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[PMID]:28867213
[Au] Autor:Song Y; Yang L
[Ad] Endereço:Medical College, Hangzhou Normal University, No.16 Xueling Road, Xiasha Higher Education Park, Hangzhou 310036, Zhejiang, PR China. Electronic address: sygp_0@163.com.
[Ti] Título:Transgenerational pancreatic impairment with Igf2/H19 epigenetic alteration induced by p,p'-DDE exposure in early life.
[So] Source:Toxicol Lett;280:222-231, 2017 Oct 05.
[Is] ISSN:1879-3169
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:The hypothesis of fetal origins indicates that exposures in early development could induce epigenetic modifications in the male germ-line, affecting the susceptibility of adult-onset disease for generations. p,p'-DDE, the primary metabolite of persistent organochlorine pesticide DDT, is highly correlated with impaired glucose tolerance (IGT) and a strong contributing factor to type 2 diabetes. In our previous study, ancestral p,p'-DDE exposure could induce transgenerational impaired male fertility with sperm Igf2 hypomethylation. It is still unknown whether this germline epigenetic defect would affect the somatic tissue endocrine pancreas. Gestating F0 generation females were exposed to p,p'-DDE from gestation day 8 to 15. The F1 male offspring were mated with female to produce F2 progeny. F3 generation was obtained by intercrossing the control and treated male and female of F2 generation and divided as C♂-C♀, DDE♂-DDE♀, DDE♂-C♀ and C♂-DDE♀. Results indicated that F1 offspring in p,p'-DDE group exhibited impaired glucose tolerance (IGT), abnormal insulin secretion, ß-cell dysfunction and altered Igf2 and H19 expression induced by Igf2/H19 hypomethylation, which could be transferred to the F3 offspring through the male germ line. IGT and abnormal insulin secretion were more obvious in males than those in females. Ancestral p,p'-DDE exposure could induce transgenerational pancreatic impairment with Igf2/H19 epigenetic defect.
[Mh] Termos MeSH primário: Epigênese Genética
Etil-Éteres/toxicidade
Fator de Crescimento Insulin-Like II/metabolismo
Células Secretoras de Insulina/metabolismo
RNA Longo não Codificante/metabolismo
[Mh] Termos MeSH secundário: Animais
Diabetes Mellitus
Exposição Ambiental
Feminino
Regulação da Expressão Gênica/efeitos dos fármacos
Teste de Tolerância a Glucose
Fator de Crescimento Insulin-Like II/genética
Masculino
Pancrelipase/genética
Pancrelipase/metabolismo
RNA Longo não Codificante/genética
RNA Mensageiro/genética
RNA Mensageiro/metabolismo
Ratos
Ratos Sprague-Dawley
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Ethyl Ethers); 0 (H19 long non-coding RNA); 0 (RNA, Long Noncoding); 0 (RNA, Messenger); 0 (insulin-like growth factor II, rat); 0JJZ8LER32 (bis(2-chloro-1-methylethyl) ether); 53608-75-6 (Pancrelipase); 67763-97-7 (Insulin-Like Growth Factor II)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171017
[Lr] Data última revisão:
171017
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170905
[St] Status:MEDLINE


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[PMID]:28301545
[Au] Autor:Needell JC; Dinarello CA; Ir D; Robertson CE; Ryan SM; Kroehl ME; Frank DN; Zipris D
[Ad] Endereço:Barbara Davis Center for Childhood Diabetes, University of Colorado Denver, Aurora, Colorado, United States of America.
[Ti] Título:Implication of the intestinal microbiome as a potential surrogate marker of immune responsiveness to experimental therapies in autoimmune diabetes.
