
Estadiamento de Neoplasias
Tumores Neuroendócrinos/fisiopatologia
Hormônios Pancreáticos
Neoplasias Pancreáticas/fisiopatologia
Hormônios Peptídicos
Fatores Sexuais
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Pancreatic Hormones); 0 (Peptide Hormones)
[Em] Mês de entrada:1702
[Cu] Atualização por classe:170206
[Lr] Data última revisão:
170206
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:160713
[St] Status:MEDLINE
[do] DOI:10.1080/21548331.2016.1210474


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[PMID]:27300574
[Au] Autor:Md Moin AS; Dhawan S; Shieh C; Butler PC; Cory M; Butler AE
[Ad] Endereço:Larry L. Hillblom Islet Research Center, University of California, Los Angeles, David Geffen School of Medicine, Los Angeles, California 90095-7073.
[Ti] Título:Increased Hormone-Negative Endocrine Cells in the Pancreas in Type 1 Diabetes.
[So] Source:J Clin Endocrinol Metab;101(9):3487-96, 2016 Sep.
[Is] ISSN:1945-7197
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:CONTEXT AND OBJECTIVE: Type 1 diabetes (T1D) is characterized by a ß-cell deficit due to autoimmune inflammatory-mediated ß-cell destruction. It has been proposed the deficit in ß-cell mass in T1D may be in part due to ß-cell degranulation to chromogranin-positive, hormone-negative (CPHN) cells. DESIGN, SETTING, AND PARTICIPANTS: We investigated the frequency and distribution of CPHN cells in the pancreas of 15 individuals with T1D, 17 autoantibody-positive nondiabetic individuals, and 17 nondiabetic controls. RESULTS: CPHN cells were present at a low frequency in the pancreas from nondiabetic and autoantibody-positive, brain-dead organ donors but are more frequently found in the pancreas from donors with T1D (islets: 1.11% ± 0.20% vs 0.26% ± 0.06 vs 0.27% ± 0.10% of islet endocrine cells, T1D vs autoantibody positive [AA+] vs nondiabetic [ND]; T1D vs AA+, and ND, P < .001). CPHN cells are most commonly found in the single cells and small clusters of endocrine cells rather than within established islets (clusters: 18.99% ± 2.09% vs 9.67% ± 1.49% vs 7.42% ± 1.26% of clustered endocrine cells, T1D vs AA+ vs ND; T1D vs AA+ and ND, P < .0001), mimicking the distribution present in neonatal pancreas. CONCLUSIONS: From these observations, we conclude that CPHN cells are more frequent in T1D and, as in type 2 diabetes, are distributed in a pattern comparable with the neonatal pancreas, implying a possible attempted regeneration. In contrast to rodents, CPHN cells are insufficient to account for loss of ß-cell mass in T1D.
[Mh] Termos MeSH primário: Diabetes Mellitus Tipo 1/patologia
Células Endócrinas/patologia
Células Secretoras de Insulina/patologia
Pâncreas/patologia
Hormônios Pancreáticos/metabolismo
[Mh] Termos MeSH secundário: Adulto
Autoanticorpos/sangue
Biomarcadores/análise
Estudos de Casos e Controles
Degranulação Celular
Cromograninas/metabolismo
Diabetes Mellitus Tipo 1/complicações
Diabetes Mellitus Tipo 1/imunologia
Diabetes Mellitus Tipo 1/metabolismo
Células Endócrinas/imunologia
Células Endócrinas/metabolismo
Feminino
Seguimentos
Seres Humanos
Células Secretoras de Insulina/imunologia
Células Secretoras de Insulina/metabolismo
Masculino
Pâncreas/imunologia
Pâncreas/metabolismo
Prognóstico
Regeneração
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Autoantibodies); 0 (Biomarkers); 0 (Chromogranins); 0 (Pancreatic Hormones)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170902
[Lr] Data última revisão:
170902
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:160615
[St] Status:MEDLINE
[do] DOI:10.1210/jc.2016-1350


  5 / 1183 MEDLINE  
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[PMID]:27180174
[Au] Autor:Konagaya S; Iwata H
[Ad] Endereço:Institute for Frontier Medical Sciences, Kyoto University, 53 Kawahara-cho, Shogoin, Sakyo-ku, Kyoto 606-8507, Japan.
