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[PMID]:28853885
[Au] Autor:Huard K; Ahn K; Amor P; Beebe DA; Borzilleri KA; Chrunyk BA; Coffey SB; Cong Y; Conn EL; Culp JS; Dowling MS; Gorgoglione MF; Gutierrez JA; Knafels JD; Lachapelle EA; Pandit J; Parris KD; Perez S; Pfefferkorn JA; Price DA; Raymer B; Ross TT; Shavnya A; Smith AC; Subashi TA; Tesz GJ; Thuma BA; Tu M; Weaver JD; Weng Y; Withka JM; Xing G; Magee TV
[Ad] Endereço:Medicine Design, Pfizer Inc. , 1 Portland Street, Cambridge, Massachusetts 02139, United States.
[Ti] Título:Discovery of Fragment-Derived Small Molecules for in Vivo Inhibition of Ketohexokinase (KHK).
[So] Source:J Med Chem;60(18):7835-7849, 2017 Sep 28.
[Is] ISSN:1520-4804
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Increased fructose consumption and its subsequent metabolism have been implicated in hepatic steatosis, dyslipidemia, obesity, and insulin resistance in humans. Since ketohexokinase (KHK) is the principal enzyme responsible for fructose metabolism, identification of a selective KHK inhibitor may help to further elucidate the effect of KHK inhibition on these metabolic disorders. Until now, studies on KHK inhibition with small molecules have been limited due to the lack of viable in vivo pharmacological tools. Herein we report the discovery of 12, a selective KHK inhibitor with potency and properties suitable for evaluating KHK inhibition in rat models. Key structural features interacting with KHK were discovered through fragment-based screening and subsequent optimization using structure-based drug design, and parallel medicinal chemistry led to the identification of pyridine 12.
[Mh] Termos MeSH primário: Desenho de Drogas
Frutoquinases/antagonistas & inibidores
Inibidores de Proteínas Quinases/química
Inibidores de Proteínas Quinases/farmacologia
Bibliotecas de Moléculas Pequenas/química
Bibliotecas de Moléculas Pequenas/farmacologia
[Mh] Termos MeSH secundário: Animais
Cristalografia por Raios X
Frutoquinases/química
Frutoquinases/metabolismo
Seres Humanos
Masculino
Simulação de Acoplamento Molecular
Piridinas/química
Piridinas/farmacologia
Ratos
Ratos Sprague-Dawley
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Protein Kinase Inhibitors); 0 (Pyridines); 0 (Small Molecule Libraries); EC 2.7.1.- (Fructokinases); EC 2.7.1.3 (ketohexokinase)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171016
[Lr] Data última revisão:
171016
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170831
[St] Status:MEDLINE
[do] DOI:10.1021/acs.jmedchem.7b00947


  2 / 221 MEDLINE  
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[PMID]:28441933
[Au] Autor:Riggs JW; Cavales PC; Chapiro SM; Callis J
[Ad] Endereço:Department of Molecular and Cellular Biology, College of Biological Sciences, University of California, 1 Shields Ave, Davis, CA, 95616, USA.
[Ti] Título:Identification and biochemical characterization of the fructokinase gene family in Arabidopsis thaliana.
[So] Source:BMC Plant Biol;17(1):83, 2017 Apr 26.
[Is] ISSN:1471-2229
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Fructose is an abundant sugar in plants as it is a breakdown product of both major sucrose-cleaving enzymes. To enter metabolism, fructose is phosphorylated by a fructokinase (FRK). Known FRKs are members of a diverse family of carbohydrate/purine kinases known as the phosphofructokinase B (pfkB) family. The complete complement of active fructokinases has not been reported for any plant species. RESULTS: Protein sequence analysis of the 22 Arabidopsis thaliana pfkB members identified eight highly related predicted proteins, including one with previously demonstrated FRK activity. For one, At1g50390, the predicted open reading frame is half the size of active FRKs, and only incompletely spliced RNAs were identified, which led to a premature stop codon, both indicating that this gene does not produce active FRK. The remaining seven proteins were expressed in E. coli and phosphorylated fructose specifically in vitro leading us to propose a unifying nomenclature (FRK1-7). Substrate inhibition was observed for fructose in all FRKs except FRK1. Fructose binding was on the same order of magnitude for FRK1-6, between 260 and 480 µM. FRK7 was an outlier with a fructose Km of 12 µM. ATP binding was similar for all FRKs and ranged between 52 and 280 µM. YFP-tagged AtFRKs were cytosolic, except plastidic FRK3. T-DNA alleles with non-detectable wild-type RNAs in five of the seven active FRK genes produced no overt phenotype. We extended our sequence comparisons to include putative FRKs encoded in other plant sequenced genomes. We observed that different subgroups expanded subsequent to speciation. CONCLUSIONS: Arabidopsis thaliana as well as all other plant species analyzed contain multiple copies of genes encoding FRK activity. Sequence comparisons among multiple species identified a minimal set of three distinct FRKs present on all species investigated including a plastid-localized form. The selective expansion of specific isozymes results in differences in FRK gene number among species. AtFRKs exhibit substrate inhibition, typical of their mammalian counterparts with the single AtFRK1 lacking this property, suggesting it may have a distinct in vivo role. Results presented here provide a starting point for the engineering of specific FRKs to affect biomass production.