[So] Source:PLoS One;12(3):e0173968, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Type 1 diabetes (T1D) is an autoimmune proinflammatory disease with no effective intervention. A major obstacle in developing new immunotherapies for T1D is the lack of means for monitoring immune responsiveness to experimental therapies. The LEW1.WR1 rat develops autoimmunity following infection with the parvovirus Kilham rat virus (KRV) via mechanisms linked with activation of proinflammatory pathways and alterations in the gut bacterial composition. We used this animal to test the hypothesis that intervention with agents that block innate immunity and diabetes is associated with a shift in the gut microbiota. We observed that infection with KRV results in the induction of proinflammatory gene activation in both the spleen and pancreatic lymph nodes. Furthermore, administering animals the histone deacetylase inhibitor ITF-2357 and IL-1 receptor antagonist (Anakinra) induced differential STAT-1 and the p40 unit of IL-12/IL-23 gene expression. Sequencing of bacterial 16S rRNA genes demonstrated that both ITF-2357 and Anakinra alter microbial diversity. ITF-2357 and Anakinra modulated the abundance of 23 and 8 bacterial taxa in KRV-infected animals, respectively, of which 5 overlapped between the two agents. Lastly, principal component analysis implied that ITF-2357 and Anakinra induce distinct gut microbiomes compared with those from untreated animals or rats provided KRV only. Together, the data suggest that ITF-2357 and Anakinra differentially influence the innate immune system and the intestinal microbiota and highlight the potential use of the gut microbiome as a surrogate means of assessing anti-inflammatory immune effects in type 1 diabetes.
[Mh] Termos MeSH primário: Biomarcadores/metabolismo
Diabetes Mellitus Tipo 1/terapia
Intestinos/microbiologia
Microbiota
[Mh] Termos MeSH secundário: Animais
Biodiversidade
Diabetes Mellitus Tipo 1/imunologia
Diabetes Mellitus Tipo 1/microbiologia
Fezes/microbiologia
Sequenciamento de Nucleotídeos em Larga Escala
Ácidos Hidroxâmicos/farmacologia
Imunidade Inata
Proteína Antagonista do Receptor de Interleucina 1/farmacologia
Linfonodos/efeitos dos fármacos
Linfonodos/imunologia
Microbiota/efeitos dos fármacos
Pancrelipase/efeitos dos fármacos
Pancrelipase/imunologia
Parvovirus/patogenicidade
Análise de Componente Principal
RNA Ribossômico 16S/genética
Ratos
Ratos Endogâmicos Lew
Baço/efeitos dos fármacos
Baço/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (Hydroxamic Acids); 0 (Interleukin 1 Receptor Antagonist Protein); 0 (RNA, Ribosomal, 16S); 53608-75-6 (Pancrelipase); Z02132R2QQ (givinostat hydrochloride)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170907
[Lr] Data última revisão:
170907
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170317
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0173968


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[PMID]:27802195
[Au] Autor:Yang Z; Li D; Liu Z; Miao X; Yang L; Zou Q; Yuan Y
[Ad] Endereço:Research Laboratory of Hepatobiliary Diseases, Second Xiangya Hospital, Central South University, Changsha, Hunan, China.
[Ti] Título:BIRC7 and KLF4 expression in benign and malignant lesions of pancreas and their clinicopathological significance.
[So] Source:Cancer Biomark;17(4):437-444, 2016.
[Is] ISSN:1875-8592
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:This study investigated the KLF4 and BIRC7 protein expression in malignant and benign pancreatic tissues by immunohistochemical staining and the clinical and pathological significance of KLF4 and BIRC7 expression in PDAC. KLF4 expression was significantly lower, whereas BIRC7 expression was significantly higher in PDAC than that in peritumoral tissue, benign pancreatic lesions, and normal pancreatic tissue (P < 0.01). The percentage of positive BIRC7 and negative KLF4 expression was significantly lower in PDAC patients with well differentiated tumors, maximum tumor size < 3 cm, no lymph node metastasis, no invasion to the surrounding tissues and organs, and TNM stage I/II stage disease than in patients with poorly differentiated tumor, maximum tumor size > 5 cm, lymph node metastasis, invasion to surrounding tissues and organs, and TNM stage III/IV disease (P < 0.05 or P < 0.01). Kaplan-Meier survival analysis showed that the differentiation, maximum tumor size, TNM stage, lymph node metastasis, invasion, negative KLF4 expression, and positive BIRC7 expression were significantly associated with the short survival of patients with PDAC (P < 0.05 or P < 0.01). Cox multivariate analysis revealed that positive BIRC7 expression and negative KLF4 expression were independent poor prognosis factors in PDAC patients. In conclusions, positive BIRC7 expression and negative KLF4 expression are associated with the progression of PDAC and poor prognosis in patients with PDAC.
