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  1 / 134409 MEDLINE  
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[PMID]:29353037
[Au] Autor:Lu Z; Liu Y; Shi Y; Shi X; Wang X; Xu C; Zhao H; Dong Q
[Ad] Endereço:Department of Neurology, Yueyang Hospital of Integrated Traditional Chinese and Western Medicine, Shanghai University of Traditional Chinese Medicine, Shanghai 200437, PR China.
[Ti] Título:Curcumin protects cortical neurons against oxygen and glucose deprivation/reoxygenation injury through flotillin-1 and extracellular signal-regulated kinase1/2 pathway.
[So] Source:Biochem Biophys Res Commun;496(2):515-522, 2018 02 05.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:In this study, we provided evidence that curcumin could be a promising therapeutic agent for ischemic stroke by activating neuroprotective signaling pathways. Post oxygen and glucose deprivation/reoxygenation (OGD/R), primary mouse cortical neurons treated with curcumin exhibited a significant decrease in cell death, LDH release and enzyme caspase-3 activity under OGD/R circumstances, which were abolished by flotillin-1 downregulation or extracellular signal-regulated kinase (ERK) inhibitor. Moreover, flotillin-1 knockdown led to suppression of curcumin-mediated ERK phosphorylation under OGD/R condition. Based on these findings, we concluded that curcumin could confer neuroprotection against OGD/R injury through a novel flotillin-1 and ERK1/2 pathway.
[Mh] Termos MeSH primário: Isquemia Encefálica/tratamento farmacológico
Curcumina/farmacologia
Sistema de Sinalização das MAP Quinases/efeitos dos fármacos
Proteínas de Membrana/metabolismo
Neurônios/efeitos dos fármacos
Fármacos Neuroprotetores/farmacologia
[Mh] Termos MeSH secundário: Animais
Isquemia Encefálica/metabolismo
Células Cultivadas
Córtex Cerebelar/citologia
Córtex Cerebelar/efeitos dos fármacos
Feminino
Glucose/metabolismo
Masculino
Camundongos Endogâmicos BALB C
Neurônios/metabolismo
Oxigênio/metabolismo
Traumatismo por Reperfusão/tratamento farmacológico
Traumatismo por Reperfusão/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Membrane Proteins); 0 (Neuroprotective Agents); 0 (flotillins); IT942ZTH98 (Curcumin); IY9XDZ35W2 (Glucose); S88TT14065 (Oxygen)
[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:180122
[St] Status:MEDLINE


  2 / 134409 MEDLINE  
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[PMID]:29351321
[Au] Autor:Khan MA; Arif Z; Khan MA; Moinuddin; Alam K
[Ad] Endereço:Department of Biochemistry, J.N. Medical College, Faculty of Medicine, Aligarh Muslim University, Aligarh, Uttar Pradesh, India.
[Ti] Título:Methylglyoxal produces more changes in biochemical and biophysical properties of human IgG under high glucose compared to normal glucose level.
[So] Source:PLoS One;13(1):e0191014, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Hyperglycaemia triggers increased production of methylglyoxal which can cause gross modification in proteins' structure vis-a-vis function though advanced glycation end products (AGEs). The AGEs may initiate vascular and nonvascular pathologies. In this study, we have examined the biochemical and biophysical changes in human IgG under normal and high glucose after introducing methylglyoxal into the assay mixture. This non-enzymatic reaction mainly engaged lysine residues as indicated by TNBS results. The UV results showed hyperchromicity in modified-IgG samples while fluorescence data supported AGEs formation during the course of reaction. Shift in amide I and amide II band position indicated perturbations in secondary structure. Increase carbonyl content and decrease in sulfhydryl suggests that the modification is accompanied by oxidative stress. All modified-IgG samples showed more thermostability than native IgG; the highest Tm was shown by IgG-high glucose-MGO variant. Results of ANS, Congo red and Thioflavin T dyes clearly suggest increase in hydrophobic patches and aggregation, respectively. SEM and TEM images support aggregates generation in modified-IgG samples.