[Mh] Termos MeSH primário: Arabidopsis/genética
Frutoquinases/genética
Genes de Plantas
Proteínas de Plantas/genética
[Mh] Termos MeSH secundário: Arabidopsis/enzimologia
DNA Bacteriano
Frutoquinases/metabolismo
Frutose/metabolismo
Genoma de Planta
Isoenzimas/genética
Família Multigênica
Mutagênese Insercional
Fosforilação
Proteínas de Plantas/metabolismo
Especificidade da Espécie
Especificidade por Substrato
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (DNA, Bacterial); 0 (Isoenzymes); 0 (Plant Proteins); 0 (T-DNA); 30237-26-4 (Fructose); EC 2.7.1.- (Fructokinases)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171108
[Lr] Data última revisão:
171108
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170427
[St] Status:MEDLINE
[do] DOI:10.1186/s12870-017-1031-5


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[PMID]:28336548
[Au] Autor:Kishida K; Pearce SC; Yu S; Gao N; Ferraris RP
[Ad] Endereço:Department of Pharmacology, Physiology and Neurosciences, New Jersey Medical School, Rutgers University, Newark, New Jersey; and.
[Ti] Título:Nutrient sensing by absorptive and secretory progenies of small intestinal stem cells.
[So] Source:Am J Physiol Gastrointest Liver Physiol;312(6):G592-G605, 2017 Jun 01.
[Is] ISSN:1522-1547
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Nutrient sensing triggers responses by the gut-brain axis modulating hormone release, feeding behavior and metabolism that become dysregulated in metabolic syndrome and some cancers. Except for absorptive enterocytes and secretory enteroendocrine cells, the ability of many intestinal cell types to sense nutrients is still unknown; hence we hypothesized that progenitor stem cells (intestinal stem cells, ISC) possess nutrient sensing ability inherited by progenies during differentiation. We directed via modulators of Wnt and Notch signaling differentiation of precursor mouse intestinal crypts into specialized organoids each containing ISC, enterocyte, goblet, or Paneth cells at relative proportions much higher than in situ as determined by mRNA expression and immunocytochemistry of cell type biomarkers. We identified nutrient sensing cell type(s) by increased expression of fructolytic genes in response to a fructose challenge. Organoids comprised primarily of enterocytes, Paneth, or goblet, but not ISC, cells responded specifically to fructose without affecting nonfructolytic genes. Sensing was independent of Wnt and Notch modulators and of glucose concentrations in the medium but required fructose absorption and metabolism. More mature enterocyte- and goblet-enriched organoids exhibited stronger fructose responses. Remarkably, enterocyte organoids, upon forced dedifferentiation to reacquire ISC characteristics, exhibited a markedly extended lifespan and retained fructose sensing ability, mimicking responses of some dedifferentiated cancer cells. Using an innovative approach, we discovered that nutrient sensing is likely repressed in progenitor ISCs then irreversibly derepressed during specification into sensing-competent absorptive or secretory lineages, the surprising capacity of Paneth and goblet cells to detect fructose, and the important role of differentiation in modulating nutrient sensing. Small intestinal stem cells differentiate into several cell types transiently populating the villi. We used specialized organoid cultures each comprised of a single cell type to demonstrate that ) differentiation seems required for nutrient sensing, ) secretory goblet and Paneth cells along with enterocytes sense fructose, suggesting that sensing is acquired after differentiation is triggered but before divergence between absorptive and secretory lineages, and ) forcibly dedifferentiated enterocytes exhibit fructose sensing and lifespan extension.
