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[PMID]:29302038
[Au] Autor:Lucas S; Omata Y; Hofmann J; Böttcher M; Iljazovic A; Sarter K; Albrecht O; Schulz O; Krishnacoumar B; Krönke G; Herrmann M; Mougiakakos D; Strowig T; Schett G; Zaiss MM
[Ad] Endereço:Department of Internal Medicine 3, Rheumatology and Immunology, Friedrich-Alexander-University Erlangen-Nürnberg (FAU) and Universitätsklinikum Erlangen, 91054, Erlangen, Germany.
[Ti] Título:Short-chain fatty acids regulate systemic bone mass and protect from pathological bone loss.
[So] Source:Nat Commun;9(1):55, 2018 01 04.
[Is] ISSN:2041-1723
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Microbial metabolites are known to modulate immune responses of the host. The main metabolites derived from microbial fermentation of dietary fibers in the intestine, short-chain fatty acids (SCFA), affect local and systemic immune functions. Here we show that SCFA are regulators of osteoclast metabolism and bone mass in vivo. Treatment of mice with SCFA as well as feeding with a high-fiber diet significantly increases bone mass and prevents postmenopausal and inflammation-induced bone loss. The protective effects of SCFA on bone mass are associated with inhibition of osteoclast differentiation and bone resorption in vitro and in vivo, while bone formation is not affected. Mechanistically, propionate (C3) and butyrate (C4) induce metabolic reprogramming of osteoclasts resulting in enhanced glycolysis at the expense of oxidative phosphorylation, thereby downregulating essential osteoclast genes such as TRAF6 and NFATc1. In summary, these data identify SCFA as potent regulators of osteoclast metabolism and bone homeostasis.
[Mh] Termos MeSH primário: Reabsorção Óssea/metabolismo
Osso e Ossos/metabolismo
Ácidos Graxos Voláteis/metabolismo
Osteoclastos/metabolismo
[Mh] Termos MeSH secundário: Animais
Densidade Óssea/efeitos dos fármacos
Reabsorção Óssea/prevenção & controle
Osso e Ossos/efeitos dos fármacos
Butiratos/metabolismo
Butiratos/farmacologia
Fibras na Dieta/administração & dosagem
Ácidos Graxos Voláteis/farmacologia
Feminino
Expressão Gênica/efeitos dos fármacos
Glicólise/efeitos dos fármacos
Seres Humanos
Camundongos Endogâmicos C57BL
Osteoclastos/efeitos dos fármacos
Propionatos/metabolismo
Propionatos/farmacologia
Substâncias Protetoras/metabolismo
Substâncias Protetoras/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Butyrates); 0 (Dietary Fiber); 0 (Fatty Acids, Volatile); 0 (Propionates); 0 (Protective Agents)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180106
[St] Status:MEDLINE
[do] DOI:10.1038/s41467-017-02490-4


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[PMID]:29363966
[Au] Autor:Van den Abbeele P; Taminiau B; Pinheiro I; Duysburgh C; Jacobs H; Pijls L; Marzorati M
[Ad] Endereço:ProDigest bvba , Technologiepark 3, 9052 Ghent, Belgium.
[Ti] Título:Arabinoxylo-Oligosaccharides and Inulin Impact Inter-Individual Variation on Microbial Metabolism and Composition, Which Immunomodulates Human Cells.
[So] Source:J Agric Food Chem;66(5):1121-1130, 2018 Feb 07.