[Mh] Termos MeSH primário: Glucose/química
Imunoglobulina G/química
Aldeído Pirúvico/farmacologia
[Mh] Termos MeSH secundário: Fenômenos Biofísicos
Seres Humanos
Microscopia Eletrônica de Varredura
Microscopia Eletrônica de Transmissão
Estresse Oxidativo
Desnaturação Proteica
Espectrometria de Fluorescência
Espectrofotometria Ultravioleta
Espectroscopia de Infravermelho com Transformada de Fourier
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Immunoglobulin G); 722KLD7415 (Pyruvaldehyde); IY9XDZ35W2 (Glucose)
[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:180120
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0191014


  3 / 134409 MEDLINE  
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[PMID]:29337061
[Au] Autor:Li Q; Qin Z; Nie F; Bi H; Zhao R; Pan B; Ma J; Xie X
[Ad] Endereço:Department of Plastic and Reconstructive Surgery, Peking University Third Hospital, Beijing, 100191, China.
[Ti] Título:Metabolic reprogramming in keloid fibroblasts: Aerobic glycolysis and a novel therapeutic strategy.
[So] Source:Biochem Biophys Res Commun;496(2):641-647, 2018 02 05.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Keloids, tumor-like fibroproliferative cutaneous lesions, were reported in metabolic disturbance. However, the metabolic character remains unclear. The purpose of this study is to determine if glycolytic reprogramming is important for the pathogenesis of keloids and to assess the inhibition potential of glycolysis in keloid treatment. An intracellular metabolic profile assay was used to compare metabolic phenotypes between normal skin fibroblasts and keloid fibroblasts (NFs and KFs). Our data indicated that KFs underwent reprogramming of their metabolic phonotype from oxidative phosphorylation to aerobic glycolysis (Warburg effect) with augmented glycolysis and glycolytic capacity. Both gene and protein assays showed that the expression of glycolytic enzymes was upregulated in KFs compared to NFs. Our data showed higher glucose influx and lactate production in KFs compared to NFs. Furthermore, the proliferation of KFs was suppressed in a dose-dependent and time-dependent manner after inhibition of glycolysis with 2-deoxy-glucose (2-DG). Taken together, these findings suggested that keloids underwent a reprogrammed metabolic phenotype of aerobic glycolysis. This was essential for keloid hyperplasia, and glycolytic inhibitors might provide a potential treatment for keloids.
[Mh] Termos MeSH primário: Fibroblastos/patologia
Queloide/patologia
[Mh] Termos MeSH secundário: Proliferação Celular/efeitos dos fármacos
Células Cultivadas
Desoxiglucose/farmacologia
Fibroblastos/efeitos dos fármacos
Fibroblastos/metabolismo
Regulação da Expressão Gênica
Glucose/metabolismo
Glicólise/efeitos dos fármacos
Seres Humanos
Queloide/tratamento farmacológico
Queloide/genética
Queloide/metabolismo
Ácido Láctico/metabolismo
Consumo de Oxigênio
Pele/metabolismo
Pele/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
33X04XA5AT (Lactic Acid); 9G2MP84A8W (Deoxyglucose); IY9XDZ35W2 (Glucose)
[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:180117
[St] Status:MEDLINE


  4 / 134409 MEDLINE  
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[PMID]:29324792
[Au] Autor:Cibicek N; Ehrmann J; Proskova J; Vecera R
[Ad] Endereço:Department of Medical Chemistry and Biochemistry, Faculty of Medicine and Dentistry, Palacky University, Olomouc, Czech Republic.
[Ti] Título:Critical evaluation of colon submucosal microdialysis in awake, mobile rats.