[Mh] Termos MeSH primário: Diferenciação Celular
Linhagem da Célula
Frutose/metabolismo
Absorção Intestinal
Mucosa Intestinal/metabolismo
Secreções Intestinais/metabolismo
Intestino Delgado/metabolismo
Células-Tronco/metabolismo
[Mh] Termos MeSH secundário: Animais
Células Cultivadas
Enterócitos/metabolismo
Enterócitos/secreção
Frutoquinases/genética
Frutoquinases/metabolismo
Regulação Enzimológica da Expressão Gênica
Genótipo
Proteínas Facilitadoras de Transporte de Glucose/genética
Proteínas Facilitadoras de Transporte de Glucose/metabolismo
Células Caliciformes/metabolismo
Células Caliciformes/secreção
Mucosa Intestinal/citologia
Mucosa Intestinal/secreção
Secreções Intestinais/secreção
Intestino Delgado/citologia
Intestino Delgado/secreção
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Organoides/metabolismo
Organoides/secreção
Celulas de Paneth/metabolismo
Celulas de Paneth/secreção
Fenótipo
Transdução de Sinais
Células-Tronco/secreção
Fatores de Tempo
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Glucose Transport Proteins, Facilitative); 0 (Slc2a5 protein, mouse); 30237-26-4 (Fructose); EC 2.7.1.- (Fructokinases); EC 2.7.1.3 (ketohexokinase)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170811
[Lr] Data última revisão:
170811
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170325
[St] Status:MEDLINE
[do] DOI:10.1152/ajpgi.00416.2016


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[PMID]:28241431
[Au] Autor:Iizuka K
[Ad] Endereço:Department of Diabetes and Endocrinology, Graduate School of Medicine, Gifu University, Gifu 501-1194, Japan. kiizuka@gifu-u.ac.jp.
[Ti] Título:The Role of Carbohydrate Response Element Binding Protein in Intestinal and Hepatic Fructose Metabolism.
[So] Source:Nutrients;9(2), 2017 Feb 22.
[Is] ISSN:2072-6643
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:Many articles have discussed the relationship between fructose consumption and the incidence of obesity and related diseases. Fructose is absorbed in the intestine and metabolized in the liver to glucose, lactate, glycogen, and, to a lesser extent, lipids. Unabsorbed fructose causes bacterial fermentation, resulting in irritable bowl syndrome. Therefore, understanding the mechanisms underlying intestinal and hepatic fructose metabolism is important for the treatment of metabolic syndrome and fructose malabsorption. Carbohydrate response element binding protein (ChREBP) is a glucose-activated transcription factor that controls approximately 50% of de novo lipogenesis in the liver. ChREBP target genes are involved in glycolysis (Glut2, liver pyruvate kinase), fructolysis (Glut5, ketohexokinase), and lipogenesis (acetyl CoA carboxylase, fatty acid synthase). ChREBP gene deletion protects against high sucrose diet-induced and leptin-deficient obesity, because mice cannot consume fructose or sucrose. Moreover, ChREBP contributes to some of the physiological effects of fructose on sweet taste preference and glucose production through regulation of ChREBP target genes, such as fibroblast growth factor-21 and glucose-6-phosphatase catalytic subunits. Thus, ChREBP might play roles in fructose metabolism. Restriction of excess fructose intake will be beneficial for preventing not only metabolic syndrome but also irritable bowl syndrome.
[Mh] Termos MeSH primário: Fatores de Transcrição de Zíper de Leucina e Hélice-Alça-Hélix Básicos/fisiologia
Frutose/metabolismo
Intestinos/metabolismo
Fígado/metabolismo
[Mh] Termos MeSH secundário: Animais
Frutoquinases/genética
Frutose/efeitos adversos
Expressão Gênica/fisiologia
Transportador de Glucose Tipo 5/genética
Glicólise/genética
Glicólise/fisiologia
Seres Humanos
Absorção Intestinal/fisiologia
Síndrome do Intestino Irritável/etiologia
Síndrome do Intestino Irritável/prevenção & controle
Lipogênese/genética
Lipogênese/fisiologia
Síndrome Metabólica/etiologia
Síndrome Metabólica/prevenção & controle
Camundongos
Camundongos Knockout
Proteínas Nucleares/deficiência
Proteínas Nucleares/genética
Proteínas Nucleares/fisiologia
Fatores de Transcrição/deficiência
Fatores de Transcrição/genética
Fatores de Transcrição/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Basic Helix-Loop-Helix Leucine Zipper Transcription Factors); 0 (Glucose Transporter Type 5); 0 (MLXIPL protein, human); 0 (Mlxipl protein, mouse); 0 (Nuclear Proteins); 0 (Transcription Factors); 30237-26-4 (Fructose); EC 2.7.1.- (Fructokinases); EC 2.7.1.3 (ketohexokinase)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170301
[St] Status:MEDLINE


  5 / 221 MEDLINE  
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[PMID]:28222695
[Au] Autor:Chen Y; Zhang Q; Hu W; Zhang X; Wang L; Hua X; Yu Q; Ming R; Zhang J
[Ad] Endereço:Center for Genomics and Biotechnology, Fujian Provincial Key Laboratory of Haixia Applied Plant Systems Biology, Haixia Institute of Science and Technology (HIST), Fujian Agriculture and Forestry University, Fuzhou, 350002, China.
