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[PMID]:28464795
[Au] Autor:Marandel L; Panserat S; Plagnes-Juan E; Arbenoits E; Soengas JL; Bobe J
[Ad] Endereço:INRA, UPPA, UMR 1419 Nutrition, Metabolism, Aquaculture, F-64310, Saint Pée sur Nivelle, France. lucie.marandel@inra.fr.
[Ti] Título:Evolutionary history of glucose-6-phosphatase encoding genes in vertebrate lineages: towards a better understanding of the functions of multiple duplicates.
[So] Source:BMC Genomics;18(1):342, 2017 05 02.
[Is] ISSN:1471-2164
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Glucose-6-phosphate (G6pc) is a key enzyme involved in the regulation of the glucose homeostasis. The present study aims at revisiting and clarifying the evolutionary history of g6pc genes in vertebrates. RESULTS: g6pc duplications happened by successive rounds of whole genome duplication that occurred during vertebrate evolution. g6pc duplicated before or around Osteichthyes/Chondrichthyes radiation, giving rise to g6pca and g6pcb as a consequence of the second vertebrate whole genome duplication. g6pca was lost after this duplication in Sarcopterygii whereas both g6pca and g6pcb then duplicated as a consequence of the teleost-specific whole genome duplication. One g6pca duplicate was lost after this duplication in teleosts. Similarly one g6pcb2 duplicate was lost at least in the ancestor of percomorpha. The analysis of the evolution of spatial expression patterns of g6pc genes in vertebrates showed that all g6pc were mainly expressed in intestine and liver whereas teleost-specific g6pcb2 genes were mainly and surprisingly expressed in brain and heart. g6pcb2b, one gene previously hypothesised to be involved in the glucose intolerant phenotype in trout, was unexpectedly up-regulated (as it was in liver) by carbohydrates in trout telencephalon without showing significant changes in other brain regions. This up-regulation is in striking contrast with expected glucosensing mechanisms suggesting that its positive response to glucose relates to specific unknown processes in this brain area. CONCLUSIONS: Our results suggested that the fixation and the divergence of g6pc duplicated genes during vertebrates' evolution may lead to adaptive novelty and probably to the emergence of novel phenotypes related to glucose homeostasis.
[Mh] Termos MeSH primário: Evolução Molecular
Glucose-6-Fosfatase/genética
Vertebrados/genética
[Mh] Termos MeSH secundário: Animais
Encéfalo/efeitos dos fármacos
Encéfalo/metabolismo
Carboidratos da Dieta/farmacologia
Regulação Enzimológica da Expressão Gênica/efeitos dos fármacos
Coração/efeitos dos fármacos
Seres Humanos
Miocárdio/metabolismo
Filogenia
Sintenia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Dietary Carbohydrates); EC 3.1.3.9 (Glucose-6-Phosphatase)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:180104
[Lr] Data última revisão:
180104
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170504
[St] Status:MEDLINE
[do] DOI:10.1186/s12864-017-3727-1


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[PMID]:29053971
[Au] Autor:Hebbandi Nanjundappa R; Ronchi F; Wang J; Clemente-Casares X; Yamanouchi J; Sokke Umeshappa C; Yang Y; Blanco J; Bassolas-Molina H; Salas A; Khan H; Slattery RM; Wyss M; Mooser C; Macpherson AJ; Sycuro LK; Serra P; McKay DM; McCoy KD; Santamaria P
[Ad] Endereço:Julia McFarlane Diabetes Research Centre (JMDRC), University of Calgary, Calgary AB T2N 4N1, Canada; Department of Microbiology, Immunology, and Infectious Diseases, Snyder Institute for Chronic Diseases, University of Calgary, Calgary AB T2N 4N1, Canada.
[Ti] Título:A Gut Microbial Mimic that Hijacks Diabetogenic Autoreactivity to Suppress Colitis.
[So] Source:Cell;171(3):655-667.e17, 2017 Oct 19.