[So] Source:PLoS One;13(1):e0191041, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Sensors able to record large bowel physiology and biochemistry in situ in awake rodents are lacking. Microdialysis is a mini-invasive technique that may be utilized to continuously deliver or recover low-molecular substances from various tissues. In this experiment we evaluated the feasibility of in vivo microdialysis to monitor extracellular fluid chemistry in the descending colon submucosa of conscious, freely moving rodents. Following surgical implantation of a microdialysis probe, male Wistar rats were housed in metabolic cages where they were analgized and clinically followed for four days with free access to standard diet and water. To assess local microcirculation and probe function, glucose, lactate, glucose-to-lactate ratio and urea clearance were determined in the dialysates from the three postoperative days with focus on the final 24-h period. In an attempt to mitigate the expected tissue inflammatory response, one group of animals had the catheters perfused with 5-aminosalicylic acid-enriched medium with final concentration 1 µmol/L. For verification of probe position and the assessment of the surrounding foreign body reaction, standard histological and immunohistochemical methods were employed. Microdialysis of rat gut is associated with considerable technical challenges that may lead to the loss of probe function and high drop-out rate. In this setting, limited data did not allow to draw any firm conclusion regarding local anti-inflammatory effectiveness of 5-aminosalicylic acid perfusion. Although intestinal microdialysis may be suitable for larger anesthetized animals, low reproducibility of the presented method compromises its routine experimental use in awake and freely moving small-sized rodents.
[Mh] Termos MeSH primário: Colo/fisiologia
[Mh] Termos MeSH secundário: Animais
Colo/irrigação sanguínea
Glucose/metabolismo
Mucosa Intestinal/fisiologia
Ácido Láctico/metabolismo
Masculino
Microcirculação
Microdiálise
Ratos
Ratos Wistar
Ureia/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
33X04XA5AT (Lactic Acid); 8W8T17847W (Urea); IY9XDZ35W2 (Glucose)
[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:180112
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0191041


  5 / 134409 MEDLINE  
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[PMID]:28463898
[Au] Autor:Gastaldelli A; Gaggini M; DeFronzo R
[Ad] Endereço:aCardiometabolic Risk Laboratory, Institute of Clinical Physiology, National Research Council, Pisa, Italy bUniversity of Texas Health Science Center at San Antonio, TX, USA.
[Ti] Título:Glucose kinetics: an update and novel insights into its regulation by glucagon and GLP-1.
[So] Source:Curr Opin Clin Nutr Metab Care;20(4):300-309, 2017 Jul.
[Is] ISSN:1473-6519
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:PURPOSE OF REVIEW: Glucagon and GLP-1 share the same origin (i.e., proglucagon); primarily GLP-1 is generated from intestinal L-cells and glucagon from pancreatic α-cell, but intestinal glucagon and pancreatic GLP-1 secretion is likely. Glucose kinetics are tightly regulated by pancreatic hormones insulin and glucagon, but other hormones, including glucagon-like peptide-1 (GLP-1), also play an important role. The purpose of this review is to describe the recent findings on the mechanisms by which these two hormones regulate glucose kinetics. RECENT FINDINGS: Recent findings showed new important mechanisms of action of glucagon and GLP-1 in the regulation of glucose metabolism. Knock out of glucagon receptors protects against hyperglycemia without causing hypoglycemia. GLP-1 not only stimulates insulin secretion, but it has also an independent effect on the liver and inhibits glucose production. Moreover, when coinfused with glucagon, GLP-1 limits the hyperglycemic effects. Both hormones have also central effects on gastric emptying (delayed), intestinal motility (reduced), and satiety (increased). SUMMARY: The implications of these findings are very important for the management of type 2 diabetes given that GLP-1 receptor agonist are currently approved for the treatment of hyperglycemia and glucagon receptor antagonists and GLP-1/glucagon dual agonists are under development.
