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  1 / 10811 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


  2 / 10811 MEDLINE  
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[PMID]:29459024
[Au] Autor:Fang P; Yu M; Min W; Wan D; Han S; Shan Y; Wang R; Shi M; Zhang Z; Bo P
[Ad] Endereço:Department of Physiology, Nanjing University of Chinese Medicine Hanlin College, Taizhou, Jiangsu 225300, China; Department of Endocrinology, Clinical Medical College, Yangzhou University, Yangzhou, Jiangsu 225001, China.
[Ti] Título:Effect of baicalin on GLUT4 expression and glucose uptake in myotubes of rats.
[So] Source:Life Sci;196:156-161, 2018 Mar 01.
[Is] ISSN:1879-0631
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:AIMS: Although baicalin could attenuate obesity-induced insulin resistance, the detailed mechanism of baicalin on glucose uptake has not been sufficiently explored as yet. The aim of this study was to survey if baicalin might facilitate glucose uptake and to explore its signal mechanisms in L6 myotubes. MATERIALS AND METHODS: L6 myotubes were treated with 100, 200, 400 µM baicalin for 6 h, 12 h and 24 h in this study. Then 2-NBDG and insulin signal protein levels in myotubes of L6 cells were examined. KEY FINDINGS: We discovered that administration of baicalin enhanced GLUT4, PGC-1α, pP38MAPK, pAKT and pAS160 contents, as well as GLUT4 mRNA and PGC-1α mRNA levels in L6 myotubes. The beneficial metabolic changes elicited by baicalin were abrogated in myotubes of L6 by P38MAPK or AKT inhibitors. SIGNIFICANCE: These results suggest that baicalin promoted glucose uptake in myotubes by differential regulation on P38MAPK and AKT activity. In conclusion, these data provide insight that baicalin is a powerful and promising agent for the treament of hyperglycemia via AKT/AS160/GLUT4 and P38MAPK/PGC1α/GLUT4 pathway.
[Mh] Termos MeSH primário: Flavonoides/farmacologia
Transportador de Glucose Tipo 4/biossíntese
Glucose/metabolismo
Hipoglicemiantes/farmacologia
Fibras Musculares Esqueléticas/metabolismo
[Mh] Termos MeSH secundário: 4-Cloro-7-nitrobenzofurazano/análogos & derivados
4-Cloro-7-nitrobenzofurazano/metabolismo
Animais
Células Cultivadas
Desoxiglucose/análogos & derivados
Desoxiglucose/metabolismo
Insulina/metabolismo
Fibras Musculares Esqueléticas/efeitos dos fármacos
Músculo Esquelético/efeitos dos fármacos
Músculo Esquelético/metabolismo
Proteína Oncogênica v-akt/efeitos dos fármacos
Proteína Oncogênica v-akt/metabolismo
Coativador 1-alfa do Receptor gama Ativado por Proliferador de Peroxissomo/efeitos dos fármacos
Coativador 1-alfa do Receptor gama Ativado por Proliferador de Peroxissomo/metabolismo
Ratos
Transdução de Sinais/efeitos dos fármacos
Frações Subcelulares/efeitos dos fármacos
Frações Subcelulares/metabolismo
Proteínas Quinases p38 Ativadas por Mitógeno/efeitos dos fármacos
Proteínas Quinases p38 Ativadas por Mitógeno/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Flavonoids); 0 (Glucose Transporter Type 4); 0 (Hypoglycemic Agents); 0 (Insulin); 0 (Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha); 0 (Ppargc1a protein, rat); 0 (Slc2a4 protein, rat); 347Q89U4M5 (baicalin); 9G2MP84A8W (Deoxyglucose); EC 2.7.11.1 (Oncogene Protein v-akt); EC 2.7.11.24 (p38 Mitogen-Activated Protein Kinases); EQF2794IRE (4-Chloro-7-nitrobenzofurazan); IY9XDZ35W2 (Glucose); JE4F4P486R (2-(N-(7-nitrobenz-2-oxa-1,3-diazol-4-yl)amino)-2-deoxyglucose)
[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:180221
[St] Status:MEDLINE


  3 / 10811 MEDLINE  
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[PMID]:29176801
[Au] Autor:Xing J; Singh S; Zhao Y; Duan Y; Guo H; Hu C; Ma A; George R; Xing JZ; Kalluri A; Macwan I; Patra P; Chen J
[Ad] Endereço:Department of Electrical and Computer Engineering, University of Alberta, Edmonton, Canada.