[Is] ISSN:1097-4172
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The gut microbiota contributes to the development of normal immunity but, when dysregulated, can promote autoimmunity through various non-antigen-specific effects on pathogenic and regulatory lymphocytes. Here, we show that an integrase expressed by several species of the gut microbial genus Bacteroides encodes a low-avidity mimotope of the pancreatic ß cell autoantigen islet-specific glucose-6-phosphatase-catalytic-subunit-related protein (IGRP ). Studies in germ-free mice monocolonized with integrase-competent, integrase-deficient, and integrase-transgenic Bacteroides demonstrate that the microbial epitope promotes the recruitment of diabetogenic CD8+ T cells to the gut. There, these effectors suppress colitis by targeting microbial antigen-loaded, antigen-presenting cells in an integrin ß7-, perforin-, and major histocompatibility complex class I-dependent manner. Like their murine counterparts, human peripheral blood T cells also recognize Bacteroides integrase. These data suggest that gut microbial antigen-specific cytotoxic T cells may have therapeutic value in inflammatory bowel disease and unearth molecular mimicry as a novel mechanism by which the gut microbiota can regulate normal immune homeostasis. PAPERCLIP.
[Mh] Termos MeSH primário: Autoantígenos/imunologia
Bacteroides/imunologia
Colite/imunologia
Microbioma Gastrointestinal
Glucose-6-Fosfatase/imunologia
[Mh] Termos MeSH secundário: Adulto
Animais
Bacteroides/classificação
Bacteroides/enzimologia
Colite/microbiologia
Feminino
Glucose-6-Fosfatase/genética
Seres Humanos
Tecido Linfoide/imunologia
Masculino
Camundongos
Camundongos Endogâmicos BALB C
Camundongos Endogâmicos NOD
Meia-Idade
Mimetismo Molecular
Linfócitos T/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Autoantigens); EC 3.1.3.9 (Glucose-6-Phosphatase); EC 3.1.3.9. (G6PC2 protein, human); EC 3.1.3.9. (G6pc2 protein, mouse)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171101
[Lr] Data última revisão:
171101
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171021
[St] Status:MEDLINE


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[PMID]:28835389
[Au] Autor:Ying Z; Zhang H; Su W; Zhou L; Wang F; Li Y; Zhang L; Wang T
[Ad] Endereço:College of Animal Science and Technology, Nanjing Agricultural University, Nanjing, People's Republic of China.
[Ti] Título:Dietary Methionine Restriction Alleviates Hyperglycemia in Pigs with Intrauterine Growth Restriction by Enhancing Hepatic Protein Kinase B Signaling and Glycogen Synthesis.
[So] Source:J Nutr;147(10):1892-1899, 2017 Oct.
[Is] ISSN:1541-6100
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Individuals with intrauterine growth restriction (IUGR) are prone to developing type 2 diabetes mellitus (T2DM). Dietary methionine restriction (MR) improves insulin sensitivity and glucose homeostasis in individuals with normal birth weight (NBW). This study investigated the effects of MR on plasma glucose concentration and hepatic and muscle glucose metabolism in pigs with IUGR. Thirty female NBW and 60 same-sex spontaneous IUGR piglets (Landrace × Yorkshire) were selected. After weaning (day 21), the piglets were fed diets with adequate methionine (NBW-CON and IUGR-CON) or 30% less methionine (IUGR-MR) ( = 6). At day 180, 1 pig with a body weight near the mean of each replication was selected for biochemical analysis. The IUGR-CON group showed 41.6%, 68.6%, and 67.1% higher plasma glucose concentration, hepatic phosphoenolpyruvate carboxykinase activity, and glucose-6-phosphatase activity, respectively, than the NBW-CON group ( < 0.05). Muscle glycogen content and glycogen synthase activity were 36.9% and 38.8% lower, respectively, in the IUGR-CON than the NBW-CON group ( < 0.05), respectively, and there was decreased hepatic and muscle protein kinase B phosphorylation in the IUGR-CON group ( < 0.05). Compared with the IUGR-CON pigs, the IUGR-MR pigs had 28.7% lower plasma glucose concentrations ( < 0.05), which were similar to those of the NBW-CON pigs ( ≥ 0.05). The hepatic glycogen content and glycogen synthase activity of the IUGR-MR pigs were 62.9% and 50.8% higher than those of the IUGR-CON pigs ( < 0.05) and 53.5% and 84.3% higher than the NBW-CON pigs ( < 0.05), respectively. The IUGR-MR pigs' hepatic and muscle protein kinase B phosphorylation was higher than that of the IUGR-CON pigs ( < 0.05) and similar to that of the NBW-CON pigs ( ≥ 0.05). MR attenuates hyperglycemia in IUGR pigs by enhancing hepatic protein kinase B signaling and glycogen synthesis, implying a potential nutritional strategy to prevent type 2 diabetes mellitus in IUGR offspring.