[Ti] Título:Evolution and expression of the fructokinase gene family in Saccharum.
[So] Source:BMC Genomics;18(1):197, 2017 Feb 21.
[Is] ISSN:1471-2164
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Sugarcane is an important sugar crop contributing up to about 80% of the world sugar production. Efforts to characterize the genes involved in sugar metabolism at the molecular level are growing since increasing sugar content is a major goal in the breeding of new sugarcane varieties. Fructokinases (FRK) are the main fructose phosphorylating enzymes with high substrate specificity and affinity. RESULTS: In this study, by combining comparative genomics approaches with BAC resources, seven fructokinase genes were identified in S. spontaneum. Phylogenetic analysis based on representative monocotyledon and dicotyledon plant species suggested that the FRK gene family is ancient and its evolutionary history can be traced in duplicated descending order: SsFRK4, SsFRK6/SsFRK7,SsFRK5, SsFRK3 and SsFRK1/SsFRK2. Among the close orthologs, the number and position of exons in FRKs were conserved; in contrast, the size of introns varied among the paralogous FRKs in Saccharum. Genomic constraints were analyzed within the gene alleles and between S. spontaneum and Sorghum bicolor, and gene expression analysis was performed under drought stress and with exogenous applications of plant hormones. FRK1, which was under strong functional constraint selection, was conserved among the gene allelic haplotypes, and displayed dominant expression levels among the gene families in the control conditions, suggesting that FRK1 plays a major role in the phosphorylation of fructose. FRK3 and FRK5 were dramatically induced under drought stress, and FRK5 was also found to increase its expression levels in the mature stage of Saccharum. Similarly, FRK3 and FRK5 were induced in response to drought stress in Saccharum. FRK2 and FRK7 displayed lower expression levels than the other FRK family members; FRK2 was under strong genomic selection constraints whereas FRK7 was under neutral selection. FRK7 may have become functionally redundant in Saccharum through pseudogenization. FRK4 and FRK6 shared the most similar expression pattern: FRK4 was revealed to have higher expression levels in mature tissues than in premature tissues of Saccharum, and FRK6 presented a slight increase under drought stress. CONCLUSIONS: Our study presents a comprehensive genomic study of the entire FRK gene family in Saccharum, providing the foundations for approaches to characterize the molecular mechanism regulated by the SsFRK family in sugarcane.
[Mh] Termos MeSH primário: Evolução Molecular
Frutoquinases/genética
Regulação da Expressão Gênica de Plantas
Família Multigênica
Saccharum/genética
[Mh] Termos MeSH secundário: Alelos
Sequência de Aminoácidos
Sequência Conservada
Éxons
Frutoquinases/química
Haplótipos
Íntrons
Filogenia
Domínios Proteicos/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
EC 2.7.1.- (Fructokinases); EC 2.7.1.4 (fructokinase)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170911
[Lr] Data última revisão:
170911
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170223
[St] Status:MEDLINE
[do] DOI:10.1186/s12864-017-3535-7


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[PMID]:28034722
[Au] Autor:Oppelt SA; Zhang W; Tolan DR
[Ad] Endereço:Program in Molecular Biology, Cell Biology, and Biochemistry, Boston University, 5 Cummington Mall, Boston, MA, USA.
[Ti] Título:Specific regions of the brain are capable of fructose metabolism.
[So] Source:Brain Res;1657:312-322, 2017 Feb 15.