[Mh] Termos MeSH primário: Peptídeo 1 Semelhante ao Glucagon/fisiologia
Glucagon/fisiologia
Glucose/metabolismo
[Mh] Termos MeSH secundário: Animais
Diabetes Mellitus Tipo 2/tratamento farmacológico
Jejum
Esvaziamento Gástrico/fisiologia
Motilidade Gastrointestinal/fisiologia
Glucagon/sangue
Glucagon/farmacologia
Peptídeo 1 Semelhante ao Glucagon/farmacologia
Receptor do Peptídeo Semelhante ao Glucagon 1/agonistas
Receptor do Peptídeo Semelhante ao Glucagon 1/fisiologia
Gluconeogênese/efeitos dos fármacos
Glucose/biossíntese
Homeostase
Seres Humanos
Hiperglicemia/tratamento farmacológico
Cinética
Fígado/efeitos dos fármacos
Fígado/metabolismo
Receptores de Glucagon/antagonistas & inibidores
Receptores de Glucagon/fisiologia
Saciação/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Glucagon-Like Peptide-1 Receptor); 0 (Receptors, Glucagon); 89750-14-1 (Glucagon-Like Peptide 1); 9007-92-5 (Glucagon); IY9XDZ35W2 (Glucose)
[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:170503
[St] Status:MEDLINE
[do] DOI:10.1097/MCO.0000000000000384


  6 / 134409 MEDLINE  
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[PMID]:28946120
[Au] Autor:Zhao F; Jiang G; Wei P; Wang H; Ru S
[Ad] Endereço:Marine Life Science College, Ocean University of China, 5 Yushan Road, Qingdao, 266003 Shandong Province, PR China.
[Ti] Título:Bisphenol S exposure impairs glucose homeostasis in male zebrafish (Danio rerio).
[So] Source:Ecotoxicol Environ Saf;147:794-802, 2018 Jan.
[Is] ISSN:1090-2414
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Bisphenol S (BPS) is a substitute of the plastic additive bisphenol A (BPA). Its concentrations detected in surface waters and urine samples are on the same order of magnitude as BPA. Human exposure to BPA has been implicated in the development of diabetes mellitus; however, whether BPS can disrupt glucose homeostasis and increase blood glucose concentration remains unclear. We extensively investigated the effects of environmentally relevant concentrations of BPS on glucose metabolism in male zebrafish (Danio rerio) and the underlying mechanisms of these effects. Male zebrafish were exposed to 1, 10, or 100µg/L of BPS for 28 d. Fasting blood glucose (FBG) levels, glycogen levels in the liver and muscle, and mRNA levels of key glucose metabolic enzymes and the activities of the encoded proteins in tissues were evaluated to assess the effect of BPS on glucose metabolism. Plasma insulin levels and expression of preproinsulin and glucagon genes in the visceral tissue were also evaluated. Compared with the control group, exposure to 1 and 10µg/L of BPS significantly increased FBG levels but decreased insulin levels. Gluconeogenesis and glycogenolysis in the liver were promoted, and glycogen synthesis in the liver and muscle and glycolysis in the muscle were inhibited. Exposure to 100µg/L of BPS did not significantly alter plasma insulin and blood glucose levels, but nonetheless pronouncedly interfered with gluconeogenesis, glycogenolysis, glycolysis, and glycogen synthesis. Our data indicates that BPS at environmentally relevant concentrations impairs glucose homeostasis of male zebrafish possibly by hampering the physiological effect of insulin; higher BPS doses also pronouncedly interfered with glucose metabolism.
[Mh] Termos MeSH primário: Glucose/metabolismo
Homeostase/efeitos dos fármacos
Fenóis/toxicidade
Sulfonas/toxicidade
Poluentes Químicos da Água/toxicidade
Peixe-Zebra/metabolismo
[Mh] Termos MeSH secundário: Animais
Relação Dose-Resposta a Droga
Glucagon/genética
Glicogênio/biossíntese
Insulina/sangue
Insulina/genética
Fígado/efeitos dos fármacos
Fígado/metabolismo
Masculino
Músculos/efeitos dos fármacos
Músculos/metabolismo
Precursores de Proteínas/sangue
Precursores de Proteínas/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Insulin); 0 (Phenols); 0 (Protein Precursors); 0 (Sulfones); 0 (Water Pollutants, Chemical); 61116-24-3 (preproinsulin); 80-09-1 (bis(4-hydroxyphenyl)sulfone); 9005-79-2 (Glycogen); 9007-92-5 (Glucagon); IY9XDZ35W2 (Glucose)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170926
[St] Status:MEDLINE


  7 / 134409 MEDLINE  
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[PMID]:29416045
[Au] Autor:Basco D; Zhang Q; Salehi A; Tarasov A; Dolci W; Herrera P; Spiliotis I; Berney X; Tarussio D; Rorsman P; Thorens B
[Ad] Endereço:Center for Integrative Genomics, University of Lausanne, 1015, Lausanne, Switzerland.