[Mh] Termos MeSH primário: Proteínas Adaptadoras de Transdução de Sinal/biossíntese
Carcinoma Ductal Pancreático/metabolismo
Proteínas Inibidoras de Apoptose/biossíntese
Fatores de Transcrição Kruppel-Like/biossíntese
Proteínas de Neoplasias/biossíntese
Neoplasias Pancreáticas/metabolismo
[Mh] Termos MeSH secundário: Proteínas Adaptadoras de Transdução de Sinal/genética
Biomarcadores Tumorais/biossíntese
Biomarcadores Tumorais/genética
Carcinoma Ductal Pancreático/genética
Carcinoma Ductal Pancreático/patologia
Progressão da Doença
Regulação para Baixo
Feminino
Seres Humanos
Imuno-Histoquímica
Proteínas Inibidoras de Apoptose/genética
Fatores de Transcrição Kruppel-Like/genética
Masculino
Meia-Idade
Proteínas de Neoplasias/genética
Neoplasias Pancreáticas/genética
Neoplasias Pancreáticas/patologia
Pancreatite Crônica/genética
Pancreatite Crônica/metabolismo
Pancreatite Crônica/patologia
Pancrelipase/metabolismo
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Adaptor Proteins, Signal Transducing); 0 (BIRC7 protein, human); 0 (Biomarkers, Tumor); 0 (GKLF protein); 0 (Inhibitor of Apoptosis Proteins); 0 (Kruppel-Like Transcription Factors); 0 (Neoplasm Proteins); 53608-75-6 (Pancrelipase)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:170309
[Lr] Data última revisão:
170309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161102
[St] Status:MEDLINE
[do] DOI:10.3233/CBM-160660


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[PMID]:27618657
[Au] Autor:Woo SM; Joo J; Kim SY; Park SJ; Han SS; Kim TH; Koh YH; Chung SH; Kim YH; Moon H; Hong EK; Lee WJ
[Ad] Endereço:Center for Liver Cancer, National Cancer Center, Republic of Korea. Electronic address: wsm@ncc.re.kr.
[Ti] Título:Efficacy of pancreatic exocrine replacement therapy for patients with unresectable pancreatic cancer in a randomized trial.
[So] Source:Pancreatology;16(6):1099-1105, 2016 Nov - Dec.
[Is] ISSN:1424-3911
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Weight loss in pancreatic cancer is associated with maldigestion due to pancreatic duct obstruction. Pancreatic exocrine replacement therapy (PERT) may significantly improve fat and protein absorption. OBJECTIVES: This prospective, double-blind, randomized, placebo-controlled phase II trial assessed whether PERT could reduce or prevent weight loss in patients with unresectable pancreatic cancer. METHODS: Sixty seven patients with unresectable pancreatic cancer were randomized to receive enteric coated PERT, consisting of 6-9 capsules of pancreatin (457.7 mg/capsule), or placebo. Patients took two capsules each three times daily during main meals and one capsule each up to three times daily when having between-meal snacks. The primary endpoint was the percentage change in body weight at eight weeks. RESULTS: The mean percentage change in body weight (1.49% [1.12 kg] vs. 2.99% [1.63 kg], P = 0.381) and the mean percent change in Patient-Generated Subjective Global Assessment (PG-SGA) score (8.85% vs. 15.69%, p = 0.18) did not differ significantly between the PERT and placebo groups. There was no improvement in quality of life and overall survival did not differ significantly between the PERT and placebo groups (5.84 months vs 8.13 months, p = 0.744). CONCLUSIONS: PERT did not reduce weight loss in patients with unresectable pancreatic cancer. Larger randomized trials are needed to identify those patients who may benefit from PERT. TRIAL REGISTRATION: ClinicalTrials.gov Number NCT01587534.