[Ti] Título:Increasing vaccine production using pulsed ultrasound waves.
[So] Source:PLoS One;12(11):e0187048, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Vaccination is a safe and effective approach to prevent deadly diseases. To increase vaccine production, we propose that a mechanical stimulation can enhance protein production. In order to prove this hypothesis, Sf9 insect cells were used to evaluate the increase in the expression of a fusion protein from hepatitis B virus (HBV S1/S2). We discovered that the ultrasound stimulation at a frequency of 1.5 MHz, intensity of 60 mW/cm2, for a duration of 10 minutes per day increased HBV S1/S2 by 27%. We further derived a model for transport through a cell membrane under the effect of ultrasound waves, tested the key assumptions of the model through a molecular dynamics simulation package, NAMD (Nanoscale Molecular Dynamics program) and utilized CHARMM force field in a steered molecular dynamics environment. The results show that ultrasound waves can increase cell permeability, which, in turn, can enhance nutrient / waste exchange thus leading to enhanced vaccine production. This finding is very meaningful in either shortening vaccine production time, or increasing the yield of proteins for use as vaccines.
[Mh] Termos MeSH primário: Vacinas contra Hepatite B/biossíntese
Ondas Ultrassônicas
[Mh] Termos MeSH secundário: 4-Cloro-7-nitrobenzofurazano/análogos & derivados
4-Cloro-7-nitrobenzofurazano/metabolismo
Animais
Western Blotting
Permeabilidade da Membrana Celular
Desoxiglucose/análogos & derivados
Desoxiglucose/metabolismo
Vacinas contra Hepatite B/imunologia
Simulação de Dinâmica Molecular
Fosfatidilcolinas/química
Proteínas/metabolismo
Células Sf9
Sonicação
Termodinâmica
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Hepatitis B Vaccines); 0 (Phosphatidylcholines); 0 (Proteins); 9G2MP84A8W (Deoxyglucose); EDS2L3ODLV (1,2-oleoylphosphatidylcholine); EQF2794IRE (4-Chloro-7-nitrobenzofurazan); JE4F4P486R (2-(N-(7-nitrobenz-2-oxa-1,3-diazol-4-yl)amino)-2-deoxyglucose)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171219
[Lr] Data última revisão:
171219
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171128
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0187048


  4 / 10811 MEDLINE  
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[PMID]:28899903
[Au] Autor:Pedroso JAB; de Mendonca POR; Fortes MAS; Tomaz I; Pecorali VL; Auricino TB; Costa IC; Lima LB; Furigo IC; Bueno DN; Ramos-Lobo AM; Lotfi CFP; Donato J
[Ad] Endereço:Department of Physiology and BiophysicsInstitute of Biomedical Sciences, University of São Paulo, São Paulo, Brazil.
[Ti] Título:SOCS3 expression in SF1 cells regulates adrenal differentiation and exercise performance.
[So] Source:J Endocrinol;235(3):207-222, 2017 Dec.