[Ti] Título:α-cell glucokinase suppresses glucose-regulated glucagon secretion.
[So] Source:Nat Commun;9(1):546, 2018 02 07.
[Is] ISSN:2041-1723
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Glucagon secretion by pancreatic α-cells is triggered by hypoglycemia and suppressed by high glucose levels; impaired suppression of glucagon secretion is a hallmark of both type 1 and type 2 diabetes. Here, we show that α-cell glucokinase (Gck) plays a role in the control of glucagon secretion. Using mice with α-cell-specific inactivation of Gck (αGckKO mice), we find that glucokinase is required for the glucose-dependent increase in intracellular ATP/ADP ratio and the closure of K channels in α-cells and the suppression of glucagon secretion at euglycemic and hyperglycemic levels. αGckKO mice display hyperglucagonemia in the fed state, which is associated with increased hepatic gluconeogenic gene expression and hepatic glucose output capacity. In adult mice, fed hyperglucagonemia is further increased and glucose intolerance develops. Thus, glucokinase governs an α-cell metabolic pathway that suppresses secretion at or above normoglycemic levels; abnormal suppression of glucagon secretion deregulates hepatic glucose metabolism and, over time, induces a pre-diabetic phenotype.
[Mh] Termos MeSH primário: Células Secretoras de Glucagon/metabolismo
Glucagon/secreção
Glucoquinase/genética
Intolerância à Glucose/metabolismo
Glucose/metabolismo
Hipoglicemia/metabolismo
[Mh] Termos MeSH secundário: Difosfato de Adenosina/metabolismo
Trifosfato de Adenosina/metabolismo
Animais
Transporte Biológico
Feminino
Expressão Gênica
Células Secretoras de Glucagon/patologia
Glucoquinase/deficiência
Intolerância à Glucose/genética
Intolerância à Glucose/patologia
Hipoglicemia/genética
Hipoglicemia/patologia
Insulina/metabolismo
Canais KATP/genética
Canais KATP/metabolismo
Fígado/metabolismo
Masculino
Camundongos
Camundongos Knockout
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Insulin); 0 (KATP Channels); 61D2G4IYVH (Adenosine Diphosphate); 8L70Q75FXE (Adenosine Triphosphate); 9007-92-5 (Glucagon); EC 2.7.1.2 (Glucokinase); IY9XDZ35W2 (Glucose)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180307
[Lr] Data última revisão:
180307
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180209
[St] Status:MEDLINE
[do] DOI:10.1038/s41467-018-03034-0


  8 / 134409 MEDLINE  
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[PMID]:28453664
[Au] Autor:Krag TO; Ruiz-Ruiz C; Vissing J
[Ad] Endereço:Copenhagen Neuromuscular Center, Department of Neurology, Rigshospitalet, University of Copenhagen, 2100 Copenhagen, Denmark.
[Ti] Título:Glycogen Synthesis in Glycogenin 1-Deficient Patients: A Role for Glycogenin 2 in Muscle.
[So] Source:J Clin Endocrinol Metab;102(8):2690-2700, 2017 Aug 01.
[Is] ISSN:1945-7197
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Context: Glycogen storage disease (GSD) type XV is a rare disease caused by mutations in the GYG1 gene that codes for the core molecule of muscle glycogen, glycogenin 1. Nonetheless, glycogen is present in muscles of glycogenin 1-deficient patients, suggesting an alternative for glycogen buildup. A likely candidate is glycogenin 2, an isoform expressed in the liver and heart but not in healthy skeletal muscle. Objective: We wanted to investigate the formation of glycogen and changes in glycogen metabolism in patients with GSD type XV. Design, Setting, and Patients: Two patients with mutations in the GYG1 gene were investigated for histopathology, ultrastructure, and expression of proteins involved in glycogen synthesis and metabolism. Results: Apart from occurrence of polyglucosan (PG) bodies in few fibers, glycogen appeared normal in most cells, and the concentration was normal in patients with GSD type XV. We found that glycogenin 1 was absent, but glycogenin 2 was present in the patients, whereas the opposite was the case in healthy controls. Electron microscopy revealed that glycogen was present between and not inside myofibrils in type II fibers, compromising the ultrastructure of these fibers, and only type I fibers contained PG bodies. We also found significant changes to the expression levels of several enzymes directly involved in glycogen and glucose metabolism. Conclusions: To our knowledge, this is the first report demonstrating expression of glycogenin 2 in glycogenin 1-deficient patients, suggesting that glycogenin 2 rescues the formation of glycogen in patients with glycogenin 1 deficiency.