[Mh] Termos MeSH primário: Terapia de Reposição Hormonal/métodos
Pâncreas Exócrino
Neoplasias Pancreáticas/terapia
Pancreatina/uso terapêutico
Pancrelipase/uso terapêutico
[Mh] Termos MeSH secundário: Adulto
Idoso
Peso Corporal/efeitos dos fármacos
Método Duplo-Cego
Feminino
Seres Humanos
Masculino
Meia-Idade
Pancreatina/administração & dosagem
Pancrelipase/administração & dosagem
Estudos Prospectivos
Qualidade de Vida
Análise de Sobrevida
Resultado do Tratamento
Perda de Peso
[Pt] Tipo de publicação:CLINICAL TRIAL, PHASE II; JOURNAL ARTICLE; RANDOMIZED CONTROLLED TRIAL
[Nm] Nome de substância:
53608-75-6 (Pancrelipase); 8049-47-6 (Pancreatin)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170404
[Lr] Data última revisão:
170404
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160913
[Cl] Clinical Trial:ClinicalTrial
[St] Status:MEDLINE


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[PMID]:27560634
[Au] Autor:Baldane S; Ipekci SH; Kebapcilar L
[Ti] Título:Pancrelipase treatment in a patient with the history of Roux-en-Y gastric bypass operation that developed resistant hypocalcemia secondary to total thyroidectomy.
[So] Source:Endocr Regul;50(1):27-31, 2016 Jan.
[Is] ISSN:1210-0668
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: Roux-en-Y gastric bypass (RYGB) is an independent risk factor for moderate hypocalcaemia and may lead to the development of resistant hypocalcaemia following thyroid surgery. Subject and Results. A 35-year old female patient was referred to our hospital by her family physician for treatment of resistant hypocalcaemia. The patient underwent RYGB three years ago and a total thyroidectomy for a benign thyroid nodule one year ago. Calcitriol, calcium carbonate, magnesium oxide, and ergocalciferol therapeutic dosages were incremented. Despite dosage increments, the desired calcium levels were not achieved. In the sixth month after admission to our hospital, pancrelipase was added to patient's treatment scheme. On the following visit, a good calcium increase had been achieved. CONCLUSION: This report presents a case history of RYGB and resistant hypocalcaemia, which developed after thyroid surgery and positively responded to pancrelipase treatment.
[Mh] Termos MeSH primário: Derivação Gástrica/efeitos adversos
Hipocalcemia/tratamento farmacológico
Pancrelipase/uso terapêutico
Tireoidectomia/efeitos adversos
[Mh] Termos MeSH secundário: Adulto
Cálcio na Dieta/metabolismo
Feminino
Seres Humanos
Hipocalcemia/etiologia
Absorção Intestinal
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Calcium, Dietary); 53608-75-6 (Pancrelipase)
[Em] Mês de entrada:1612
[Cu] Atualização por classe:161230
[Lr] Data última revisão:
161230
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160826
[St] Status:MEDLINE


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[PMID]:27522847
[Au] Autor:Felicilda-Reynaldo RF; Kenneally M
[Ti] Título:Digestive Enzyme Replacement Therapy: Pancreatic Enzymes and Lactase.
[So] Source:Medsurg Nurs;25(3):182-5, 2016 May-Jun.
[Is] ISSN:1092-0811
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Maldigestion occurs when digestive enzymes are lacking to help break complex food components into absorbable nutrients within the gastrointestinal tract. Education is needed to help patients manage the intricacies of digestive enzyme replacement therapies and ensure their effectiveness in reducing symptoms of maldigestion.