[Is] ISSN:1479-6805
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Many hormones/cytokines are secreted in response to exercise and cytokine signaling may play a pivotal role in the training adaptations. To investigate the importance of cytokine signaling during vertical ladder climbing, a resistance exercise model, we produced mice lacking SOCS3 protein exclusively in steroidogenic factor-1 (SF1) cells (SF1 Socs3 KO mice). SF1 expression is found in steroidogenic cells of the adrenal cortex and gonads, as well as in neurons of the ventromedial nucleus of the hypothalamus. Histological markers of the fetal adrenal zone (or X-zone in rodents) were still present in adult males and postpartum SF1 Socs3 KO females, suggesting a previously unrecognized effect of SOCS3 on the terminal differentiation of the adrenal gland. This change led to a distinct distribution of lipid droplets along the adrenal cortex. Under basal conditions, adult SF1 Socs3 KO mice exhibited similar adrenal weight, and plasma ACTH and corticosterone concentrations. Nonetheless, SF1 Socs3 KO mice exhibited a blunted ACTH-induced corticosterone secretion. The overall metabolic responses induced by resistance training remained unaffected in SF1 Socs3 KO mice, including changes in body adiposity, glucose tolerance and energy expenditure. However, training performance and glucose control during intense resistance exercise were impaired in SF1 Socs3 KO mice. Furthermore, a reduced counter-regulatory response to 2-deoxy-d-glucose was observed in mutant mice. These findings revealed a novel participation of SOCS3 regulating several endocrine and metabolic aspects. Therefore, cytokine signaling in SF1 cells exerts an important role to sustain training performance possibly by promoting the necessary metabolic adjustments during exercise.
[Mh] Termos MeSH primário: Diferenciação Celular/fisiologia
Fator Esteroidogênico 1/metabolismo
Proteína 3 Supressora da Sinalização de Citocinas/metabolismo
[Mh] Termos MeSH secundário: Adiposidade/genética
Adiposidade/fisiologia
Glândulas Suprarrenais/metabolismo
Animais
Diferenciação Celular/genética
Corticosterona/secreção
Desoxiglucose/metabolismo
Feminino
Masculino
Camundongos
Camundongos Knockout
Hipófise/metabolismo
Fator Esteroidogênico 1/genética
Proteína 3 Supressora da Sinalização de Citocinas/genética
Testículo/metabolismo
Testosterona/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Socs3 protein, mouse); 0 (Steroidogenic Factor 1); 0 (Suppressor of Cytokine Signaling 3 Protein); 0 (steroidogenic factor 1, mouse); 3XMK78S47O (Testosterone); 9G2MP84A8W (Deoxyglucose); W980KJ009P (Corticosterone)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171020
[Lr] Data última revisão:
171020
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170914
[St] Status:MEDLINE
[do] DOI:10.1530/JOE-17-0255


  5 / 10811 MEDLINE  
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[PMID]:28859155
[Au] Autor:Yoshitomi H; Tsuru R; Li L; Zhou J; Kudo M; Liu T; Gao M
[Ad] Endereço:School of Pharmaceutical Sciences, Mukogawa Women's University, Hyogo, Japan.
[Ti] Título:Cyclocarya paliurus extract activates insulin signaling via Sirtuin1 in C2C12 myotubes and decreases blood glucose level in mice with impaired insulin secretion.
[So] Source:PLoS One;12(8):e0183988, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Diabetes is caused by the lack of release or action of insulin. Some foods and supplements can compensate for this deficiency; thus, they can aid in the prevention or treatment of diabetes. The aim of this study was to investigate the effects of Cyclocarya paliurus extract (CPE) on insulin signaling and its capacity to correct hyperglycemia in the absence of insulin. To investigate the hypoglycemic effects of CPE, C2C12 cells were exposed to CPE (50 and 100 µg/mL). CPE promoted 2-(N-(7-Nitrobenz-2-oxa-1,3-diazol-4-yl)Amino)-2-Deoxyglucose (2NBDG) uptake into the cells via translocation of glucose transporter 4 (Glut4) to the plasma membrane. In addition, CPE enhanced tyrosine phosphorylation of insulin receptor substrate and activated phosphatidylinositol 3-kinase and protein kinase B (Akt) via sirtuin1 in C2C12 cells. Moreover, we found that oral administration of CPE (1 g/kg) to streptozotocin-induced hyperglycemic mice produced a progressive decrease in plasma glucose levels at 1 h after single dosing. At that point, CPE significantly increased the expression of skeletal muscle membrane Glut4 and enhanced the phosphorylation of Akt. These results suggest that CPE exerts antidiabetic effects similar to those of insulin, and may be an oral therapeutic alternative for the management of diabetes.