[Mh] Termos MeSH primário: Glucosiltransferases/genética
Glucosiltransferases/metabolismo
Glicogênio/biossíntese
Glicoproteínas/genética
Músculo Esquelético/metabolismo
[Mh] Termos MeSH secundário: Idoso
Metabolismo dos Carboidratos
Estudos de Casos e Controles
Feminino
Glucanos/metabolismo
Glucose/metabolismo
Glicogênio/metabolismo
Glicogênio/ultraestrutura
Doença de Depósito de Glicogênio/genética
Glicoproteínas/metabolismo
Seres Humanos
Microscopia Eletrônica
Meia-Idade
Fibras Musculares de Contração Rápida/ultraestrutura
Músculo Esquelético/patologia
Músculo Esquelético/ultraestrutura
Miofibrilas/ultraestrutura
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Glucans); 0 (Glycoproteins); 0 (glycogenin); 9005-79-2 (Glycogen); 9012-72-0 (polyglucosan); EC 2.4.1.- (Glucosyltransferases); EC 2.4.1.186 (GYG2 protein, human); IY9XDZ35W2 (Glucose)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170429
[St] Status:MEDLINE
[do] DOI:10.1210/jc.2017-00399


  9 / 134409 MEDLINE  
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[PMID]:27775923
[Au] Autor:Ortuño-Lizarán I; Vilariño-Feltrer G; Martínez-Ramos C; Pradas MM; Vallés-Lluch A
[Ad] Endereço:Centre for Biomaterials and Tissue Engineering, Universitat Politècnica de València, Cno. de Vera s/n, E-46022, Valencia, Spain. Networking Research Center on Bioengineering, Biomaterials and Nanomedicine (CIBER-BBN), Spain.
[Ti] Título:Influence of synthesis parameters on hyaluronic acid hydrogels intended as nerve conduits.
[So] Source:Biofabrication;8(4):045011, 2016 10 24.
[Is] ISSN:1758-5090
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Hydrogels have widely been proposed lately as strategies for neural tissue regeneration, but there are still some issues to be solved before their efficient use in tissue engineering of trauma, stroke or the idiopathic degeneration of the nervous system. In a previous work of the authors a novel Schwann-cell structure with the shape of a hollow cylinder was obtained using a three-dimensional conduit based in crosslinked hyaluronic acid as template. This original engineered tissue of tightly joined Schwann cells obtained in a conduit lumen having 400 µm in diameter is a consequence of specific cell-material interactions. In the present work we analyze the influence of the hydrogel concentration and of the drying process on the physicochemical and biological performance of the resulting tubular scaffolds, and prove that the cylinder-like cell sheath obtains also in scaffolds of a larger inner diameter. The diffusion of glucose and of the protein BSA through the scaffolds is studied and characterized, as well as the enzymatic degradation kinetics of the lyophilized conduits. This can be modulated from a couple of weeks to several months by varying the concentration of hyaluronic acid in the starting solution. These findings allow to improve the performance of hyaluronan intended for neural conduits, and open the way to scaffolds with tunable degradation rate adapted to the site and severity of the injury.