[Is] ISSN:1520-5118
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Fecal batch fermentations coupled to cocultures of epithelial cells and macrophages were used to compare how arabinoxylo-oligosaccharides (AXOS) and inulin modulate gut microbial activity and composition of three different human donors and subsequently the epithelial permeability and immune response. Both inulin and AXOS decreased the pH during incubation (-1.5 pH units), leading to increased productions of acetate, propionate, and butyrate. Differences in terms of metabolites production could be linked to specific microbial alterations at genus level upon inulin/AXOS supplementation (i.e., Bifidobacterium, Bacteroides, Prevotella and unclassified Erysipelotrichaceae), as shown by 16S-targeted Illumina sequencing. Both products stimulated gut barrier and immune function with increases in TEER, NF-KB, IL-10, and IL-6. Ingredients with different structures selectively modulate the microbiota of a specific donor leading to differential changes at metabolic level. The extent of this effect is donor specific and is linked to a final specific modulation of the host's immune system.
[Mh] Termos MeSH primário: Microbioma Gastrointestinal/efeitos dos fármacos
Imunomodulação/efeitos dos fármacos
Inulina/farmacologia
Oligossacarídeos/farmacologia
Xilanos/farmacologia
[Mh] Termos MeSH secundário: Acetatos/metabolismo
Butiratos/metabolismo
Células CACO-2
Fezes/microbiologia
Fermentação
Microbioma Gastrointestinal/imunologia
Microbioma Gastrointestinal/fisiologia
Seres Humanos
Concentração de Íons de Hidrogênio
Propionatos/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Acetates); 0 (Butyrates); 0 (Oligosaccharides); 0 (Propionates); 0 (Xylans); 9005-80-5 (Inulin); 9040-27-1 (arabinoxylan)
[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:180125
[St] Status:MEDLINE
[do] DOI:10.1021/acs.jafc.7b04611


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[PMID]:29233468
[Au] Autor:Li Q; Ding C; Meng T; Lu W; Liu W; Hao H; Cao L
[Ad] Endereço:State Key Laboratory of Natural Medicines, Key Laboratory of Drug Metabolism and Pharmacokinetics, China Pharmaceutical University, Nanjing, 210009, China.
[Ti] Título:Butyrate suppresses motility of colorectal cancer cells via deactivating Akt/ERK signaling in histone deacetylase dependent manner.
[So] Source:J Pharmacol Sci;135(4):148-155, 2017 Dec.
[Is] ISSN:1347-8648
[Cp] País de publicação:Japan
[La] Idioma:eng
[Ab] Resumo:Butyrate is a typical short chain fatty acid produced by gut microbiota of which the dysmetabolism has been consistently associated with colorectal diseases. However, whether butyrate affects metastatic colorectal cancer is not clear. In this study we investigated in vitro the effect of butyrate on motility, a significant metastatic factor of colorectal cancer cells and explored the potential mechanism. By using wound healing and transwell-based invasion models, we demonstrated that pretreatment of butyrate significantly inhibited motility of HCT116, HT29, LOVO and HCT8 cells, this activity was further attributed to deactivation of Akt1 and ERK1/2. Suberanilohydroxamic acid (SAHA), another HDAC inhibitor, mimicked the inhibitory effect of butyrate on cell motility and deactivation of Akt/ERK. Furthermore, by silencing of HDAC3 with siRNA, we confirmed dependence of butyrate's effect on HDAC3, the similar reduced cell motility observed under HDAC3 silencing also indicates the significance of HDAC itself in cell motility. In conclusion, we confirmed the HDAC3-relied activity of butyrate on inhibiting motility of colorectal cancer cells via deactivating Akt/ERK signaling. Our data indicate that modulating butyrate metabolism is an effective therapeutic strategy of metastatic colorectal cancer; and HDAC3 might be a novel target for management of colorectal cancer metastasis.