[Ti] Título:Reproducible preparation of spheroids of pancreatic hormone positive cells from human iPS cells: An in vitro study.
[So] Source:Biochim Biophys Acta;1860(9):2008-16, 2016 09.
[Is] ISSN:0006-3002
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Transplantation of islets of Langerhans is regarded as a promising therapy for type 1 diabetes. A large number of ß-cells are required for the treatment of human type 1 diabetes. Pluripotent stem cells, such as embryonic stem cells and induced pluripotent stem cells, have been considered as new sources for cell replacement therapy. METHODS: Cell aggregates were prepared from human iPS cells using agarose microwell plates and differentiated into pancreatic endocrine cells by changing the culture media with different additives. RESULTS: After 20days of culture, approximately 30% of cells in aggregates were positive for C-peptide. After another 14days in culture, the cells gained an ability to alter C-peptide release in response to changes in the glucose concentration. CONCLUSIONS: Uniform aggregates of human iPSCs were easily prepared on agarose microwell plates and efficiently differentiated into the pancreatic endocrine lineage. Thus, aggregate culture is a suitable method for preparing islet-like aggregates from human iPSCs. GENERAL SIGNIFICANCE: Our results indicate that the microwell plate is suitable for scaling up the preparation of pancreatic endocrine cells from human iPS cells in a robotic system.
[Mh] Termos MeSH primário: Células-Tronco Pluripotentes Induzidas/citologia
Hormônios Pancreáticos/metabolismo
[Mh] Termos MeSH secundário: Peptídeo C/metabolismo
Diferenciação Celular/fisiologia
Linhagem da Célula/fisiologia
Células Cultivadas
Diabetes Mellitus Tipo 1/metabolismo
Células-Tronco Embrionárias/citologia
Células-Tronco Embrionárias/metabolismo
Células Endócrinas/citologia
Células Endócrinas/metabolismo
Glucose
Seres Humanos
Células-Tronco Pluripotentes Induzidas/metabolismo
Insulina/metabolismo
Células Secretoras de Insulina/citologia
Células Secretoras de Insulina/metabolismo
Células-Tronco Pluripotentes/citologia
Células-Tronco Pluripotentes/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (C-Peptide); 0 (Insulin); 0 (Pancreatic Hormones); IY9XDZ35W2 (Glucose)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171026
[Lr] Data última revisão:
171026
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160516
[St] Status:MEDLINE


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[PMID]:27173509
[Au] Autor:Pendharkar SA; Asrani VM; Xiao AY; Yoon HD; Murphy R; Windsor JA; Petrov MS
[Ad] Endereço:Department of Surgery, University of Auckland, Auckland, New Zealand;
[Ti] Título:Relationship between pancreatic hormones and glucose metabolism: A cross-sectional study in patients after acute pancreatitis.
[So] Source:Am J Physiol Gastrointest Liver Physiol;311(1):G50-8, 2016 Jul 01.
[Is] ISSN:1522-1547
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Abnormal glucose metabolism is present in almost 40% of patients after acute pancreatitis, but its pathophysiology has been poorly investigated. Pancreatic hormone derangements have been sparingly studied to date, and their relationship with abnormal glucose metabolism is largely unknown. The aim was to investigate the associations between pancreatic hormones and glucose metabolism after acute pancreatitis, including the effect of potential confounders. This was a cross-sectional study of 83 adult patients after acute pancreatitis. Fasting venous blood was collected from all patients and used for analysis of insulin, glucagon, pancreatic polypeptide, amylin, somatostatin, C-peptide, glucose, and hemoglobin A1c. Statistical analyses were conducted using the modified Poisson regression, multivariable linear regression, and Spearman's correlation. Age, sex, body mass index, recurrence of acute pancreatitis, duration from first attack, severity, and etiology were adjusted for. Increased insulin was significantly associated with abnormal glucose metabolism after acute pancreatitis, in both unadjusted (P = 0.038) and adjusted (P = 0.001) analyses. Patients with abnormal glucose metabolism also had significantly decreased pancreatic polypeptide (P = 0.001) and increased amylin (P = 0.047) in adjusted analyses. Somatostatin, C-peptide, and glucagon were not changed significantly in both unadjusted and adjusted analyses. Increased insulin resistance and reduced insulin clearance may be important components of hyperinsulinemic compensation in patients after acute pancreatitis. Increased amylin and reduced pancreatic polypeptide fasting levels characterize impaired glucose homeostasis. Clinical studies investigating islet-cell hormonal responses to mixed-nutrient meal testing and euglycemic-hyperinsulinemic clamps are now warranted for further insights into the role of pancreatic hormones in glucose metabolism derangements secondary to pancreatic diseases.