[Mh] Termos MeSH primário: Diabetes Mellitus Experimental/tratamento farmacológico
Medicamentos de Ervas Chinesas/farmacologia
Fagaceae/química
Hipoglicemiantes/farmacologia
Insulina/agonistas
Transdução de Sinais/efeitos dos fármacos
Sirtuína 1/genética
[Mh] Termos MeSH secundário: 4-Cloro-7-nitrobenzofurazano/análogos & derivados
4-Cloro-7-nitrobenzofurazano/metabolismo
Animais
Transporte Biológico/efeitos dos fármacos
Linhagem Celular
Desoxiglucose/análogos & derivados
Desoxiglucose/metabolismo
Diabetes Mellitus Experimental/genética
Diabetes Mellitus Experimental/metabolismo
Diabetes Mellitus Experimental/patologia
Medicamentos de Ervas Chinesas/isolamento & purificação
Regulação da Expressão Gênica
Transportador de Glucose Tipo 4/genética
Transportador de Glucose Tipo 4/metabolismo
Hipoglicemiantes/isolamento & purificação
Insulina/metabolismo
Proteínas Substratos do Receptor de Insulina/genética
Proteínas Substratos do Receptor de Insulina/metabolismo
Masculino
Camundongos
Camundongos Endogâmicos ICR
Fibras Musculares Esqueléticas/citologia
Fibras Musculares Esqueléticas/efeitos dos fármacos
Fibras Musculares Esqueléticas/metabolismo
Músculo Esquelético/efeitos dos fármacos
Músculo Esquelético/metabolismo
Fosfatidilinositol 3-Quinase/genética
Fosfatidilinositol 3-Quinase/metabolismo
Fosforilação/efeitos dos fármacos
Transporte Proteico
Proteínas Proto-Oncogênicas c-akt/genética
Proteínas Proto-Oncogênicas c-akt/metabolismo
Sirtuína 1/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Drugs, Chinese Herbal); 0 (Glucose Transporter Type 4); 0 (Hypoglycemic Agents); 0 (Insulin); 0 (Insulin Receptor Substrate Proteins); 0 (Irs1 protein, mouse); 0 (Slc2a4 protein, mouse); 9G2MP84A8W (Deoxyglucose); EC 2.7.1.137 (Phosphatidylinositol 3-Kinase); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt); EC 3.5.1.- (Sirt1 protein, mouse); EC 3.5.1.- (Sirtuin 1); EQF2794IRE (4-Chloro-7-nitrobenzofurazan); JE4F4P486R (2-(N-(7-nitrobenz-2-oxa-1,3-diazol-4-yl)amino)-2-deoxyglucose)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170901
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0183988


  6 / 10811 MEDLINE  
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[PMID]:28858121
[Au] Autor:Wang XY; Zhao YF; Liu Y; Yang YK; Wu N
[Ad] Endereço:aDepartment of Diagnostic Radiology bPET/CT Center cDepartment of Thoracic Surgery, National Cancer Center/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.
[Ti] Título:Prognostic value of metabolic variables of [18F]FDG PET/CT in surgically resected stage I lung adenocarcinoma.
[So] Source:Medicine (Baltimore);96(35):e7941, 2017 Sep.