[Mh] Termos MeSH primário: Terapia de Reposição de Enzimas
Insuficiência Pancreática Exócrina/tratamento farmacológico
Fármacos Gastrointestinais/uso terapêutico
Lactase/uso terapêutico
Intolerância à Lactose/tratamento farmacológico
Pancrelipase/uso terapêutico
[Mh] Termos MeSH secundário: Fármacos Gastrointestinais/farmacologia
Seres Humanos
Lactase/farmacologia
Pancrelipase/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Gastrointestinal Agents); 53608-75-6 (Pancrelipase); EC 3.2.1.108 (Lactase)
[Em] Mês de entrada:1701
[Cu] Atualização por classe:170113
[Lr] Data última revisão:
170113
[Sb] Subgrupo de revista:N
[Da] Data de entrada para processamento:160816
[St] Status:MEDLINE


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[PMID]:27518039
[Au] Autor:Brock A; Aldag I; Edskes S; Hartmann M; Herzog T; Uhl W; Schnekenburger J
[Ad] Endereço:aBiomedical Technology Center of the Medical Faculty, University of Muenster bCilian AG, Muenster cDepartment of Surgery, St Josef-Hospital Bochum, Ruhr-University Bochum, Bochum, Germany.
[Ti] Título:Novel ciliate lipases for enzyme replacement during exocrine pancreatic insufficiency.
[So] Source:Eur J Gastroenterol Hepatol;28(11):1305-12, 2016 Nov.
[Is] ISSN:1473-5687
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:AIM AND OBJECTIVES: Exocrine pancreatic insufficiency caused by inflammation or pancreatic tumors results in nutrient malfunction by a lack of digestive enzymes and neutralization compounds. Despite satisfactory clinical results with current enzyme therapies, a normalization of fat absorption in patients is rare. An individualized therapy is required that includes high dosage of enzymatic units, usage of enteric coating, and addition of gastric proton pump inhibitors. The key goal to improve this therapy is to identify digestive enzymes with high activity and stability in the gastrointestinal tract. METHODS: We cloned and analyzed three novel ciliate lipases derived from Tetrahymena thermophila. Using highly precise pH-STAT-titration and colorimetric methods, we determined stability and lipolytic activity under physiological conditions in comparison with commercially available porcine and fungal digestive enzyme preparations. We measured from pH 2.0 to 9.0, with different bile salts concentrations, and substrates such as olive oil and fat derived from pig diet. RESULTS: Ciliate lipases CL-120, CL-130, and CL-230 showed activities up to 220-fold higher than Creon, pancreatin standard, and rizolipase Nortase within a pH range from pH 2.0 to 9.0. They are highly active in the presence of bile salts and complex pig diet substrate, and more stable after incubation in human gastric juice compared with porcine pancreatic lipase and rizolipase. CONCLUSIONS: The newly cloned and characterized lipases fulfilled all requirements for high activity under physiological conditions. These novel enzymes are therefore promising candidates for an improved enzyme replacement therapy for exocrine pancreatic insufficiency.
[Mh] Termos MeSH primário: Terapia de Reposição de Enzimas/métodos
Insuficiência Pancreática Exócrina/tratamento farmacológico
Lipase/química
[Mh] Termos MeSH secundário: Amilases/química
Ração Animal
Animais
Ácidos e Sais Biliares
Clonagem Molecular/métodos
Colorimetria/métodos
Combinação de Medicamentos
Endopeptidases/química
Fermentação
Suco Gástrico/enzimologia
Seres Humanos
Concentração de Íons de Hidrogênio
Lipase/genética
Lipólise
Pancrelipase/química
Sus scrofa
Tetrahymena thermophila/enzimologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Bile Acids and Salts); 0 (Drug Combinations); 53608-75-6 (Pancrelipase); 84932-46-7 (nortase); EC 3.1.1.3 (Lipase); EC 3.2.1.- (Amylases); EC 3.4.- (Endopeptidases)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170817
[Lr] Data última revisão:
170817
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160813
[St] Status:MEDLINE
[do] DOI:10.1097/MEG.0000000000000720


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[PMID]:27460666
[Au] Autor:Gurgul-Convey E; Mehmeti I; Plötz T; Jörns A; Lenzen S
[Ad] Endereço:Institute of Clinical Biochemistry, Hannover Medical School, Carl-Neuberg-Str. 1, 30625, Hannover, Germany.
[Ti] Título:Sensitivity profile of the human EndoC-ßH1 beta cell line to proinflammatory cytokines.