[Mh] Termos MeSH primário: Butiratos/farmacologia
Movimento Celular/efeitos dos fármacos
Neoplasias Colorretais/tratamento farmacológico
Neoplasias Colorretais/patologia
Histona Desacetilases/metabolismo
Sistema de Sinalização das MAP Quinases/efeitos dos fármacos
[Mh] Termos MeSH secundário: Butiratos/metabolismo
Butiratos/uso terapêutico
Linhagem Celular Tumoral
Inibidores de Histona Desacetilases
Histona Desacetilases/fisiologia
Seres Humanos
Ácidos Hidroxâmicos/farmacologia
Terapia de Alvo Molecular
Metástase Neoplásica
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Butyrates); 0 (Histone Deacetylase Inhibitors); 0 (Hydroxamic Acids); 58IFB293JI (vorinostat); EC 3.5.1.98 (Histone Deacetylases); EC 3.5.1.98 (histone deacetylase 3)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180222
[Lr] Data última revisão:
180222
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171214
[St] Status:MEDLINE


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[PMID]:29225125
[Au] Autor:Shimada N; Takasawa R; Tanuma SI
[Ad] Endereço:Faculty of Pharmaceutical Sciences, Tokyo University of Science, 2641 Yamazaki, Noda, Chiba 278-8510, Japan.
[Ti] Título:Interdependence of GLO I and PKM2 in the Metabolic shift to escape apoptosis in GLO I-dependent cancer cells.
[So] Source:Arch Biochem Biophys;638:1-7, 2018 01 15.
[Is] ISSN:1096-0384
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Many cancer cells undergo metabolic reprogramming known as the Warburg effect, which is characterized by a greater dependence on glycolysis for ATP generation, even under normoxic conditions. Glyoxalase I (GLO I) is a rate-limiting enzyme involved in the detoxification of cytotoxic methylglyoxal formed in glycolysis and which is known to be highly expressed in many cancer cells. Thus, specific inhibitors of GLO I are expected to be effective anticancer drugs. We previously discovered a novel GLO I inhibitor named TLSC702. Although the strong inhibitory activity of TLSC702 was observed in the in vitro enzyme assay, higher concentrations were required to induce apoptosis at the cellular level. One of the proposed reasons for this difference is that cancer cells alter the energy metabolism leading them to become more dependent on mitochondrial respiration than glycolysis (Metabolic shift) to avoid apoptosis induction. Thus, we assumed that combination of TLSC702 with shikonin-a specific inhibitor of pyruvate kinase M2 (PKM2) that acts as a driver of TCA cycle by supplying pyruvate and which is known to be specifically expressed in cancer cells-would have anticancer effects. We herein show the anticancer effects of combination treatment with TLSC702 and shikonin, and a possible anticancer mechanism.
[Mh] Termos MeSH primário: Apoptose
Proteínas de Transporte/metabolismo
Lactoilglutationa Liase/metabolismo
Proteínas de Membrana/metabolismo
Proteínas de Neoplasias/metabolismo
Neoplasias/enzimologia
Piruvato Quinase/metabolismo
Hormônios Tireóideos/metabolismo
[Mh] Termos MeSH secundário: Butiratos/farmacologia
Proteínas de Transporte/antagonistas & inibidores
Proteínas de Transporte/genética
Linhagem Celular Tumoral
Ciclo do Ácido Cítrico/efeitos dos fármacos
Ensaios de Seleção de Medicamentos Antitumorais
Seres Humanos
Lactoilglutationa Liase/antagonistas & inibidores
Lactoilglutationa Liase/genética
Proteínas de Membrana/antagonistas & inibidores
Proteínas de Membrana/genética
Naftoquinonas/farmacologia
Proteínas de Neoplasias/antagonistas & inibidores
Proteínas de Neoplasias/genética
Neoplasias/tratamento farmacológico
Neoplasias/genética
Neoplasias/patologia
Piruvato Quinase/antagonistas & inibidores
Piruvato Quinase/genética
Ácido Pirúvico/metabolismo
Tiazóis/farmacologia
Hormônios Tireóideos/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (3-(1,3-benzothiazol-2-yl)-4-(4-methoxyphenyl)but-3-enoic acid); 0 (Butyrates); 0 (Carrier Proteins); 0 (Membrane Proteins); 0 (Naphthoquinones); 0 (Neoplasm Proteins); 0 (Thiazoles); 0 (Thyroid Hormones); 0 (thyroid hormone-binding proteins); 3IK6592UBW (shikonin); 8558G7RUTR (Pyruvic Acid); EC 2.7.1.40 (Pyruvate Kinase); EC 4.4.1.5 (GLO1 protein, human); EC 4.4.1.5 (Lactoylglutathione Lyase)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180214
[Lr] Data última revisão:
180214
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171212
[St] Status:MEDLINE


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[PMID]:29236389
[Au] Autor:Holota YV; Holubenko OO; Ostapchuk AM; Serhiychuk TM; Zakordonets LV; Tolstanova GM
[Ti] Título:Fecal short-chain fatty acids at different time points after ceftriaxone administration in rats.