[Mh] Termos MeSH primário: Glicemia/metabolismo
Hormônios Pancreáticos/sangue
Pancreatite/sangue
Pancreatite/enzimologia
[Mh] Termos MeSH secundário: Doença Aguda
Adulto
Idoso
Biomarcadores/sangue
Distribuição de Qui-Quadrado
Estudos Transversais
Jejum/sangue
Feminino
Glucagon/sangue
Hemoglobina A Glicada/metabolismo
Seres Humanos
Hiperinsulinismo/sangue
Hiperinsulinismo/etiologia
Insulina/sangue
Resistência à Insulina
Polipeptídeo Amiloide das Ilhotas Pancreáticas/sangue
Modelos Lineares
Masculino
Meia-Idade
Análise Multivariada
Polipeptídeo Pancreático/sangue
Pancreatite/complicações
Pancreatite/diagnóstico
Somatostatina/sangue
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (Blood Glucose); 0 (Glycated Hemoglobin A); 0 (Insulin); 0 (Islet Amyloid Polypeptide); 0 (Pancreatic Hormones); 0 (hemoglobin A1c protein, human); 51110-01-1 (Somatostatin); 59763-91-6 (Pancreatic Polypeptide); 9007-92-5 (Glucagon)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160514
[St] Status:MEDLINE
[do] DOI:10.1152/ajpgi.00074.2016


  7 / 1183 MEDLINE  
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[PMID]:27162024
[Au] Autor:Yadav R; Kakkar A; Sharma A; Malik PS; Sharma MC
[Ad] Endereço:a Departments of Pathology and Medical Oncology , All India Institute of Medical Sciences , New Delhi , India.
[Ti] Título:Study of clinicopathological features, hormone immunoexpression, and loss of ATRX and DAXX expression in pancreatic neuroendocrine tumors.
[So] Source:Scand J Gastroenterol;51(8):994-9, 2016 Aug.
[Is] ISSN:1502-7708
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:OBJECTIVES: Neuroendocrine tumors of the pancreas (PanNETs) are rare neoplasms, and not much is known about their pathogenesis. We aimed to evaluate ATRX/DAXX immunoexpression in PanNETs a cohort of well-characterized PanNETs. METHODS: PanNETs diagnosed over a 10-year period were retrieved and clinicopathogical features reviewed. Immuohistochemistry for pancreatic hormones, and for ATRX and DAXX was performed. RESULTS: Sixty-eight PanNETs were included (30 males and 38 females) with median age of 39 years. Histologically, there were 37 Grade 1 (54.4%), 27 Grade 2 (39.7%), and 4 Grade 3 (5.9%) cases. On immunostaining for hormones, insulin expression was most frequent (22 cases; 38.6%), followed by gastrin (7 cases; 12.3%); 25 cases (43.9%) were negative for all hormones. Loss of ATRX/DAXX immunoexpression was noted in 18 cases (39.1%), and was significantly more frequent in tumors larger than 5 cm. Lymphovascular invasion, infiltrative borders, and infiltration of adjacent organs were also more frequent in tumors with loss of ATRX/DAXX immunoreactivity. A little over half the tumors with ATRX/DAXX loss showed negative immunostaining for all hormones (55.6%). CONCLUSION: Loss of ATRX/DAXX expression is frequent in PanNETs, indicating a role in their pathogenesis. As ATRX/DAXX loss is more frequent in larger tumors, and in those with lymphovascular invasion, adjacent organ infiltration and infiltrative borders, this suggests that loss of ATRX/DAXX expression is a late event in pathogenesis and is associated with an aggressive phenotype. Immunohistochemical detection of ATRX/DAXX loss is a simple method for ATRX/DAXX evaluation and can easily be incorporated into routine pathological evaluation of PanNETs.