[So] Source:Diabetologia;59(10):2125-33, 2016 Oct.
[Is] ISSN:1432-0428
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:AIMS/HYPOTHESIS: The aim of this study was to perform a detailed analysis of cytokine toxicity in the new human EndoC-ßH1 beta cell line. METHODS: The expression profile of the antioxidative enzymes in the new human EndoC-ßH1 beta cells was characterised and compared with that of primary beta cells in the human pancreas. The effects of proinflammatory cytokines on reactive oxygen species formation, insulin secretory responsiveness and apoptosis of EndoC-ßH1 beta cells were determined. RESULTS: EndoC-ßH1 beta cells were sensitive to the toxic action of proinflammatory cytokines. Glucose-dependent stimulation of insulin secretion and an increase in the ATP/ADP ratio was abolished by proinflammatory cytokines without induction of IL-1ß expression. Cytokine-mediated caspase-3 activation was accompanied by reactive oxygen species formation and developed more slowly than in rodent beta cells. Cytokines transiently increased the expression of unfolded protein response genes, without inducing endoplasmic reticulum stress-marker genes. Cytokine-mediated NFκB activation was too weak to induce inducible nitric oxide synthase expression. The resultant lack of nitric oxide generation in EndoC-ßH1 cells, in contrast to rodent beta cells, makes these cells dependent on exogenously generated nitric oxide, which is released from infiltrating immune cells in human type 1 diabetes, for full expression of proinflammatory cytokine toxicity. CONCLUSIONS/INTERPRETATION: EndoC-ßH1 beta cells are characterised by an imbalance between H2O2-generating and -inactivating enzymes, and react to cytokine exposure in a similar manner to primary human beta cells. They are a suitable beta cell surrogate for cytokine-toxicity studies.
[Mh] Termos MeSH primário: Citocinas/farmacologia
Células Secretoras de Insulina/efeitos dos fármacos
Células Secretoras de Insulina/metabolismo
[Mh] Termos MeSH secundário: Western Blotting
Caspase 3/metabolismo
Linhagem Celular
Citometria de Fluxo
Imunofluorescência
Glucose/metabolismo
Seres Humanos
Peróxido de Hidrogênio/metabolismo
Insulina/metabolismo
Estresse Oxidativo/efeitos dos fármacos
Pancrelipase/metabolismo
Espécies Reativas de Oxigênio
Reação em Cadeia da Polimerase Via Transcriptase Reversa
Transdução de Sinais/efeitos dos fármacos
Superóxido Dismutase-1/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cytokines); 0 (Insulin); 0 (Reactive Oxygen Species); 53608-75-6 (Pancrelipase); BBX060AN9V (Hydrogen Peroxide); EC 1.15.1.1 (Superoxide Dismutase-1); EC 3.4.22.- (Caspase 3); IY9XDZ35W2 (Glucose)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170828
[Lr] Data última revisão:
170828
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160728
[St] Status:MEDLINE
[do] DOI:10.1007/s00125-016-4060-y


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[PMID]:26970531
[Au] Autor:Fabroni S; Ballistreri G; Amenta M; Romeo FV; Rapisarda P
[Ad] Endereço:Consiglio per la Ricerca in Agricoltura e l'Analisi dell'Economia Agraria (CREA), Centro di Ricerca per l'Agrumicoltura e le Colture Mediterranee, Corso Savoia 190, 95024, Acireale, Italy.
[Ti] Título:Screening of the anthocyanin profile and in vitro pancreatic lipase inhibition by anthocyanin-containing extracts of fruits, vegetables, legumes and cereals.
[So] Source:J Sci Food Agric;96(14):4713-4723, 2016 Nov.