[Mh] Termos MeSH primário: Diabetes Mellitus Tipo 2/metabolismo
Retardo do Crescimento Fetal
Glicogênio/biossíntese
Hiperglicemia/dietoterapia
Fígado/metabolismo
Metionina/administração & dosagem
Proteínas Proto-Oncogênicas c-akt/metabolismo
[Mh] Termos MeSH secundário: Ração Animal
Animais
Animais Recém-Nascidos
Peso ao Nascer
Glicemia/metabolismo
Diabetes Mellitus Tipo 2/prevenção & controle
Dieta
Feminino
Glucose-6-Fosfatase/metabolismo
Glicogênio/metabolismo
Hiperglicemia/metabolismo
Resistência à Insulina
Masculino
Metionina/metabolismo
Metionina/farmacologia
Músculos/metabolismo
Fosfoenolpiruvato Carboxiquinase (GTP)/metabolismo
Fosforilação
Transdução de Sinais
Suínos
Desmame
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Blood Glucose); 9005-79-2 (Glycogen); AE28F7PNPL (Methionine); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt); EC 3.1.3.9 (Glucose-6-Phosphatase); EC 4.1.1.32 (Phosphoenolpyruvate Carboxykinase (GTP))
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171012
[Lr] Data última revisão:
171012
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170825
[St] Status:MEDLINE
[do] DOI:10.3945/jn.117.253427


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[PMID]:28817664
[Au] Autor:MacCormack TJ; Rundle AM; Malek M; Raveendran A; Meli MV
[Ad] Endereço:Department of Chemistry and Biochemistry, Mount Allison University, Sackville, NB, Canada.
[Ti] Título:Gold nanoparticles partition to and increase the activity of glucose-6-phosphatase in a synthetic phospholipid membrane system.
[So] Source:PLoS One;12(8):e0183274, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Engineered nanomaterials can alter the structure and/or function of biological membranes and membrane proteins but the underlying mechanisms remain unclear. We addressed this using a Langmuir phospholipid monolayer containing an active transmembrane protein, glucose-6-phosphatase (G6Pase). Gold nanoparticles (nAu) with varying ligand shell composition and hydrophobicity were synthesized, and their partitioning in the membrane and effects on protein activity characterized. nAu incorporation did not alter the macroscopic properties of the membrane. Atomic force microscopy showed that when co-spread with other components prior to membrane compression, nAu preferentially interacted with G6Pase and each other in a functional group-dependent manner. Under these conditions, all nAu formulations reduced G6Pase aggregation in the membrane, enhancing catalytic activity 5-6 fold. When injected into the subphase beneath pre-compressed monolayers, nAu did not affect G6Pase activity over 60 minutes, implying they were unable to interact with the protein under these conditions. A small but significant quenching of tryptophan fluorescence showed that nAu interacted with G6Pase in aqueous suspension. nAu also significantly reduced the hydrodynamic diameter of G6Pase in aqueous suspension and promoted catalytic activity, likely via a similar mechanism to that observed in co-spread monolayers. Overall, our results show that nAu can incorporate into membranes and associate preferentially with membrane proteins under certain conditions and that partitioning is dependent upon ligand shell chemistry and composition. Once incorporated, nAu can alter the distribution of membrane proteins and indirectly affect their function by improving active site accessibility, or potentially by changing their native structure and distribution in the membrane.
[Mh] Termos MeSH primário: Glucose-6-Fosfatase/metabolismo
Ouro/química
Lipídeos de Membrana/metabolismo
Nanopartículas Metálicas
Fosfolipídeos/metabolismo
[Mh] Termos MeSH secundário: Microscopia de Força Atômica
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Membrane Lipids); 0 (Phospholipids); 7440-57-5 (Gold); EC 3.1.3.9 (Glucose-6-Phosphatase)
[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:170818
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0183274


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[PMID]:28783164
[Au] Autor:Ivarsdottir EV; Steinthorsdottir V; Daneshpour MS; Thorleifsson G; Sulem P; Holm H; Sigurdsson S; Hreidarsson AB; Sigurdsson G; Bjarnason R; Thorsson AV; Benediktsson R; Eyjolfsson G; Sigurdardottir O; Olafsson I; Zeinali S; Azizi F; Thorsteinsdottir U; Gudbjartsson DF; Stefansson K
[Ad] Endereço:deCODE Genetics/Amgen, Inc., Reykjavik, Iceland.
[Ti] Título:Effect of sequence variants on variance in glucose levels predicts type 2 diabetes risk and accounts for heritability.
[So] Source:Nat Genet;49(9):1398-1402, 2017 Sep.