[Is] ISSN:1536-5964
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The objective of this study was to assess the prognostic value of metabolic tumor burden measured by positron emission tomography/computed tomography (PET/CT) in patients with stage I lung adenocarcinoma.We reviewed 127 consecutive patients with pathologically proven stage I lung adenocarcinoma who underwent pretreatment [18F]FDG PET/CT scans in our hospital from 2005 June to 2012 June. The maximum, mean, and peak standardized uptake value (SUVmax, SUVmean, and SUVpeak), metabolic tumor volume (MTV), total lesion glycolysis (TLG), and computed tomography volume (CTV) were measured. The Kaplan-Meier and Cox proportional hazards model were used with age, gender, TNM stage, clinical stage, histological grade, nodule type, tumor size, and metabolic parameters to predict progression-free survival (PFS). The cut-off point was determined through receiver-operating characteristic curve.In univariate analysis, the histological grade, nodule type, diameter (cut-off value of 2.0 cm), CTV (6.56 cm), SUVmax (3.25 g/mL), SUVmean (1.58 g/mL), SUVpeak (1.84 g/mL), MTV (4.80 cm), and TLG (10.40) were significantly associated with PFS (all P value < .05). Patients with poorly differentiated adenocarcinoma, solid nodule type, large size, and high metabolic tumor burden were associated with poor prognosis. In multivariate analysis, only histological grade was independent prognostic factors for progression with a P value of .005 (RR, 0.355; 95% CI, 0.173-0.728). Among 5 PET/CT metabolic parameters, only MTV was independent prognostic factors for progression with a P value of .031 (RR, 1.118; 95% CI, 1.010-1.237).Histological grade was an independent predictor for progression in patients with stage I lung adenocarcinoma. Among 5 PET/CT metabolic parameters, only MTV was an independent predictor for progression.
[Mh] Termos MeSH primário: Adenocarcinoma/diagnóstico por imagem
Adenocarcinoma/cirurgia
Neoplasias Pulmonares/diagnóstico por imagem
Neoplasias Pulmonares/cirurgia
[Mh] Termos MeSH secundário: Adenocarcinoma/mortalidade
Adenocarcinoma/patologia
Desoxiglucose/análogos & derivados
Feminino
Seres Humanos
Estimativa de Kaplan-Meier
Neoplasias Pulmonares/mortalidade
Neoplasias Pulmonares/patologia
Masculino
Meia-Idade
Gradação de Tumores
Estadiamento de Neoplasias
Tomografia Computadorizada com Tomografia por Emissão de Pósitrons
Prognóstico
Modelos de Riscos Proporcionais
Compostos Radiofarmacêuticos
Estudos Retrospectivos
Carga Tumoral
[Pt] Tipo de publicação:JOURNAL ARTICLE; OBSERVATIONAL STUDY
[Nm] Nome de substância:
0 (Radiopharmaceuticals); 14685-79-1 (2-chloro-2-deoxyglucose); 9G2MP84A8W (Deoxyglucose)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170918
[Lr] Data última revisão:
170918
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170901
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000007941


  7 / 10811 MEDLINE  
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[PMID]:28820081
[Au] Autor:Nakamura S; Tanabe K; Yoshinaga K; Shimura F; Oku T
[Ad] Endereço:1Institute of Food, Nutrition and Health,Jumonji University,2-1-28 Sugasawa,Niiza,Saitama 352-8510,Japan.
[Ti] Título:Effects of 1,5-anhydroglucitol on postprandial blood glucose and insulin levels and hydrogen excretion in rats and healthy humans.
[So] Source:Br J Nutr;118(2):81-91, 2017 Jul.
[Is] ISSN:1475-2662
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The inhibition by 1,5-anhydro-d-glucitol (1,5-AG) was determined on disaccharidases of rats and humans. Then, the metabolism and fate of 1,5-AG was investigated in rats and humans. Although 1,5-AG inhibited about 50 % of sucrase activity in rat small intestine, the inhibition was less than half of d-sorbose. 1,5-AG strongly inhibited trehalase and lactase, whereas d-sorbose inhibited them very weakly. 1,5-AG noncompetitively inhibited sucrase. The inhibition of 1,5-AG on sucrase and maltase was similar between humans and rats. 1,5-AG in serum increased 30 min after oral administration of 1,5-AG (600 mg) in rats, and mostly 100 % of 1,5-AG was excreted into the urine 24 h after administration. 1,5-AG in serum showed a peak 30 min after ingestion of 1,5-AG (20 g) by healthy subjects, and decreased gradually over 180 min. About 60 % of 1,5-AG was excreted into the urine for 9 h following ingestion. Hydrogen was scarcely excreted in both rats and humans 24 h after administration of 1,5-AG. Furthermore, 1,5-AG significantly suppressed the blood glucose elevation, and hydrogen excretion was increased following the simultaneous ingestion of sucrose and 1,5-AG in healthy subjects. 1,5-AG also significantly suppressed the blood glucose elevation following the simultaneous ingestion of glucose and 1,5-AG; however, hydrogen excretion was negligible. The available energy of 1,5-AG, which is absorbed readily from the small intestine and excreted quickly into the urine, is 0 kJ/g (0 kcal/g). Furthermore, 1,5-AG might suppress the blood glucose elevation through the inhibition of sucrase, as well as intestinal glucose absorption.