[Is] ISSN:1097-0010
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: The phytotherapic treatment of overweight and/or moderate obesity is growing widely, thus there is a great interest towards the phenolic compounds of fruits and vegetables which may inhibit pancreatic lipase enzyme. In this study, we report the chemical composition and in vitro pancreatic lipase inhibitory activity of 13 freeze-dried anthocyanin-containing extracts of different Mediterranean plants: fruits (blood orange, pomegranate, blackberry, mulberry and sumac), citrus by-products (blood orange peel), citrus vegetative tissues (young lemon shoots); vegetables (red cabbage and violet cauliflower), legume seeds (black bean), cereals (black rice), and cereal processing by-products (black rice hull). Total phenols and anthocyanins were determined. Individual anthocyanins were identified by UHPLC-PDA-ESI/MS . RESULTS: Results revealed a wide variation in the distribution of anthocyanin compounds. Blood orange and pomegranate juice extracts had the highest total anthocyanin content and exhibited the strongest inhibition of pancreatic lipase in vitro. CONCLUSION: Inhibitory activity was positively correlated with anthocyanin content. In appropriate formulations, anthocyanin-containing extracts could find a use as anti-obesity agents. © 2016 Society of Chemical Industry.
[Mh] Termos MeSH primário: Antocianinas/química
Fabaceae/química
Frutas/química
Pancrelipase/antagonistas & inibidores
Extratos Vegetais/farmacologia
Verduras/química
[Mh] Termos MeSH secundário: Antocianinas/genética
Antocianinas/metabolismo
Grãos Comestíveis/química
Extratos Vegetais/química
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anthocyanins); 0 (Plant Extracts); 53608-75-6 (Pancrelipase)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170519
[Lr] Data última revisão:
170519
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160313
[St] Status:MEDLINE
[do] DOI:10.1002/jsfa.7708


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[PMID]:26775768
[Au] Autor:Smith RC; Smith SF; Wilson J; Pearce C; Wray N; Vo R; Chen J; Ooi CY; Oliver M; Katz T; Turner R; Nikfarjam M; Rayner C; Horowitz M; Holtmann G; Talley N; Windsor J; Pirola R; Neale R; Working Party of the Australasian Pancreatic Club
[Ad] Endereço:Department of Surgery, University of Sydney, NSW, Australia; Australasian Pancreatic Club, Australia. Electronic address: Ross.smith@sydney.edu.au.
[Ti] Título:Summary and recommendations from the Australasian guidelines for the management of pancreatic exocrine insufficiency.
[So] Source:Pancreatology;16(2):164-80, 2016 Mar-Apr.
[Is] ISSN:1424-3911
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:AIM: Because of increasing awareness of variations in the use of pancreatic exocrine replacement therapy, the Australasian Pancreatic Club decided it was timely to re-review the literature and create new Australasian guidelines for the management of pancreatic exocrine insufficiency (PEI). METHODS: A working party of expert clinicians was convened and initially determined that by dividing the types of presentation into three categories for the likelihood of PEI (definite, possible and unlikely) they were able to consider the difficulties of diagnosing PEI and relate these to the value of treatment for each diagnostic category. RESULTS AND CONCLUSIONS: Recent studies confirm that patients with chronic pancreatitis receive similar benefit from pancreatic exocrine replacement therapy (PERT) to that established in children with cystic fibrosis. Severe acute pancreatitis is frequently followed by PEI and PERT should be considered for these patients because of their nutritional requirements. Evidence is also becoming stronger for the benefits of PERT in patients with unresectable pancreatic cancer. However there is as yet no clear guide to help identify those patients in the 'unlikely' PEI group who would benefit from PERT. For example, patients with coeliac disease, diabetes mellitus, irritable bowel syndrome and weight loss in the elderly may occasionally be given a trial of PERT, but determining its effectiveness will be difficult. The starting dose of PERT should be from 25,000-40,000 IU lipase taken with food. This may need to be titrated up and there may be a need for proton pump inhibitors in some patients to improve efficacy.
[Mh] Termos MeSH primário: Pancreatopatias/terapia
Guias de Prática Clínica como Assunto
[Mh] Termos MeSH secundário: Australásia
Seres Humanos
Pancrelipase/uso terapêutico
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
53608-75-6 (Pancrelipase)
[Em] Mês de entrada:1612
[Cu] Atualização por classe:161230
[Lr] Data última revisão:
161230
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160119
[St] Status:MEDLINE



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