[Is] ISSN:1546-1718
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Sequence variants that affect mean fasting glucose levels do not necessarily affect risk for type 2 diabetes (T2D). We assessed the effects of 36 reported glucose-associated sequence variants on between- and within-subject variance in fasting glucose levels in 69,142 Icelanders. The variant in TCF7L2 that increases fasting glucose levels increases between-subject variance (5.7% per allele, P = 4.2 × 10 ), whereas variants in GCK and G6PC2 that increase fasting glucose levels decrease between-subject variance (7.5% per allele, P = 4.9 × 10 and 7.3% per allele, P = 7.5 × 10 , respectively). Variants that increase mean and between-subject variance in fasting glucose levels tend to increase T2D risk, whereas those that increase the mean but reduce variance do not (r = 0.61). The variants that increase between-subject variance increase fasting glucose heritability estimates. Intuitively, our results show that increasing the mean and variance of glucose levels is more likely to cause pathologically high glucose levels than increase in the mean offset by a decrease in variance.
[Mh] Termos MeSH primário: Glicemia/metabolismo
Diabetes Mellitus Tipo 2/genética
Predisposição Genética para Doença/genética
Variação Genética
[Mh] Termos MeSH secundário: Alelos
Índice de Massa Corporal
Diabetes Mellitus Tipo 2/sangue
Jejum
Feminino
Frequência do Gene
Glucoquinase/genética
Glucose-6-Fosfatase/genética
Hemoglobina A Glicada/metabolismo
Seres Humanos
Islândia
Masculino
Penetrância
Polimorfismo de Nucleotídeo Único
Fatores de Risco
Proteína 2 Semelhante ao Fator 7 de Transcrição/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Blood Glucose); 0 (Glycated Hemoglobin A); 0 (TCF7L2 protein, human); 0 (Transcription Factor 7-Like 2 Protein); EC 2.7.1.2 (Glucokinase); EC 3.1.3.9 (Glucose-6-Phosphatase); EC 3.1.3.9. (G6PC2 protein, human)
[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:170808
[St] Status:MEDLINE
[do] DOI:10.1038/ng.3928


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[PMID]:28711683
[Au] Autor:Veiga FMS; Graus-Nunes F; Rachid TL; Barreto AB; Mandarim-de-Lacerda CA; Souza-Mello V
[Ad] Endereço:Laboratory of Morphometry, Metabolism and Cardiovascular Disease, Biomedical Center, Institute of Biology, State University of Rio de Janeiro, Brazil.
[Ti] Título:Anti-obesogenic effects of WY14643 (PPAR-alpha agonist): Hepatic mitochondrial enhancement and suppressed lipogenic pathway in diet-induced obese mice.
[So] Source:Biochimie;140:106-116, 2017 Sep.
[Is] ISSN:1638-6183
[Cp] País de publicação:France
[La] Idioma:eng
[Ab] Resumo:Non-alcoholic fatty liver disease (NAFLD) presents with growing prevalence worldwide, though its pharmacological treatment remains to be established. This study aimed to evaluate the effects of a PPAR-alpha agonist on liver tissue structure, ultrastructure, and metabolism, focusing on gene and protein expression of de novo lipogenesis and gluconeogenesis pathways, in diet-induced obese mice. Male C57BL/6 mice (three months old) received a control diet (C, 10% of lipids, n = 10) or a high-fat diet (HFD, 50% of lipids, n = 10) for ten weeks. These groups were subdivided to receive the treatment (n = 5 per group): C, C-alpha (PPAR-alpha agonist, 2.5 mg/kg/day mixed in the control diet), HFD and HFD-alpha group (PPAR-alpha agonist, 2.5 mg/kg/day mixed in the HFD). The effects were compared with biometrical, biochemical, molecular biology and transmission electron microscopy (TEM) analyses. HFD showed greater body mass (BM) and insulinemia than C, both of which were tackled by the treatment in the HFD-alpha group. Increased hepatic protein expression of glucose-6-phosphatase, CHREBP and gene expression of PEPCK in HFD points to increased gluconeogenesis. Treatment rescued these parameters in the HFD-alpha group, eliciting a reduced hepatic glucose output, confirmed by the smaller GLUT2 expression in HFD-alpha than in HFD. Conversely, favored de novo lipogenesis was found in the HFD group by the increased expression of PPAR-gamma, and its target gene SREBP-1, FAS and GK when compared to C. The treatment yielded a marked reduction in the expression of all lipogenic factors. TEM analyses showed a greater numerical density of mitochondria per area of tissue in treated than in untreated groups, suggesting an increase in beta-oxidation and the consequent NAFLD control. PPAR-alpha activation reduced BM and treated insulin resistance (IR) and NAFLD by increasing the number of mitochondria and reducing hepatic gluconeogenesis and de novo lipogenesis protein and gene expressions in a murine obesity model.