[Mh] Termos MeSH primário: Proteínas Adaptadoras de Transdução de Sinal/análise
DNA Helicases/análise
Tumores Neuroendócrinos/patologia
Proteínas Nucleares/análise
Neoplasias Pancreáticas/patologia
[Mh] Termos MeSH secundário: Proteínas Adaptadoras de Transdução de Sinal/imunologia
Adulto
DNA Helicases/imunologia
Feminino
Gastrinas/análise
Seres Humanos
Imuno-Histoquímica
Insulina/análise
Masculino
Tumores Neuroendócrinos/metabolismo
Proteínas Nucleares/imunologia
Hormônios Pancreáticos
Neoplasias Pancreáticas/metabolismo
Proteína Nuclear Ligada ao X
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Adaptor Proteins, Signal Transducing); 0 (DAXX protein, human); 0 (Gastrins); 0 (Insulin); 0 (Nuclear Proteins); 0 (Pancreatic Hormones); EC 3.6.4.- (DNA Helicases); EC 3.6.4.12 (ATRX protein, human); EC 3.6.4.12 (X-linked Nuclear Protein)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160511
[St] Status:MEDLINE
[do] DOI:10.3109/00365521.2016.1170195


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[PMID]:27016982
[Ti] Título:Discussion.
[So] Source:J Am Coll Surg;222(4):542-4, 2016 Apr.
[Is] ISSN:1879-1190
[Cp] País de publicação:United States
[La] Idioma:eng
[Mh] Termos MeSH primário: Cromogranina A/metabolismo
Neoplasias Duodenais/metabolismo
Neoplasias Duodenais/mortalidade
Tumores Neuroendócrinos/metabolismo
Tumores Neuroendócrinos/mortalidade
Hormônios Pancreáticos/metabolismo
[Mh] Termos MeSH secundário: Feminino
Seres Humanos
Masculino
[Pt] Tipo de publicação:COMMENT; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Chromogranin A); 0 (Pancreatic Hormones)
[Em] Mês de entrada:1608
[Cu] Atualização por classe:160328
[Lr] Data última revisão:
160328
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:160328
[St] Status:MEDLINE


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[PMID]:27007848
[Au] Autor:Stanley SA; Kelly L; Latcha KN; Schmidt SF; Yu X; Nectow AR; Sauer J; Dyke JP; Dordick JS; Friedman JM
[Ad] Endereço:Laboratory of Molecular Genetics, Rockefeller University, New York, New York 10065, USA.
[Ti] Título:Bidirectional electromagnetic control of the hypothalamus regulates feeding and metabolism.
[So] Source:Nature;531(7596):647-50, 2016 Mar 31.
[Is] ISSN:1476-4687
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Targeted, temporally regulated neural modulation is invaluable in determining the physiological roles of specific neural populations or circuits. Here we describe a system for non-invasive, temporal activation or inhibition of neuronal activity in vivo and its use to study central nervous system control of glucose homeostasis and feeding in mice. We are able to induce neuronal activation remotely using radio waves or magnetic fields via Cre-dependent expression of a GFP-tagged ferritin fusion protein tethered to the cation-conducting transient receptor potential vanilloid 1 (TRPV1) by a camelid anti-GFP antibody (anti-GFP-TRPV1). Neuronal inhibition via the same stimuli is achieved by mutating the TRPV1 pore, rendering the channel chloride-permeable. These constructs were targeted to glucose-sensing neurons in the ventromedial hypothalamus in glucokinase-Cre mice, which express Cre in glucose-sensing neurons. Acute activation of glucose-sensing neurons in this region increases plasma glucose and glucagon, lowers insulin levels and stimulates feeding, while inhibition reduces blood glucose, raises insulin levels and suppresses feeding. These results suggest that pancreatic hormones function as an effector mechanism of central nervous system circuits controlling blood glucose and behaviour. The method we employ obviates the need for permanent implants and could potentially be applied to study other neural processes or used to regulate other, even dispersed, cell types.