[Mh] Termos MeSH primário: Glicemia/análise
Desoxiglucose/farmacologia
Insulina/sangue
Período Pós-Prandial
[Mh] Termos MeSH secundário: Adulto
Animais
Desoxiglucose/farmacocinética
Dissacaridases/antagonistas & inibidores
Inibidores Enzimáticos/farmacologia
Feminino
Glucose/administração & dosagem
Glucose/farmacocinética
Inibidores de Glicosídeo Hidrolases/farmacologia
Seres Humanos
Hidrogênio/urina
Absorção Intestinal
Intestino Delgado/enzimologia
Masculino
Ratos
Ratos Wistar
Sacarase/antagonistas & inibidores
Sacarose/administração & dosagem
alfa-Glucosidases
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Blood Glucose); 0 (Enzyme Inhibitors); 0 (Glycoside Hydrolase Inhibitors); 0 (Insulin); 54BB3B7XMZ (1,5-anhydroglucitol); 57-50-1 (Sucrose); 7YNJ3PO35Z (Hydrogen); 9G2MP84A8W (Deoxyglucose); EC 3.2.1.- (Disaccharidases); EC 3.2.1.20 (alpha-Glucosidases); EC 3.2.1.48 (Sucrase); IY9XDZ35W2 (Glucose)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170825
[Lr] Data última revisão:
170825
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170819
[St] Status:MEDLINE
[do] DOI:10.1017/S0007114517001866


  8 / 10811 MEDLINE  
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[PMID]:28798141
[Au] Autor:Tavakoli S; Downs K; Short JD; Nguyen HN; Lai Y; Jerabek PA; Goins B; Toczek J; Sadeghi MM; Asmis R
[Ad] Endereço:From the Department of Radiology (S.T.) and Department of Medicine (S.T.), University of Pittsburgh, PA; Department of Cellular and Structural Biology (K.D), Department of Pharmacology (J.D.S.), Department of Biochemistry (H.N.N., R.A.), Department of Clinical Laboratory Sciences (Y.L., R.A.), Depar
[Ti] Título:Characterization of Macrophage Polarization States Using Combined Measurement of 2-Deoxyglucose and Glutamine Accumulation: Implications for Imaging of Atherosclerosis.
[So] Source:Arterioscler Thromb Vasc Biol;37(10):1840-1848, 2017 Oct.
[Is] ISSN:1524-4636
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: Despite the early promising results of F-fluorodeoxyglucose positron emission tomography for assessment of vessel wall inflammation, its accuracy in prospective identification of vulnerable plaques has remained limited. Additionally, previous studies have indicated that F-fluorodeoxyglucose uptake alone may not allow for accurate identification of specific macrophage activation states. We aimed to determine whether combined measurement of glucose and glutamine accumulation-the 2 most important bioenergetic substrates for macrophages-improves the distinction of macrophage inflammatory states and can be utilized to image atherosclerosis. APPROACH AND RESULTS: Murine peritoneal macrophages (MΦ) were activated ex vivo into proinflammatory states with either lipopolysaccharide (MΦ ) or interferon-γ+tumor necrosis factor-α (MΦ ). An alternative polarization phenotype was induced with interleukin-4 (MΦ ). The pronounced increase in 2-deoxyglucose uptake distinguishes MΦ from MΦ , MΦ , and unstimulated macrophages (MΦ ). Despite having comparable levels of 2-deoxyglucose accumulation, MΦ can be distinguished from both MΦ and MΦ based on the enhanced glutamine accumulation, which was associated with increased expression of a glutamine transporter, . Ex vivo autoradiography experiments demonstrated distinct and heterogenous patterns of F-fluorodeoxyglucose and C-glutamine accumulation in atherosclerotic lesions of low-density lipoprotein receptor-null mice fed a high-fat diet. CONCLUSIONS: Combined assessment of glutamine and 2-deoxyglucose accumulation improves the ex vivo identification of macrophage activation states. Combined ex vivo metabolic imaging demonstrates heterogenous and distinct patterns of substrate accumulation in atherosclerotic lesions. Further studies are required to define the in vivo significance of glutamine uptake in atherosclerosis and its potential application in identification of vulnerable plaques.