[Is] ISSN:1872-6240
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:High fructose consumption in the Western diet correlates with disease states such as obesity and metabolic syndrome complications, including type II diabetes, chronic kidney disease, and non-alcoholic fatty acid liver disease. Liver and kidneys are responsible for metabolism of 40-60% of ingested fructose, while the physiological fate of the remaining fructose remains poorly understood. The primary metabolic pathway for fructose includes the fructose-transporting solute-like carrier transport proteins 2a (SLC2a or GLUT), including GLUT5 and GLUT9, ketohexokinase (KHK), and aldolase. Bioinformatic analysis of gene expression encoding these proteins (glut5, glut9, khk, and aldoC, respectively) identifies other organs capable of this fructose metabolism. This analysis predicts brain, lymphoreticular tissue, placenta, and reproductive tissues as possible additional organs for fructose metabolism. While expression of these genes is highest in liver, the brain is predicted to have expression levels of these genes similar to kidney. RNA in situ hybridization of coronal slices of adult mouse brains validate the in silico expression of glut5, glut9, khk, and aldoC, and show expression across many regions of the brain, with the most notable expression in the cerebellum, hippocampus, cortex, and olfactory bulb. Dissected samples of these brain regions show KHK and aldolase enzyme activity 5-10 times the concentration of that in liver. Furthermore, rates of fructose oxidation in these brain regions are 15-150 times that of liver slices, confirming the bioinformatics prediction and in situ hybridization data. This suggests that previously unappreciated regions across the brain can use fructose, in addition to glucose, for energy production.
[Mh] Termos MeSH primário: Encéfalo/metabolismo
Frutose/metabolismo
[Mh] Termos MeSH secundário: Análise de Variância
Animais
Western Blotting
Biologia Computacional
Frutoquinases/metabolismo
Frutose-Bifosfato Aldolase/metabolismo
Expressão Gênica
Proteínas Facilitadoras de Transporte de Glucose/metabolismo
Hexoquinase/metabolismo
Hibridização In Situ
Fígado/metabolismo
Masculino
Camundongos Endogâmicos C57BL
Oxirredução
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Glucose Transport Proteins, Facilitative); 0 (Slc2a5 protein, mouse); 0 (Slc2a9 protein, mouse); 30237-26-4 (Fructose); EC 2.7.1.- (Fructokinases); EC 2.7.1.1 (Hexokinase); EC 2.7.1.3 (ketohexokinase); EC 4.1.2.13 (Fructose-Bisphosphate Aldolase)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170807
[Lr] Data última revisão:
170807
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161231
[St] Status:MEDLINE


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[PMID]:28003190
[Au] Autor:Roncal-Jimenez CA; Milagres T; Andres-Hernando A; Kuwabara M; Jensen T; Song Z; Bjornstad P; Garcia GE; Sato Y; Sanchez-Lozada LG; Lanaspa MA; Johnson RJ
[Ad] Endereço:Division of Renal Diseases and Hypertension, University of Colorado, Aurora, Colorado.
[Ti] Título:Effects of exogenous desmopressin on a model of heat stress nephropathy in mice.
[So] Source:Am J Physiol Renal Physiol;312(3):F418-F426, 2017 Mar 01.
[Is] ISSN:1522-1466
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Recurrent heat stress and dehydration have recently been shown experimentally to cause chronic kidney disease (CKD). One potential mediator may be vasopressin, acting via the type 2 vasopressin receptor (V receptor). We tested the hypothesis that desmopressin accelerates CKD in mice subjected to heat stress and recurrent dehydration. Recurrent exposure to heat with limited water availability was performed in male mice over a 5-wk period, with one group receiving desmopressin two times daily and the other group receiving vehicle. Two additional control groups were not exposed to heat or dehydration and received vehicle or desmopressin. The effects of the treatment on renal injury were assessed. Heat stress and recurrent dehydration induced functional changes (albuminuria, elevated urinary neutrophil gelatinase-associated protein), glomerular changes (mesangiolysis, matrix expansion), and tubulointerstitial changes (fibrosis, inflammation). Desmopressin also induced albuminuria, glomerular changes, and tubulointerstitial fibrosis in normal animals and also exacerbated injury in mice with heat stress nephropathy. Both heat stress and/or desmopressin were also associated with activation of the polyol pathway in the renal cortex, likely due to increased interstitial osmolarity. Our studies document both glomerular and tubulointerstitial injury and inflammation in heat stress nephropathy and may be clinically relevant to the pathogenesis of Mesoamerican nephropathy. Our data also suggest that vasopressin may play a role in the pathogenesis of the renal injury of heat stress nephropathy, likely via a V receptor-dependent pathway.
