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[PMID]:28987405
[Au] Autor:Botelho MJ; Vale C; Joaquim S; Costa ST; Soares F; Roque C; Matias D
[Ad] Endereço:IPMA, Portuguese Institute for the Sea and Atmosphere, Rua Alfredo Magalhães Ramalho, 6, 1495-006, Lisbon, Portugal; CIIMAR, Interdisciplinary Centre of Marine and Environmental Research, University of Porto, Rua dos Bragas 289, 4050-123, Porto, Portugal. Electronic address: mjbotelho@ipma.pt.
[Ti] Título:Combined effect of temperature and nutritional regime on the elimination of the lipophilic toxin okadaic acid in the naturally contaminated wedge shell Donax trunculus.
[So] Source:Chemosphere;190:166-173, 2018 Jan.
[Is] ISSN:1879-1298
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The influence of nutritional regime and water temperature on depuration rates of OA-group toxins in the wedge shell Donax trunculus was examined by exposing naturally contaminated specimens to three nutritional regimes (microalgae, commercial paste of microalgae, and starvation) for 14 days at 16 °C and 20 °C. Total OA was quantified in the whole soft tissues of the individuals collected in days 2, 4, 6, 8, 10, 12 and 14. Mortality, dry weight, condition index, gross biochemical composition and gametogenic stages were surveyed. Low variation of glycogen and carbohydrates during the experiments suggest that wedge shells were under non-dramatic stress conditions. Wedge shells fed with non-toxic diets showed similar depuration rates being 15 and 38% higher than in starvation, at 16 and 20 °C, respectively. Depuration rates under non-toxic diets at 20 °C were 71% higher than at 16 °C. These results highlight the influence of water temperature on the depuration rate of total OA accumulated by D. trunculus, even when the increase is of only 4 °C, as commonly observed in week time scales in the southern Portuguese coastal waters. These results open the possibility of a faster release of OA in harvested wedge shells translocated to depuration systems when under a slight increase of water temperature.
[Mh] Termos MeSH primário: Bivalves/química
Recuperação e Remediação Ambiental/métodos
Avaliação Nutricional
Ácido Okadáico/isolamento & purificação
Temperatura Ambiente
[Mh] Termos MeSH secundário: Animais
Carboidratos/análise
Dieta/efeitos adversos
Glicogênio/análise
Toxinas Marinhas/isolamento & purificação
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Carbohydrates); 0 (Marine Toxins); 1W21G5Q4N2 (Okadaic Acid); 9005-79-2 (Glycogen)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171009
[St] Status:MEDLINE


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


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


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[PMID]:29223569
[Au] Autor:Singh AK; Raj V; Keshari AK; Rai A; Kumar P; Rawat A; Maity B; Kumar D; Prakash A; De A; Samanta A; Bhattacharya B; Saha S
[Ad] Endereço:Department of Pharmaceutical Sciences, Babasaheb Bhimrao Ambedkar University, Vidya Vihar, Raebareli Road, Lucknow 226025, Uttar Pradesh, India.
[Ti] Título:Isolated mangiferin and naringenin exert antidiabetic effect via PPAR /GLUT4 dual agonistic action with strong metabolic regulation.
[So] Source:Chem Biol Interact;280:33-44, 2018 Jan 25.
[Is] ISSN:1872-7786
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:In this study, we isolated two compounds from the leaves of Salacia oblonga (SA1, mangiferin and SA2, naringenin), and their structures were confirmed by infrared spectroscopy, nuclear magnetic resonance (NMR) spectroscopy, and mass spectrometry. SA1 and SA2 were orally administered to streptozotocin-induced diabetic rats at 50 and 100 mg/kg daily for 15 days. Blood glucose level, serum lipid profile, oxidative stress parameters, histopathology, docking, molecular parameters, and NMR-based metabolic perturbation studies were performed to investigate the pharmacological activities of SA1 and SA2. Results suggested that both compounds reduced blood glucose level, restored body weight, and normalized lipid concentrations in the serum and oxidative stress biomarkers in the liver and pancreas. In addition, the docking study on several diabetes-associated targets revealed that both compounds had a strong binding affinity towards peroxisome proliferator-activated receptor gamma (PPAR ) and glucose transporter type 4 (GLUT4). Further real-time reverse transcription polymerase chain reaction and western blot analyses were performed to confirm the gene and protein expression levels of PPAR and GLUT4 in the pancreatic tissues. Data obtained from the molecular studies showed that both compounds exhibited antidiabetic effects through dual activation of PPAR /GLUT4 signaling pathways. Finally, the NMR-based metabolic studies showed that both compounds normalized the diabetogenic metabolites in the serum. Altogether, we concluded that SA1 and SA2 might be potential antidiabetic lead compounds for future drug development.
[Mh] Termos MeSH primário: Flavanonas/farmacologia
Transportador de Glucose Tipo 4/metabolismo
Hipoglicemiantes/farmacologia
PPAR gama/metabolismo
Xantonas/farmacologia
[Mh] Termos MeSH secundário: Animais
Glicemia/análise
Diabetes Mellitus Experimental/induzido quimicamente
Diabetes Mellitus Experimental/tratamento farmacológico
Flavanonas/isolamento & purificação
Flavanonas/uso terapêutico
Transportador de Glucose Tipo 4/agonistas
Transportador de Glucose Tipo 4/genética
Glicogênio/metabolismo
Hipoglicemiantes/isolamento & purificação
Hipoglicemiantes/uso terapêutico
Insulina/sangue
Lipídeos/sangue
Fígado/efeitos dos fármacos
Fígado/metabolismo
Fígado/patologia
Masculino
Simulação de Acoplamento Molecular
Estresse Oxidativo/efeitos dos fármacos
PPAR gama/agonistas
PPAR gama/genética
Pâncreas/efeitos dos fármacos
Pâncreas/metabolismo
Pâncreas/patologia
Estrutura Terciária de Proteína
Ratos
Salacia/química
Salacia/metabolismo
Transdução de Sinais/efeitos dos fármacos
Estreptozocina/toxicidade
Xantonas/isolamento & purificação
Xantonas/uso terapêutico
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Blood Glucose); 0 (Flavanones); 0 (Glucose Transporter Type 4); 0 (Hypoglycemic Agents); 0 (Insulin); 0 (Lipids); 0 (PPAR gamma); 0 (Xanthones); 1M84LD0UMD (mangiferin); 5W494URQ81 (Streptozocin); 9005-79-2 (Glycogen); HN5425SBF2 (naringenin)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180129
[Lr] Data última revisão:
180129
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171211
[St] Status:MEDLINE