[So] Source:Ukr Biochem J;89(1):50-8, 2017 Jan-Feb.
[Is] ISSN:2409-4943
[Cp] País de publicação:Ukraine
[La] Idioma:eng
[Ab] Resumo:Short-chain fatty acids (SCFAs) are major products of the microbial fermentation of dietary fiber in the colon. Recent studies suggest that these products of microbial metabolism in the gut act as signaling molecules, influence host energy homeostasis and play major immunological roles. In the present study, defined the long-term effects of ceftriaxone administration on the fecal SCFAs concentration in Wistar rats. Ceftriaxone (300 mg/kg, i.m.) was administered daily for 14 days. Rats were euthanized in 1, 15 and 56 days after ceftriaxone withdrawal. Caecal weight and fecal concentration of SCFAs by gas chromatography were measured. Ceftriaxone administration induced time-dependent rats' caecal enlargement through accumulation of undigestable substances. In 1 day after ceftriaxone withdrawal, the concentrations of acetic, propionic, butyric acids and total SCFAs were decreased 2.9-, 13.8-, 8.5-, 4.8-fold (P < 0.05), respectively. Concentration of valeric, isovaleric and caproic acids was below the detectable level. That was accompanied by decreased 4.3-fold anaerobic index and increased the relative amount of acetic acid (P < 0.05). In 56 days, concentration of SCFAs was still below control value but higher than in 1 day (except propionic acid). Anaerobic index was lower 1.3-fold (P < 0.05) vs. control. Conclusion: antibiotic therapy induced long-term disturbance in colonic microbiota metabolic activity.
[Mh] Termos MeSH primário: Antibacterianos/farmacologia
Ceftriaxona/farmacologia
Colo/efeitos dos fármacos
Ácidos Graxos Voláteis/metabolismo
Fezes/química
[Mh] Termos MeSH secundário: Ácido Acético/metabolismo
Animais
Butiratos/metabolismo
Caproatos/metabolismo
Colo/metabolismo
Esquema de Medicação
Ácidos Graxos Voláteis/antagonistas & inibidores
Injeções Intramusculares
Masculino
Ácidos Pentanoicos/metabolismo
Propionatos/metabolismo
Ratos
Ratos Wistar
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Bacterial Agents); 0 (Butyrates); 0 (Caproates); 0 (Fatty Acids, Volatile); 0 (Pentanoic Acids); 0 (Propionates); 1BR7X184L5 (isovaleric acid); 1F8SN134MX (hexanoic acid); 75J73V1629 (Ceftriaxone); GZK92PJM7B (n-pentanoic acid); JHU490RVYR (propionic acid); Q40Q9N063P (Acetic Acid)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180116
[Lr] Data última revisão:
180116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171214
[St] Status:MEDLINE
[do] DOI:10.15407/ubj89.01.050


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[PMID]:27773823
[Au] Autor:Iannucci LF; Sun J; Singh BK; Zhou J; Kaddai VA; Lanni A; Yen PM; Sinha RA
[Ad] Endereço:Dipartimento di Scienze e Tecnologie Ambientali, Biologiche e Farmaceutiche, Seconda Università degli Studi di Napoli, Caserta, Italy.