[Mh] Termos MeSH primário: Aterosclerose/diagnóstico por imagem
Desoxiglucose/metabolismo
Fluordesoxiglucose F18
Glutamina/metabolismo
Macrófagos/metabolismo
Placa Aterosclerótica/diagnóstico por imagem
Tomografia por Emissão de Pósitrons
[Mh] Termos MeSH secundário: Animais
Aorta/diagnóstico por imagem
Aorta/metabolismo
Aterosclerose/metabolismo
Autorradiografia
Camundongos
Placa Aterosclerótica/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0RH81L854J (Glutamine); 0Z5B2CJX4D (Fluorodeoxyglucose F18); 9G2MP84A8W (Deoxyglucose)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171010
[Lr] Data última revisão:
171010
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170812
[St] Status:MEDLINE
[do] DOI:10.1161/ATVBAHA.117.308848


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[PMID]:28768727
[Au] Autor:Varanasi SK; Donohoe D; Jaggi U; Rouse BT
[Ad] Endereço:Department of Genome Science and Technology, College of Arts & Sciences, University of Tennessee, Knoxville, TN 37996.
[Ti] Título:Manipulating Glucose Metabolism during Different Stages of Viral Pathogenesis Can Have either Detrimental or Beneficial Effects.
[So] Source:J Immunol;199(5):1748-1761, 2017 Sep 01.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:This report deals with physiological changes and their implication following ocular infection with HSV. This infection usually results in a blinding inflammatory reaction in the cornea, orchestrated mainly by proinflammatory CD4 T cells and constrained in severity by regulatory T cells. In the present report, we make the unexpected finding that blood glucose levels change significantly during the course of infection. Whereas levels remained normal during the early phase of infection when the virus was actively replicating in the cornea, they increased around 2-fold during the time when inflammatory responses to the virus was occurring. We could show that glucose levels influenced the extent of induction of the inflammatory T cell subset in vitro that mainly drives lesions, but not regulatory T cells. Additionally, if glucose utilization was limited in vivo as a consequence of therapy in the inflammatory phase with the drug 2-deoxy-glucose (2DG), lesions were diminished compared with untreated infected controls. In addition, lesions in 2DG-treated animals contained less proinflammatory effectors. Glucose metabolism also influenced the acute phase of infection when the replicating virus was present in the eye. Thus, therapy with 2DG to limit glucose utilization caused mice to become susceptible to the lethal effects of HSV infection, with the virus spreading to the brain causing encephalitis. Taken together, our results indicate that glucose metabolism changed during the course of HSV infection and that modulating glucose levels can influence the outcome of infection, being detrimental or beneficial according to the stage of viral pathogenesis.