[Mh] Termos MeSH primário: Ácido Hialurônico/química
Hidrogéis/química
Tecidos Suporte/química
[Mh] Termos MeSH secundário: Animais
Bovinos
Linhagem Celular
Proliferação Celular
Sobrevivência Celular
Difusão
Glucose/metabolismo
Hidrogéis/síntese química
Regeneração Nervosa
Porosidade
Ratos
Células de Schwann/citologia
Células de Schwann/metabolismo
Células de Schwann/patologia
Soroalbumina Bovina/metabolismo
Engenharia Tecidual
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Hydrogels); 27432CM55Q (Serum Albumin, Bovine); 9004-61-9 (Hyaluronic Acid); IY9XDZ35W2 (Glucose)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161025
[St] Status:MEDLINE


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[PMID]:28449948
[Au] Autor:Lutz SZ; Ullrich A; Häring HU; Ullrich S; Gerst F
[Ad] Endereço:German Center for Diabetes Research (DZD e.V.), Germany; Institute for Diabetes Research and Metabolic Diseases IDM of the Helmholtz Center Munich at the Eberhard-Karls-University of Tübingen, Germany; University Hospital Tübingen, Internal Medicine IV, Endocrinology, Diabetology, Angiology, Nephrol
[Ti] Título:Sunitinib specifically augments glucose-induced insulin secretion.
[So] Source:Cell Signal;36:91-97, 2017 Aug.
[Is] ISSN:1873-3913
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The tyrosine kinase inhibitor sunitinib is used for the treatment of numerous cancers in humans. In diabetic patients, sunitinib lowers blood glucose levels and improves glycaemic control. This study aims to analyse whether sunitinib has specific and direct effects on insulin secreting ß-cells. Regulation of insulin secretion, of cellular cAMP levels and activation of signalling pathways were examined upon exposure of rat insulinoma INS-1E cells to sunitinib under specific stimulatory and inhibitory conditions. Secreted insulin and cellular cAMP levels were measured using RIA and ELISA, respectively. Protein phosphorylations were examined on western blots. Sunitinib enhanced glucose-induced insulin secretion (GIIS) concentration-dependently, reaching a maximal stimulation at 2µM. Sunitinib further augmented insulin secretion in the presence of elevated cAMP levels and the FFAR1 agonists. Adrenaline and the PKA inhibitor H89 counteracted the stimulatory effect of sunitinib on secretion. However, sunitinib altered neither the cellular levels of cAMP nor the phosphorylation of PKA. Sunitinib did not reduce IGF-1-induced phosphorylation of AKT/PKB and ERK1/2. In conclusion, these results suggest that sunitinib stimulates GIIS by a direct effect on ß-cells, which may contribute to the glucose-lowering action of the tyrosine kinase inhibitor in humans.
[Mh] Termos MeSH primário: Glucose/farmacologia
Indóis/farmacologia
Insulina/secreção
Pirróis/farmacologia
[Mh] Termos MeSH secundário: Compostos de Anilina
Animais
Linhagem Celular
Colforsina/farmacologia
AMP Cíclico/metabolismo
Proteínas Quinases Dependentes de AMP Cíclico/antagonistas & inibidores
Proteínas Quinases Dependentes de AMP Cíclico/metabolismo
MAP Quinases Reguladas por Sinal Extracelular/metabolismo
Fator de Crescimento Insulin-Like I/metabolismo
Isoquinolinas/farmacologia
Fenilpropionatos
Fosforilação/efeitos dos fármacos
Inibidores de Proteínas Quinases/farmacologia
Ratos
Transdução de Sinais/efeitos dos fármacos
Sulfonamidas/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Aniline Compounds); 0 (H-89 dihydrochloride hydrate); 0 (Indoles); 0 (Insulin); 0 (Isoquinolines); 0 (Phenylpropionates); 0 (Protein Kinase Inhibitors); 0 (Pyrroles); 0 (Sulfonamides); 0 (TUG-469); 1F7A44V6OU (Colforsin); 67763-96-6 (Insulin-Like Growth Factor I); E0399OZS9N (Cyclic AMP); EC 2.7.11.11 (Cyclic AMP-Dependent Protein Kinases); EC 2.7.11.24 (Extracellular Signal-Regulated MAP Kinases); IY9XDZ35W2 (Glucose); V99T50803M (sunitinib)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180306
[Lr] Data última revisão:
180306
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170429
[St] Status:MEDLINE



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