[Mh] Termos MeSH primário: Desamino Arginina Vasopressina/toxicidade
Desidratação/complicações
Desidratação/tratamento farmacológico
Transtornos de Estresse por Calor/complicações
Rim/efeitos dos fármacos
Insuficiência Renal Crônica/induzido quimicamente
[Mh] Termos MeSH secundário: Albuminúria/induzido quimicamente
Albuminúria/fisiopatologia
Aldeído Redutase/metabolismo
Amônia/metabolismo
Animais
Biomarcadores/sangue
Nitrogênio da Ureia Sanguínea
Ativação do Complemento/efeitos dos fármacos
Creatinina/sangue
Desamino Arginina Vasopressina/administração & dosagem
Desidratação/patologia
Desidratação/fisiopatologia
Modelos Animais de Doenças
Fibrose
Frutoquinases/metabolismo
Transtornos de Estresse por Calor/patologia
Transtornos de Estresse por Calor/fisiopatologia
Rim/metabolismo
Rim/patologia
Rim/fisiopatologia
Masculino
Camundongos Endogâmicos C57BL
Receptores de Vasopressinas/agonistas
Receptores de Vasopressinas/metabolismo
Insuficiência Renal Crônica/patologia
Insuficiência Renal Crônica/fisiopatologia
Fatores de Risco
Equilíbrio Hidroeletrolítico/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (Receptors, Vasopressin); 7664-41-7 (Ammonia); AYI8EX34EU (Creatinine); EC 1.1.1.21 (Aldehyde Reductase); EC 2.7.1.- (Fructokinases); EC 2.7.1.4 (fructokinase); ENR1LLB0FP (Deamino Arginine Vasopressin)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170713
[Lr] Data última revisão:
170713
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161223
[St] Status:MEDLINE
[do] DOI:10.1152/ajprenal.00495.2016


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[PMID]:27852737
[Au] Autor:Song 宋志林 Z; Roncal-Jimenez CA; Lanaspa-Garcia MA; Oppelt SA; Kuwabara M; Jensen T; Milagres T; Andres-Hernando A; Ishimoto T; Garcia GE; Johnson G; MacLean PS; Sanchez-Lozada LG; Tolan DR; Johnson RJ
[Ad] Endereço:Division of Renal Diseases and Hypertension, Department of Medicine, University of Colorado, Aurora, Colorado; Zhilin.song@ucdenver.edu.
[Ti] Título:Role of fructose and fructokinase in acute dehydration-induced vasopressin gene expression and secretion in mice.
[So] Source:J Neurophysiol;117(2):646-654, 2017 Feb 01.
[Is] ISSN:1522-1598
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Fructose stimulates vasopressin in humans and can be generated endogenously by activation of the polyol pathway with hyperosmolarity. We hypothesized that fructose metabolism in the hypothalamus might partly control vasopressin responses after acute dehydration. Wild-type and fructokinase-knockout mice were deprived of water for 24 h. The supraoptic nucleus was evaluated for vasopressin and markers of the aldose reductase-fructokinase pathway. The posterior pituitary vasopressin and serum copeptin levels were examined. Hypothalamic explants were evaluated for vasopressin secretion in response to exogenous fructose. Water restriction increased serum and urine osmolality and serum copeptin in both groups of mice, although the increase in copeptin in wild-type mice was larger than that in fructokinase-knockout mice. Water-restricted, wild-type mice showed an increase in vasopressin and aldose reductase mRNA, sorbitol, fructose and uric acid in the supraoptic nucleus. In contrast, fructokinase-knockout mice showed no change in vasopressin or aldose reductase mRNA, and no changes in sorbitol or uric acid, although fructose levels increased. With water restriction, vasopressin in the pituitary of wild-type mice was significantly less than that of fructokinase-knockout mice, indicating that fructokinase-driven vasopressin secretion overrode synthesis. Fructose increased vasopressin release in hypothalamic explants that was not observed in fructokinase-knockout mice. In situ hybridization documented fructokinase mRNA in the supraoptic nucleus, paraventricular nucleus and suprachiasmatic nucleus. Acute dehydration activates the aldose reductase-fructokinase pathway in the hypothalamus and partly drives the vasopressin response. Exogenous fructose increases vasopressin release in hypothalamic explants dependent on fructokinase. Nevertheless, circulating vasopressin is maintained and urinary concentrating is not impaired. NEW & NOTEWORTHY: This study increases our understanding of the mechanisms leading to vasopressin release under conditions of water restriction (acute dehydration). Specifically, these studies suggest that the aldose reductase-fructokinase pathways may be involved in vasopressin synthesis in the hypothalamus and secretion by the pituitary in response to acute dehydration. Nevertheless, mice undergoing water restriction remain capable of maintaining sufficient vasopressin (copeptin) levels to allow normal urinary concentration. Further studies of the aldose reductase-fructokinase system in vasopressin regulation appear indicated.