[Ti] Título:Short chain fatty acids induce UCP2-mediated autophagy in hepatic cells.
[So] Source:Biochem Biophys Res Commun;480(3):461-467, 2016 Nov 18.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Short-chain fatty acids (SCFAs) are gut microbial fermentation products derived from dietary fiber sources. Although depletion of gut microflora has been linked to the development of liver disease, the direct effects of SCFAs on intracellular hepatic processes are not well understood. In this study, we demonstrated that the SCFAs, propionate and butyrate, regulated autophagic flux in hepatic cells in a cell-autonomous manner. Induction of autophagy by SCFAs required PPARγ stimulation of Uncoupling Protein 2 (UCP2) expression that was associated with reduced intracellular ATP levels and activation of PRKAA1/AMPK (protein kinase, AMP-activated, alpha 1 catalytic subunit). In addition, elimination of gut flora by chronic antibiotic treatment diminished basal hepatic autophagy in mice suggesting that gut microbiota can regulate hepatic autophagy. These findings provide novel insights into the interplay between diet, gut microbiota, short chain fatty acids, and hepatic autophagic signaling.
[Mh] Termos MeSH primário: Autofagia/fisiologia
Microbioma Gastrointestinal/fisiologia
Hepatócitos/citologia
Hepatócitos/metabolismo
Proteína Desacopladora 2/metabolismo
[Mh] Termos MeSH secundário: Animais
Butiratos/metabolismo
Linhagem Celular
Células Cultivadas
Ácidos Graxos/metabolismo
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Propionatos/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Butyrates); 0 (Fatty Acids); 0 (Propionates); 0 (Uncoupling Protein 2)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:171127
[Lr] Data última revisão:
171127
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161106
[St] Status:MEDLINE


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[PMID]:29036231
[Au] Autor:Zhang Q; Xiao X; Li M; Yu M; Ping F; Zheng J; Wang T; Wang X
[Ad] Endereço:Key Laboratory of Endocrinology, Translational Medicine Center, Ministry of Health, Department of Endocrinology, Peking Union Medical College Hospital, Peking Union Medical College, Chinese Academy of Medical Sciences, Beijing, China.
[Ti] Título:Vildagliptin increases butyrate-producing bacteria in the gut of diabetic rats.
[So] Source:PLoS One;12(10):e0184735, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Emerging evidence supports a key role for the gut microbiota in metabolic diseases, including type 2 diabetes (T2D) and obesity. The dipeptidyl peptidase-4 inhibitor vildagliptin is highly efficacious in treating T2D. However, whether vildagliptin can alter the gut microbiome is still unclear. This study aimed to identify whether vildagliptin modifies the gut microbiota structure during T2D treatment. Diabetic Sprague-Dawley (SD) rats were induced by a high-fat diet and streptozotocin injection (HFD/STZ). Diabetic rats were orally administered a low dose of vildagliptin (LV, 0.01 g/kg/d vildagliptin), high dose of vildagliptin (HV, 0.02 g/kg/d vildagliptin), or normal saline for 12 weeks. Fasting blood glucose, blood glucose after glucose loading, and serum insulin levels were significantly reduced in the LV and HV groups compared with those in the T2D group. The serum GLP-1 level increased more in the vildagliptin-treated group than in the T2D group. Pyrosequencing of the V3-V4 regions of 16S rRNA genes revealed that vildagliptin significantly altered the gut microbiota. The operational taxonomic units (OTUs) and community richness (Chao1) index were significantly reduced in the vildagliptin and diabetic groups compared with those in the control group. At the phylum level, a higher relative abundance of Bacteroidetes, lower abundance of Firmicutes, and reduced ratio of Fimicutes/Bacteroidetes were observed in the vildagliptin-treated group. Moreover, vildagliptin treatment increased butyrate-producing bacteria, including Baceroides and Erysipelotrichaeae, in the diabetic rats. Moreover, Lachnospira abundance was significantly negatively correlated with fasting blood glucose levels. In conclusion, vildagliptin treatment could benefit the communities of the gut microbiota.