[Mh] Termos MeSH primário: Gorduras na Dieta/efeitos adversos
Fígado/metabolismo
Mitocôndrias Hepáticas/metabolismo
Obesidade/tratamento farmacológico
PPAR alfa/agonistas
Pirimidinas/farmacologia
[Mh] Termos MeSH secundário: Animais
Gorduras na Dieta/farmacologia
Regulação da Expressão Gênica/efeitos dos fármacos
Glucose-6-Fosfatase/biossíntese
Resistência à Insulina
Lipogênese/efeitos dos fármacos
Fígado/patologia
Masculino
Camundongos
Mitocôndrias Hepáticas/patologia
Hepatopatia Gordurosa não Alcoólica/induzido quimicamente
Hepatopatia Gordurosa não Alcoólica/tratamento farmacológico
Hepatopatia Gordurosa não Alcoólica/metabolismo
Hepatopatia Gordurosa não Alcoólica/patologia
Proteínas Nucleares/biossíntese
Obesidade/induzido quimicamente
Obesidade/metabolismo
Obesidade/patologia
PPAR alfa/metabolismo
PPAR gama/biossíntese
Fosfoenolpiruvato Carboxiquinase (ATP)/biossíntese
Proteína de Ligação a Elemento Regulador de Esterol 1/biossíntese
Fatores de Transcrição/biossíntese
Receptor fas/biossíntese
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Dietary Fats); 0 (Fas protein, mouse); 0 (Mlxipl protein, mouse); 0 (Nuclear Proteins); 0 (PPAR alpha); 0 (PPAR gamma); 0 (Pyrimidines); 0 (Srebf1 protein, mouse); 0 (Sterol Regulatory Element Binding Protein 1); 0 (Transcription Factors); 0 (fas Receptor); 86C4MRT55A (pirinixic acid); EC 3.1.3.9 (Glucose-6-Phosphatase); EC 4.1.1.49 (Phosphoenolpyruvate Carboxykinase (ATP))
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170717
[St] Status:MEDLINE


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[PMID]:28704540
[Au] Autor:Shi Y; Li Y; Wang J; Wang C; Fan J; Zhao J; Yin L; Liu X; Zhang D; Li L
[Ad] Endereço:Department of Epidemiology and Biostatistics, College of Public Health, Zhengzhou University, Zhengzhou, Henan, PR China.
[Ti] Título:Meta-analyses of the association of G6PC2 allele variants with elevated fasting glucose and type 2 diabetes.
[So] Source:PLoS One;12(7):e0181232, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: To collectively evaluate the association of glucose-6-phosphatase catalytic unit 2 (G6PC2) allele variants with elevated fasting glucose (FG) and type 2 diabetes (T2D). DESIGN: Meta-analysis. DATA SOURCES: PubMed, Web of Knowledge and Embase databases. STUDY SELECTION: Full text articles of studies that identified an association of G6PC2 with T2D and elevated FG. PATIENT INVOLVEMENT: There was no T2D patient involvement in the analyses on the association of FG with G6PC2, there were T2D patients and non-diabetes patient involvement in the analyses on the association of T2D with G6PC2. STATISTICAL ANALYSIS: Random-effects meta-analyses were used to calculate the pool effect sizes. I2 metric and H2 tests were used to calculate the heterogeneity. Begg's funnel plot and Egger's linear regression test were done to assess publication bias. RESULTS: Of the 423 studies identified, 21 were eligible and included. Data on three loci (rs560887, rs16856187 and rs573225) were available. The G allele at rs560887 in three ethnicities, the C allele at rs16856187 and the A allele at rs573225 all had a positive association with elevated FG. Per increment of G allele at rs560887 and A allele at rs573225 resulted in a FG 0.070 mmol/l and 0.075 mmol/l higher (ß (95% CI) = 0.070 (0.060, 0.079), p = 4.635e-50 and 0.075 (0.065, 0.085), p = 5.856e-48, respectively). With regard to the relationship of rs16856187 and FG, an increase of 0.152 (95% CI: 0.034-0.270; p = 0.011) and 0.317 (95% CI: 0.193-0.442, p = 6.046e-07) was found in the standardized mean difference (SMD) of FG for the AC and CC genotypes, respectively, when compared with the AA reference genotype. However, the G-allele of rs560887 in Caucasians under the additive model and the C-allele of rs16856187 under the allele and dominant models were associated with a decreased risk of T2D (OR (95% CI) = 0.964 (0.947, 0.981), p = 0.570e-4; OR (95% CI) = 0.892 (0.832, 0.956), p = 0.001; and OR (95% CI) = 0.923(0.892, 0.955), p = 5.301e-6, respectively). CONCLUSIONS: Our meta-analyses demonstrate that all three allele variants of G6PC2 (rs560887, rs16856187 and rs573225) are associated with elevated FG, with two variants (rs560887 in the Caucasians subgroup and rs16856187 under the allele and dominant model) being associated with T2D as well. Further studies utilizing larger sample sizes and different ethnic populations are needed to extend and confirm these findings.