[Mh] Termos MeSH primário: Desidratação/fisiopatologia
Frutoquinases/deficiência
Frutose/farmacologia
Regulação da Expressão Gênica
Hipotálamo
Vasopressinas/metabolismo
Vasopressinas/secreção
[Mh] Termos MeSH secundário: Análise de Variância
Animais
Ensaio de Imunoadsorção Enzimática
Frutoquinases/genética
Regulação da Expressão Gênica/efeitos dos fármacos
Regulação da Expressão Gênica/genética
Regulação da Expressão Gênica/fisiologia
Temperatura Alta/efeitos adversos
Hipotálamo/efeitos dos fármacos
Hipotálamo/metabolismo
Hipotálamo/secreção
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Técnicas de Cultura de Órgãos
RNA Mensageiro/metabolismo
Fatores de Tempo
Vasopressinas/genética
Privação de Água
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (RNA, Messenger); 11000-17-2 (Vasopressins); 30237-26-4 (Fructose); EC 2.7.1.- (Fructokinases); EC 2.7.1.4 (fructokinase)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170920
[Lr] Data última revisão:
170920
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161118
[St] Status:MEDLINE
[do] DOI:10.1152/jn.00781.2016


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[PMID]:27465991
[Au] Autor:Roncal-Jimenez CA; Ishimoto T; Lanaspa MA; Milagres T; Hernando AA; Jensen T; Miyazaki M; Doke T; Hayasaki T; Nakagawa T; Marumaya S; Long DA; Garcia GE; Kuwabara M; Sánchez-Lozada LG; Kang DH; Johnson RJ
[Ad] Endereço:Division of Renal Diseases and Hypertension, University of Colorado, Aurora, Colorado; carlos.roncal@ucdenver.edu.
[Ti] Título:Aging-associated renal disease in mice is fructokinase dependent.
[So] Source:Am J Physiol Renal Physiol;311(4):F722-F730, 2016 Oct 01.
[Is] ISSN:1522-1466
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Aging-associated kidney disease is usually considered a degenerative process associated with aging. Recently, it has been shown that animals can produce fructose endogenously, and that this can be a mechanism for causing kidney damage in diabetic nephropathy and in association with recurrent dehydration. We therefore hypothesized that low-level metabolism of endogenous fructose might play a role in aging-associated kidney disease. Wild-type and fructokinase knockout mice were fed a normal diet for 2 yr that had minimal (<5%) fructose content. At the end of 2 yr, wild-type mice showed elevations in systolic blood pressure, mild albuminuria, and glomerular changes with mesangial matrix expansion, variable mesangiolysis, and segmental thrombi. The renal injury was amplified by provision of high-salt diet for 3 wk, as noted by the presence of glomerular hypertrophy, mesangial matrix expansion, and alpha smooth muscle actin expression, and with segmental thrombi. Fructokinase knockout mice were protected from renal injury both at baseline and after high salt intake (3 wk) compared with wild-type mice. This was associated with higher levels of active (phosphorylated serine 1177) endothelial nitric oxide synthase in their kidneys. These studies suggest that aging-associated renal disease might be due to activation of specific metabolic pathways that could theoretically be targeted therapeutically, and raise the hypothesis that aging-associated renal injury may represent a disease process as opposed to normal age-related degeneration.