[Mh] Termos MeSH primário: Adamantano/análogos & derivados
Diabetes Mellitus Experimental/tratamento farmacológico
Diabetes Mellitus Tipo 2/tratamento farmacológico
Inibidores da Dipeptidil Peptidase IV/farmacologia
Microbioma Gastrointestinal/efeitos dos fármacos
Nitrilos/farmacologia
Pirrolidinas/farmacologia
[Mh] Termos MeSH secundário: Adamantano/farmacologia
Administração Oral
Animais
Glicemia/efeitos dos fármacos
Butiratos/metabolismo
Diabetes Mellitus Experimental/sangue
Diabetes Mellitus Experimental/microbiologia
Diabetes Mellitus Tipo 2/sangue
Diabetes Mellitus Tipo 2/microbiologia
Microbioma Gastrointestinal/genética
Microbioma Gastrointestinal/fisiologia
Peptídeo 1 Semelhante ao Glucagon/sangue
Resistência à Insulina
Interleucina-6/sangue
Masculino
RNA Ribossômico 16S/genética
Distribuição Aleatória
Ratos Sprague-Dawley
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Blood Glucose); 0 (Butyrates); 0 (Dipeptidyl-Peptidase IV Inhibitors); 0 (Interleukin-6); 0 (Nitriles); 0 (Pyrrolidines); 0 (RNA, Ribosomal, 16S); 89750-14-1 (Glucagon-Like Peptide 1); I6B4B2U96P (vildagliptin); PJY633525U (Adamantane)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171031
[Lr] Data última revisão:
171031
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171017
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0184735


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[PMID]:28893958
[Au] Autor:Zheng L; Kelly CJ; Battista KD; Schaefer R; Lanis JM; Alexeev EE; Wang RX; Onyiah JC; Kominsky DJ; Colgan SP
[Ad] Endereço:Mucosal Inflammation Program, University of Colorado, Anschutz Medical Campus, Aurora, CO 80045.
[Ti] Título:Microbial-Derived Butyrate Promotes Epithelial Barrier Function through IL-10 Receptor-Dependent Repression of Claudin-2.
[So] Source:J Immunol;199(8):2976-2984, 2017 Oct 15.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Commensal interactions between the enteric microbiota and distal intestine play important roles in regulating human health. Short-chain fatty acids (SCFAs), such as butyrate, produced through anaerobic microbial metabolism represent a major energy source for the host colonic epithelium and enhance epithelial barrier function through unclear mechanisms. Separate studies revealed that the epithelial anti-inflammatory IL-10 receptor α subunit (IL-10RA) is also important for barrier formation. Based on these findings, we examined if SCFAs promote epithelial barrier through IL-10RA-dependent mechanisms. Using human intestinal epithelial cells (IECs), we discovered that SCFAs, particularly butyrate, enhanced IEC barrier formation, induced IL-10RA mRNA, IL-10RA protein, and transactivation through activated Stat3 and HDAC inhibition. Loss and gain of IL-10RA expression directly correlates with IEC barrier formation and butyrate represses permeability-promoting claudin-2 tight-junction protein expression through an IL-10RA-dependent mechanism. Our findings provide a novel mechanism by which microbial-derived butyrate promotes barrier through IL-10RA-dependent repression of claudin-2.