[Mh] Termos MeSH primário: Anti-Inflamatórios/uso terapêutico
Córnea/imunologia
Desoxiglucose/uso terapêutico
Efeitos Colaterais e Reações Adversas Relacionados a Medicamentos/imunologia
Encefalite/imunologia
Glucose/metabolismo
Herpes Simples/tratamento farmacológico
Herpesvirus Humano 1/fisiologia
Ceratite Herpética/tratamento farmacológico
Subpopulações de Linfócitos T/imunologia
Linfócitos T Reguladores/imunologia
[Mh] Termos MeSH secundário: Animais
Células Cultivadas
Córnea/virologia
Encefalite/etiologia
Feminino
Herpes Simples/imunologia
Mediadores da Inflamação/metabolismo
Ceratite Herpética/imunologia
Camundongos
Camundongos Endogâmicos C57BL
Subpopulações de Linfócitos T/virologia
Linfócitos T Reguladores/virologia
Replicação Viral
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Inflammatory Agents); 0 (Inflammation Mediators); 9G2MP84A8W (Deoxyglucose); IY9XDZ35W2 (Glucose)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170929
[Lr] Data última revisão:
170929
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170804
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1700472


  10 / 10811 MEDLINE  
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[PMID]:28605542
[Au] Autor:Mukai N; Ohara T; Hata J; Hirakawa Y; Yoshida D; Kishimoto H; Koga M; Nakamura U; Kitazono T; Kiyohara Y; Ninomiya T
[Ad] Endereço:Center for Cohort Studies, Graduate School of Medical Sciences, Kyushu University, Fukuoka 812-8582, Japan.
[Ti] Título:Alternative Measures of Hyperglycemia and Risk of Alzheimer's Disease in the Community: The Hisayama Study.
[So] Source:J Clin Endocrinol Metab;102(8):3002-3010, 2017 Aug 01.
[Is] ISSN:1945-7197
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Context and Objective: We investigated the associations of hemoglobin A1c (HbA1c), glycated albumin (GA), GA/HbA1c ratio, and 1,5-anhydroglucitol (1,5-AG) with the development of Alzheimer's disease (AD). Design and Participants: A total of 1187 community-dwelling Japanese subjects aged ≥65 years without dementia were followed up for an average of 4.8 years. Results: The age- and sex-adjusted incidence of AD increased significantly with higher quartiles of GA/HbA1c ratio, and a similar tendency was seen for GA, whereas no such association was observed for HbA1c and 1,5-AG. After adjusting for potential confounding factors, positive association of GA/HbA1c ratio with the risk of AD remained significant: the multivariable-adjusted hazard ratio (HR) was significantly higher in the third [HR = 2.11, 95% confidence interval (CI) = 1.16 to 3.82] and fourth (HR = 2.01, 95% CI = 1.09 to 3.68) quartile than in the first quartile. Among subjects with normal glucose tolerance, those with high GA/HbA1c ratio had a higher risk of AD than those with low GA/HbA1c ratio (HR = 1.82, 95% CI = 1.05 to 3.16), and a similar tendency was found in those with glucose intolerance (HR = 1.73, 95% CI = 0.96 to 3.13). No such associations were observed for HbA1c, GA, and 1,5-AG, regardless of glucose tolerance status. Conclusions: Our findings suggest that elevated GA/HbA1c ratio-but not HbA1c, GA, or 1,5-AG level-is significantly associated with the risk of AD in subjects both with and without glucose intolerance. GA/HbA1c ratio may be a useful biomarker for predicting incident AD.
[Mh] Termos MeSH primário: Doença de Alzheimer/epidemiologia
Desoxiglucose/metabolismo
Intolerância à Glucose/epidemiologia
Hemoglobina A Glicada/metabolismo
Hiperglicemia/epidemiologia
Albumina Sérica/metabolismo
[Mh] Termos MeSH secundário: Idoso
Idoso de 80 Anos ou mais
Feminino
Seguimentos
Intolerância à Glucose/metabolismo
Seres Humanos
Hiperglicemia/metabolismo
Incidência
Vida Independente
Japão/epidemiologia
Masculino
Análise Multivariada
Modelos de Riscos Proporcionais
Estudos Prospectivos
Fatores de Risco
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Glycated Hemoglobin A); 0 (Serum Albumin); 0 (glycosylated serum albumin); 0 (hemoglobin A1c protein, human); 54BB3B7XMZ (1,5-anhydroglucitol); 9G2MP84A8W (Deoxyglucose)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170613
[St] Status:MEDLINE
[do] DOI:10.1210/jc.2017-00439



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