[Mh] Termos MeSH primário: Glicemia/metabolismo
Diabetes Mellitus Tipo 2/genética
Jejum/sangue
Glucose-6-Fosfatase/genética
[Mh] Termos MeSH secundário: Adolescente
Adulto
Idoso
Glicemia/genética
Criança
Diabetes Mellitus Tipo 2/sangue
Diabetes Mellitus Tipo 2/epidemiologia
Feminino
Estudos de Associação Genética/estatística & dados numéricos
Predisposição Genética para Doença
Seres Humanos
Masculino
Meia-Idade
Polimorfismo de Nucleotídeo Único
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE; META-ANALYSIS
[Nm] Nome de substância:
0 (Blood Glucose); EC 3.1.3.9 (Glucose-6-Phosphatase); EC 3.1.3.9. (G6PC2 protein, human)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170929
[Lr] Data última revisão:
170929
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170714
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0181232


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[PMID]:28678435
[Au] Autor:Niaz K; Mabqool F; Khan F; Ismail Hassan F; Baeeri M; Navaei-Nigjeh M; Hassani S; Gholami M; Abdollahi M
[Ad] Endereço:International Campus-Tehran University of Medical Sciences (IC-TUMS), Tehran, Iran.
[Ti] Título:Molecular mechanisms of action of styrene toxicity in blood plasma and liver.
[So] Source:Environ Toxicol;32(10):2256-2266, 2017 Oct.
[Is] ISSN:1522-7278
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Styrene is an aromatic colorless hydrocarbon available in liquid form and highly volatile. In its pure form, it gives a sweet smell. The primary source of exposure in the environment is from plastic materials, rubber industries, packaging materials, insulations, and fiber glass and carpet industry. Natural sources of styrene include: few metabolites in plants which are transferred through food chain. The current study was designed to evaluate styrene toxicity, including: superoxide dismutase (SOD) and protein carbonyl, oxidative stress, glucose-6-phosphatase (G6Pase), glycogen phosphorylase (GP), and phosphoenolpyruvate carboxykinase (PEPCK) activities, adenosine triphosphate (ATP) to adenosine diphosphate (ADP) ratio, and changes in gene expressions such as glutamate dehydrogenase 1 (GLUD1), glucose transporter 2 (GLUT2), and glucokinase (GCK) in the rat liver tissue. For this purpose, styrene was dissolved in corn oil and was administered via gavage, at doses 250, 500, 1000, 1500, 2000, mg/kg/day per mL and control (corn oil) to each rat with one day off in a week, for 42 days. Plasma SOD and protein carbonyl of plasma were significantly up-regulated in 1000, 1500, and 2000 mg/kg/day styrene administrated groups (P < .001). In addition, styrene caused an increase in lipid peroxidation (LPO) and reactive oxygen species (ROS) in the dose-dependent manners in liver tissue (P < .001). Furthermore, the ferrous reducing antioxidant power (FRAP) and total thiol molecules (TTM) in styrene-treated groups were significantly decreased in liver tissue (P < .001) with increasing doses. In treated rats, styrene significantly increased G6Pase activity (P < .001) and down-regulated GP activity (P < .001) as compared to the control group. The PEPCK activity was significantly raised in a dose-dependent manner (P < .001). The ATP/ADP ratio of live cells was significantly raised by increasing the dose (P < .001). There was significantly an up-regulation of GLUD1 and GCK at 2000 mg/kg group (P < .01) and a down-regulation for GLUT2 at the same dose. While in the rest of group, GLUT2 showed up-regulation of relative fold change. By targeting genes such as GLUD1, GLUT2, and GCK, disruption of hepatic gluconeogenesis, glycogenolysis, and insulin secretory functions are obvious. The present study illustrates that induction of oxidative stress followed by changes in G6Pase, GP, and PEPCK activities and the genes responsible for glucose metabolism are the mechanisms of styrene's action in the liver.