[Mh] Termos MeSH primário: Bactérias Anaeróbias/fisiologia
Butiratos/metabolismo
Colo/patologia
Microbioma Gastrointestinal/imunologia
Mucosa Intestinal/fisiologia
Receptores de Interleucina-10/metabolismo
Junções Íntimas/metabolismo
[Mh] Termos MeSH secundário: Butiratos/imunologia
Linhagem Celular
Células Cultivadas
Claudina-2/metabolismo
Regulação da Expressão Gênica
Histona Desacetilases/metabolismo
Seres Humanos
Mucosa Intestinal/microbiologia
Mucosa Intestinal/patologia
Receptores de Interleucina-10/genética
Fator de Transcrição STAT3/genética
Fator de Transcrição STAT3/metabolismo
Simbiose
Ativação Transcricional
Migração Transendotelial e Transepitelial
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Butyrates); 0 (Claudin-2); 0 (Receptors, Interleukin-10); 0 (STAT3 Transcription Factor); EC 3.5.1.98 (Histone Deacetylases)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171101
[Lr] Data última revisão:
171101
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170913
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1700105


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[PMID]:28797773
[Au] Autor:Bakka TA; Strøm MB; Andersen JH; Gautun OR
[Ad] Endereço:Department of Chemistry, Norwegian University of Science and Technology (NTNU), NO-7491 Trondheim, Norway.
[Ti] Título:Methyl propiolate and 3-butynone: Starting points for synthesis of amphiphilic 1,2,3-triazole peptidomimetics for antimicrobial evaluation.
[So] Source:Bioorg Med Chem;25(20):5380-5395, 2017 Oct 15.
[Is] ISSN:1464-3391
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:A library of 29 small 1,4-substituted 1,2,3-triazoles was prepared for studies of antimicrobial activity. The pharmacophore model investigated with these substrates was based on small peptidomimetics of antimicrobial peptides and antimicrobials isolated from marine organisms from sub-arctic regions. Using methyl 1,2,3-triazole-carboxylates and 1,2,3-triazole methyl ketones prepared through "click" chemistry we were able to synthesize the different cationic amphiphiles through three steps or less. Several structural modifications to the lipopohilic side and hydrophilic sides of the amphiphiles were investigated and compared with regards to antimicrobial activity and cytotoxicity in particular. The most promising amphiphile 10f displayed minimum inhibitory concentrations (MICs) between 4-16µg/mL against Gram-positive Enterococcus faecalis, Staphylococcus aureus, Streptococcus agalacticae, and Gram-negative Escherichia coli and Pseudomonas aeruginosa. The decent level of antimicrobial activity and biofilm inhibition, short synthesis, and accessible reagents, makes this type of amphiphilic mimics interesting leads for further development.
[Mh] Termos MeSH primário: Alquinos/química
Antibacterianos/farmacologia
Butiratos/química
Propionatos/química
Tensoativos/farmacologia
Triazóis/farmacologia
[Mh] Termos MeSH secundário: Antibacterianos/síntese química
Antibacterianos/química
Relação Dose-Resposta a Droga
Enterococcus faecalis/efeitos dos fármacos
Escherichia coli/efeitos dos fármacos
Testes de Sensibilidade Microbiana
Estrutura Molecular
Peptidomiméticos
Pseudomonas aeruginosa/efeitos dos fármacos
Staphylococcus/efeitos dos fármacos
Relação Estrutura-Atividade
Tensoativos/síntese química
Tensoativos/química
Triazóis/síntese química
Triazóis/química
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Alkynes); 0 (Anti-Bacterial Agents); 0 (Butyrates); 0 (Peptidomimetics); 0 (Propionates); 0 (Surface-Active Agents); 0 (Triazoles); P2QW39G9LZ (propiolic acid)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171107
[Lr] Data última revisão:
171107
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170812
[St] Status:MEDLINE


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[PMID]:28731268
[Au] Autor:Zhang M; Yu XW; Xu Y; Jouhten P; Swapna GVT; Glaser RW; Hunt JF; Montelione GT; Maaheimo H; Szyperski T
[Ad] Endereço:School of Biotechnology, Key Laboratory of Industrial Biotechnology, State Key Laboratory of Food Science and Technology, Ministry of Education, Jiangnan University, Wuxi, China.