[Mh] Termos MeSH primário: Glicemia/metabolismo
Ingestão de Alimentos/fisiologia
Campos Magnéticos
Neurônios/fisiologia
Ondas de Rádio
Núcleo Hipotalâmico Ventromedial/citologia
Núcleo Hipotalâmico Ventromedial/fisiologia
[Mh] Termos MeSH secundário: Animais
Ferritinas/genética
Ferritinas/metabolismo
Glucagon/sangue
Glucoquinase/metabolismo
Homeostase
Hipoglicemia/metabolismo
Insulina/sangue
Integrases/metabolismo
Camundongos
Inibição Neural
Hormônios Pancreáticos/metabolismo
Proteínas Recombinantes de Fusão/genética
Proteínas Recombinantes de Fusão/metabolismo
Canais de Cátion TRPV/genética
Canais de Cátion TRPV/metabolismo
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Blood Glucose); 0 (Insulin); 0 (Pancreatic Hormones); 0 (Recombinant Fusion Proteins); 0 (TRPV Cation Channels); 0 (TRPV1 receptor); 9007-73-2 (Ferritins); 9007-92-5 (Glucagon); EC 2.7.1.2 (Glucokinase); EC 2.7.7.- (Cre recombinase); EC 2.7.7.- (Integrases)
[Em] Mês de entrada:1604
[Cu] Atualização por classe:171124
[Lr] Data última revisão:
171124
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160324
[St] Status:MEDLINE
[do] DOI:10.1038/nature17183


  10 / 1183 MEDLINE  
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[PMID]:26827125
[Au] Autor:Woltering EA; Beyer DT; Thiagarajan R; Ramirez RA; Wang YZ; Ricks MJ; Boudreaux JP
[Ad] Endereço:Department of Surgery, Louisiana State University Health Sciences Center, New Orleans, LA; Neuroendocrine Tumor Program, Ochsner Medical Center, Kenner, LA. Electronic address: ewolte@lsuhsc.edu.
[Ti] Título:Elevated Plasma Pancreastatin, but Not Chromogranin A, Predicts Survival in Neuroendocrine Tumors of the Duodenum.
[So] Source:J Am Coll Surg;222(4):534-42, 2016 Apr.
[Is] ISSN:1879-1190
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Neuroendocrine tumors (NETs) of the duodenum are rare, heterogeneous, and often indolent neoplasms. We hypothesized that elevated pancreastatin levels are an indicator of a poor prognosis in well-differentiated duodenal NETs. STUDY DESIGN: Data from patients diagnosed with a primary duodenal NET were analyzed. Patients that underwent esophogogastroduodenoscopy, endoscopic ultrasound, or exploratory surgery to localize their neoplasm and whose tumors were confirmed histologically were included. RESULTS: Eighty-four patients were diagnosed with duodenal NETs from January 1991 to January 2014. Seventy-five percent and 21% of patients had their tumor localized by esophogogastroduodenoscopy and endoscopic ultrasound, respectively. The remaining 4% were localized during exploratory surgery. The 5-year Kaplan-Meier survival rate for the entire cohort (N = 84) was 80%. Survival sorted by normal vs abnormal pancreastatin level was statistically significant (p < 0.0001). Five-year survival rates were 94% and 37% for normal and abnormal pancreastatin, respectively. In contrast, survival sorted by normal vs abnormal plasma chromogranin A level was not statistically significant (p = 0.24). CONCLUSIONS: Patients with primary duodenal NETs have high 5-year survival rates. Serial monitoring of plasma pancreastatin levels can identify patients who have a poor prognosis.
[Mh] Termos MeSH primário: Cromogranina A/metabolismo
Neoplasias Duodenais/metabolismo
Neoplasias Duodenais/mortalidade
Tumores Neuroendócrinos/metabolismo
Tumores Neuroendócrinos/mortalidade
Hormônios Pancreáticos/metabolismo
[Mh] Termos MeSH secundário: Idoso
Neoplasias Duodenais/cirurgia
Feminino
Seres Humanos
Estimativa de Kaplan-Meier
Masculino
Meia-Idade
Tumores Neuroendócrinos/cirurgia
Valor Preditivo dos Testes
Prognóstico
Estudos Retrospectivos
Taxa de Sobrevida
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CHGA protein, human); 0 (Chromogranin A); 0 (Pancreatic Hormones); 106477-83-2 (pancreastatin)
[Em] Mês de entrada:1608
[Cu] Atualização por classe:160328
[Lr] Data última revisão:
160328
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:160201
[St] Status:MEDLINE



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