[Mh] Termos MeSH primário: Poluentes Ambientais/toxicidade
Fígado/efeitos dos fármacos
Estireno/toxicidade
Superóxido Dismutase/sangue
[Mh] Termos MeSH secundário: Difosfato de Adenosina/metabolismo
Trifosfato de Adenosina/metabolismo
Animais
Regulação da Expressão Gênica
Glucose/metabolismo
Glucose-6-Fosfatase/metabolismo
Glicogênio Fosforilase/metabolismo
Insulina/secreção
Peptídeos e Proteínas de Sinalização Intracelular/metabolismo
Peroxidação de Lipídeos
Fígado/metabolismo
Masculino
Estresse Oxidativo
Fosfoenolpiruvato Carboxiquinase (GTP)/metabolismo
Carbonilação Proteica
Ratos Wistar
Espécies Reativas de Oxigênio/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Environmental Pollutants); 0 (Insulin); 0 (Intracellular Signaling Peptides and Proteins); 0 (Reactive Oxygen Species); 44LJ2U959V (Styrene); 61D2G4IYVH (Adenosine Diphosphate); 8L70Q75FXE (Adenosine Triphosphate); EC 1.15.1.1 (Superoxide Dismutase); EC 2.4.1.- (Glycogen Phosphorylase); EC 3.1.3.9 (Glucose-6-Phosphatase); EC 4.1.1.32 (Phosphoenolpyruvate Carboxykinase (GTP)); EC 4.1.1.32 (phosphoenolpyruvate carboxykinase 1 (soluble) protein, rat); IY9XDZ35W2 (Glucose)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171005
[Lr] Data última revisão:
171005
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170706
[St] Status:MEDLINE
[do] DOI:10.1002/tox.22441


  9 / 4499 MEDLINE  
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[PMID]:28655758
[Au] Autor:Jiang L; Xiong J; Zhan J; Yuan F; Tang M; Zhang C; Cao Z; Chen Y; Lu X; Li Y; Wang H; Wang L; Wang J; Zhu WG; Wang H
[Ad] Endereço:From the Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education), Beijing Key Laboratory of Protein Post-translational Modifications and Cell Function, Department of Biochemistry and Molecular Biology, Peking University Health Science Center.
[Ti] Título:Ubiquitin-specific peptidase 7 (USP7)-mediated deubiquitination of the histone deacetylase SIRT7 regulates gluconeogenesis.
[So] Source:J Biol Chem;292(32):13296-13311, 2017 Aug 11.
[Is] ISSN:1083-351X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Sirtuin 7 (SIRT7), a member of the NAD -dependent class III histone deacetylases, is involved in the regulation of various cellular processes and in resisting various stresses, such as hypoxia, low glucose levels, and DNA damage. Interestingly, SIRT7 is linked to the control of glycolysis, suggesting a role in glucose metabolism. Given the important roles of SIRT7, it is critical to clarify how SIRT7 activity is potentially regulated. It has been reported that some transcriptional and post-transcriptional regulatory mechanisms are involved. However, little is known how SIRT7 is regulated by the post-translational modifications. Here, we identified ubiquitin-specific peptidase 7 (USP7), a deubiquitinase, as a negative regulator of SIRT7. We showed that USP7 interacts with SIRT7 both and and we further demonstrated that SIRT7 undergoes endogenous Lys-63-linked polyubiquitination, which is removed by USP7. Although the USP7-mediated deubiquitination of SIRT7 had no effect on its stability, the deubiquitination repressed its enzymatic activity. We also showed that USP7 coordinates with SIRT7 to regulate the expression of glucose-6-phosphatase catalytic subunit ( ), a gluconeogenic gene. USP7 depletion by RNA interference increased both expression and SIRT7 enzymatic activity. Moreover, SIRT7 targeted the promoter through the transcription factor ELK4 but not through forkhead box O1 (FoxO1). In summary, SIRT7 is a USP7 substrate and has a novel role as a regulator of gluconeogenesis. Our study may provide the basis for new clinical approaches to treat metabolic disorders related to glucose metabolism.