[Ti] Título: C metabolic flux profiling of Pichia pastoris grown in aerobic batch cultures on glucose revealed high relative anabolic use of TCA cycle and limited incorporation of provided precursors of branched-chain amino acids.
[So] Source:FEBS J;284(18):3100-3113, 2017 Sep.
[Is] ISSN:1742-4658
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Carbon metabolism of Crabtree-negative yeast Pichia pastoris was profiled using C nuclear magnetic resonance (NMR) to delineate regulation during exponential growth and to study the import of two precursors for branched-chain amino acid biosynthesis, α-ketoisovalerate and α-ketobutyrate. Cells were grown in aerobic batch cultures containing (a) only glucose, (b) glucose along with the precursors, or (c) glucose and Val. The study provided the following new insights. First, C flux ratio analyses of central metabolism reveal an unexpectedly high anaplerotic supply of the tricarboxylic acid cycle for a Crabtree-negative yeast, and show that a substantial fraction of glucose catabolism proceeds through the pentose phosphate pathway. A comparison with previous flux ratio analyses for batch cultures of Crabtree-negative Pichia stipitis and Crabtree-positive Saccharomyces cerevisiae indicate that the overall regulation of central carbon metabolism in P. pastoris is intermediate in between P. stipitis and S. cerevisiae. Second, excess α-ketoisovalerate in the medium is not transported into the cytoplasm indicating that P. pastoris lacks a suitable transporter. In contrast, excess Val is efficiently taken up and largely fulfills demands for both Val and Leu for protein synthesis. Third, excess α-ketobutyrate is transported into the mitochondria for Ile biosynthesis. However, the import does not efficiently inhibit the synthesis of α-ketobutyrate from pyruvate indicating that P. pastoris has not been optimized evolutionarily to take full advantage of this carbon source. These findings have direct implications for preparing uniformly H, C, N-labeled proteins containing protonated Ile, Val, and Leu methyl groups in P. pastoris for NMR-based structural biology. ENZYMES: Acetohydroxy acid isomeroreductase (EC 1.1.1.86), branched-chain amino acid aminotransferase (BCAT, EC 2.6.1.42), fumarase (EC 4.2.1.2), malic enzyme (EC 1.1.1.39/1.1.1.40), phosphoenolpyruvate carboxykinase (EC 4.1.1.49), pyruvate carboxylase (EC 6.4.1.1), pyruvate kinase (EC 2.7.1.40), l-serine hydroxymethyltransferase (EC 2.1.2.1), threonine aldolase (EC 4.1.2.5), threonine dehydratase (EC 4.3.1.19); transketolase (EC 2.2.1.1), transaldolase (EC 2.2.1.2).
[Mh] Termos MeSH primário: Glucose/metabolismo
Isoleucina/metabolismo
Leucina/metabolismo
Metaboloma/fisiologia
Pichia/metabolismo
Valina/metabolismo
[Mh] Termos MeSH secundário: Aerobiose/fisiologia
Técnicas de Cultura Celular por Lotes
Butiratos/metabolismo
Isótopos de Carbono
Ciclo do Ácido Cítrico/fisiologia
Cetoácidos/metabolismo
Espectroscopia de Ressonância Magnética
Mitocôndrias/metabolismo
Via de Pentose Fosfato/fisiologia
Ácido Pirúvico/metabolismo
Saccharomyces cerevisiae/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Butyrates); 0 (Carbon Isotopes); 0 (Keto Acids); 04Y7590D77 (Isoleucine); 600-18-0 (alpha-ketobutyric acid); 759-05-7 (alpha-ketoisovalerate); 8558G7RUTR (Pyruvic Acid); GMW67QNF9C (Leucine); HG18B9YRS7 (Valine); IY9XDZ35W2 (Glucose)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171004
[Lr] Data última revisão:
171004
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170722
[St] Status:MEDLINE
[do] DOI:10.1111/febs.14180



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