[Mh] Termos MeSH primário: Envelhecimento/metabolismo
Albuminúria/metabolismo
Frutoquinases/metabolismo
Nefropatias/metabolismo
Rim/metabolismo
[Mh] Termos MeSH secundário: Envelhecimento/patologia
Albuminúria/genética
Albuminúria/patologia
Animais
Pressão Sanguínea/fisiologia
Creatinina/sangue
Frutoquinases/genética
Rim/patologia
Nefropatias/genética
Nefropatias/patologia
Lipocalina-2/urina
Camundongos
Camundongos Knockout
Óxido Nítrico Sintase Tipo III/metabolismo
Fosforilação
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Lipocalin-2); 126469-30-5 (Lcn2 protein, mouse); AYI8EX34EU (Creatinine); EC 1.14.13.39 (Nitric Oxide Synthase Type III); EC 2.7.1.- (Fructokinases); EC 2.7.1.4 (fructokinase)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:171001
[Lr] Data última revisão:
171001
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160729
[St] Status:MEDLINE
[do] DOI:10.1152/ajprenal.00306.2016


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[PMID]:27462084
[Au] Autor:Liu YH; Offler CE; Ruan YL
[Ad] Endereço:School of Environmental and Life Sciences and Australia-China Research Centre for Crop Science, The University of Newcastle, Callaghan, NSW, 2308, Australia (Y.-H.L., C.E.O., Y.-L.R.); and Institute of Vegetable Science, Zhejiang Academy of Agricultural Sciences, Hangzhou, 310021, China (Y.-H.L.).
[Ti] Título:Cell Wall Invertase Promotes Fruit Set under Heat Stress by Suppressing ROS-Independent Cell Death.
[So] Source:Plant Physiol;172(1):163-80, 2016 Sep.
[Is] ISSN:1532-2548
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Reduced cell wall invertase (CWIN) activity has been shown to be associated with poor seed and fruit set under abiotic stress. Here, we examined whether genetically increasing native CWIN activity would sustain fruit set under long-term moderate heat stress (LMHS), an important factor limiting crop production, by using transgenic tomato (Solanum lycopersicum) with its CWIN inhibitor gene silenced and focusing on ovaries and fruits at 2 d before and after pollination, respectively. We found that the increase of CWIN activity suppressed LMHS-induced programmed cell death in fruits. Surprisingly, measurement of the contents of H2O2 and malondialdehyde and the activities of a cohort of antioxidant enzymes revealed that the CWIN-mediated inhibition on programmed cell death is exerted in a reactive oxygen species-independent manner. Elevation of CWIN activity sustained Suc import into fruits and increased activities of hexokinase and fructokinase in the ovaries in response to LMHS Compared to the wild type, the CWIN-elevated transgenic plants exhibited higher transcript levels of heat shock protein genes Hsp90 and Hsp100 in ovaries and HspII17.6 in fruits under LMHS, which corresponded to a lower transcript level of a negative auxin responsive factor IAA9 but a higher expression of the auxin biosynthesis gene ToFZY6 in fruits at 2 d after pollination. Collectively, the data indicate that CWIN enhances fruit set under LMHS through suppression of programmed cell death in a reactive oxygen species-independent manner that could involve enhanced Suc import and catabolism, HSP expression, and auxin response and biosynthesis.
[Mh] Termos MeSH primário: Parede Celular/enzimologia
Frutas/enzimologia
Proteínas de Plantas/metabolismo
Espécies Reativas de Oxigênio/metabolismo
beta-Frutofuranosidase/metabolismo
[Mh] Termos MeSH secundário: Apoptose/genética
Catalase/genética
Catalase/metabolismo
Flores/genética
Flores/metabolismo
Frutoquinases/genética
Frutoquinases/metabolismo
Frutas/genética
Regulação da Expressão Gênica de Plantas
Proteínas de Choque Térmico/genética
Proteínas de Choque Térmico/metabolismo
Hexoquinase/genética
Hexoquinase/metabolismo
Temperatura Alta
Peróxido de Hidrogênio/metabolismo
Lycopersicon esculentum/enzimologia
Lycopersicon esculentum/genética
Lycopersicon esculentum/metabolismo
Malondialdeído/metabolismo
Proteínas de Plantas/genética
Plantas Geneticamente Modificadas
Interferência de RNA
Reação em Cadeia da Polimerase Via Transcriptase Reversa
Estresse Fisiológico
beta-Frutofuranosidase/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Heat-Shock Proteins); 0 (Plant Proteins); 0 (Reactive Oxygen Species); 4Y8F71G49Q (Malondialdehyde); BBX060AN9V (Hydrogen Peroxide); EC 1.11.1.6 (Catalase); EC 2.7.1.- (Fructokinases); EC 2.7.1.1 (Hexokinase); EC 2.7.1.4 (fructokinase); EC 3.2.1.26 (beta-Fructofuranosidase)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171006
[Lr] Data última revisão:
171006
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160728
[St] Status:MEDLINE
[do] DOI:10.1104/pp.16.00959



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