[Mh] Termos MeSH primário: Regulação Enzimológica da Expressão Gênica
Glucose-6-Fosfatase/metabolismo
Regiões Promotoras Genéticas
Processamento de Proteína Pós-Traducional
Sirtuínas/metabolismo
Ubiquitina Tiolesterase/metabolismo
Proteínas Elk-4 do Domínio ets/metabolismo
[Mh] Termos MeSH secundário: Substituição de Aminoácidos
Linhagem Celular Tumoral
Deleção de Genes
Gluconeogênese
Glucose-6-Fosfatase/antagonistas & inibidores
Glucose-6-Fosfatase/genética
Células HEK293
Seres Humanos
Hidrólise
Lisina/metabolismo
Mutação
Fragmentos de Peptídeos/antagonistas & inibidores
Fragmentos de Peptídeos/genética
Fragmentos de Peptídeos/metabolismo
Domínios e Motivos de Interação entre Proteínas
Subunidades Proteicas/genética
Subunidades Proteicas/metabolismo
Interferência de RNA
Proteínas Recombinantes de Fusão/química
Proteínas Recombinantes de Fusão/metabolismo
Sirtuínas/antagonistas & inibidores
Sirtuínas/genética
Especificidade por Substrato
Ubiquitina Tiolesterase/antagonistas & inibidores
Ubiquitina Tiolesterase/genética
Peptidase 7 Específica de Ubiquitina
Ubiquitinação
Proteínas Elk-4 do Domínio ets/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (ELK4 protein, human); 0 (Peptide Fragments); 0 (Protein Subunits); 0 (Recombinant Fusion Proteins); 0 (SIRT7 protein, human); 146481-62-1 (ets-Domain Protein Elk-4); EC 3.1.3.9 (G6PC1 protein, human); EC 3.1.3.9 (Glucose-6-Phosphatase); EC 3.4.19.12 (USP7 protein, human); EC 3.4.19.12 (Ubiquitin Thiolesterase); EC 3.4.19.12 (Ubiquitin-Specific Peptidase 7); EC 3.5.1.- (Sirtuins); K3Z4F929H6 (Lysine)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170629
[St] Status:MEDLINE
[do] DOI:10.1074/jbc.M117.780130


  10 / 4499 MEDLINE  
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[PMID]:28622511
[Au] Autor:Weis S; Carlos AR; Moita MR; Singh S; Blankenhaus B; Cardoso S; Larsen R; Rebelo S; Schäuble S; Del Barrio L; Mithieux G; Rajas F; Lindig S; Bauer M; Soares MP
[Ad] Endereço:Instituto Gulbenkian de Ciência, 2780-156 Oeiras, Portugal; Department of Anesthesiology and Intensive Care Medicine, Jena University Hospital, 07747 Jena, Germany.
[Ti] Título:Metabolic Adaptation Establishes Disease Tolerance to Sepsis.
[So] Source:Cell;169(7):1263-1275.e14, 2017 Jun 15.
[Is] ISSN:1097-4172
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Sepsis is an often lethal syndrome resulting from maladaptive immune and metabolic responses to infection, compromising host homeostasis. Disease tolerance is a defense strategy against infection that preserves host homeostasis without exerting a direct negative impact on pathogens. Here, we demonstrate that induction of the iron-sequestering ferritin H chain (FTH) in response to polymicrobial infections is critical to establish disease tolerance to sepsis. The protective effect of FTH is exerted via a mechanism that counters iron-driven oxidative inhibition of the liver glucose-6-phosphatase (G6Pase), and in doing so, sustains endogenous glucose production via liver gluconeogenesis. This is required to prevent the development of hypoglycemia that otherwise compromises disease tolerance to sepsis. FTH overexpression or ferritin administration establish disease tolerance therapeutically. In conclusion, disease tolerance to sepsis relies on a crosstalk between adaptive responses controlling iron and glucose metabolism, required to maintain blood glucose within a physiologic range compatible with host survival.
[Mh] Termos MeSH primário: Glucose/metabolismo
Ferro/metabolismo
Sepse/metabolismo
[Mh] Termos MeSH secundário: Animais
Apoferritinas/genética
Apoferritinas/metabolismo
Ceruloplasmina/metabolismo
Gluconeogênese
Glucose-6-Fosfatase/metabolismo
Camundongos
Camundongos Endogâmicos C57BL
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
9013-31-4 (Apoferritins); E1UOL152H7 (Iron); EC 1.16.3.1 (Ceruloplasmin); EC 3.1.3.9 (Glucose-6-Phosphatase); IY9XDZ35W2 (Glucose)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170922
[Lr] Data última revisão:
170922
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170617
[St] Status:MEDLINE



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