  5 / 20862 MEDLINE  
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[PMID]:28745633
[Au] Autor:De Porcellinis A; Frigaard NU; Sakuragi Y
[Ad] Endereço:Carlsberg Research Laboratory.
[Ti] Título:Determination of the Glycogen Content in Cyanobacteria.
[So] Source:J Vis Exp;(125), 2017 Jul 17.
[Is] ISSN:1940-087X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Cyanobacteria accumulate glycogen as a major intracellular carbon and energy storage during photosynthesis. Recent developments in research have highlighted complex mechanisms of glycogen metabolism, including the diel cycle of biosynthesis and catabolism, redox regulation, and the involvement of non-coding RNA. At the same time, efforts are being made to redirect carbon from glycogen to desirable products in genetically engineered cyanobacteria to enhance product yields. Several methods are used to determine the glycogen contents in cyanobacteria, with variable accuracies and technical complexities. Here, we provide a detailed protocol for the reliable determination of the glycogen content in cyanobacteria that can be performed in a standard life science laboratory. The protocol entails the selective precipitation of glycogen from the cell lysate and the enzymatic depolymerization of glycogen to generate glucose monomers, which are detected by a glucose oxidase-peroxidase (GOD-POD) enzyme coupled assay. The method has been applied to Synechocystis sp. PCC 6803 and Synechococcus sp. PCC 7002, two model cyanobacterial species that are widely used in metabolic engineering. Moreover, the method successfully showed differences in the glycogen contents between the wildtype and mutants defective in regulatory elements or glycogen biosynthetic genes.
[Mh] Termos MeSH primário: Ensaios Enzimáticos/métodos
Glicogênio/metabolismo
Synechocystis/metabolismo
[Mh] Termos MeSH secundário: Glucose/análise
Glucose/metabolismo
Glucose Oxidase/metabolismo
Manitol/metabolismo
Peroxidase/metabolismo
Synechocystis/genética
Gravação em Vídeo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
3OWL53L36A (Mannitol); 9005-79-2 (Glycogen); EC 1.1.3.4 (Glucose Oxidase); EC 1.11.1.7 (Peroxidase); IY9XDZ35W2 (Glucose)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180130
[Lr] Data última revisão:
180130
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170727
[St] Status:MEDLINE
[do] DOI:10.3791/56068


  6 / 20862 MEDLINE  
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[PMID]:29227611
[Au] Autor:Rushchak VV; Chashchyn MO
[Ti] Título:Cytochrome P450 2E1 participation in the pathogenesis of experimental metabolic syndrome in guinea pigs.
[So] Source:Ukr Biochem J;88(2):98-106, 2016 Mar-Apr.
[Is] ISSN:2409-4943
[Cp] País de publicação:Ukraine
[La] Idioma:eng
[Ab] Resumo:In this work the experimental metabolic syndrome on the basis of protamine sulfate modeling in guinea pigs was reproduced and pathological processes in the liver of experimental animals were studied. We determined the level of free radicals and markers of liver damage in the blood of experimental animals. We investigated the liver glycogen content and K+,Na+-ATPase activity in the liver of experimental animals as well as measured the cytochrome P450 2E1 (CY P2E1) expression ­ one of the main factors of oxidative stress. Evidence of development of hepatotoxic processes, increasing of the CY P2E1 level as well as of the free radical level in the animals with metabolic syndrome were found. Using of CY P2E1 inhibitors had shown that the free radical level in the blood of experimental animals depended on the level of the enzyme expression and activity. The obtained results suggest that the changes in the CY P2E1 expression play an important role in the development of hepatotoxic processes upon experimental metabolic syndrome. It was assumed that pharmacological correction of the enzyme expression may be an important mechanism for the influence on the metabolic syndrome clinical course.
[Mh] Termos MeSH primário: Inibidores do Citocromo P-450 CYP2E1/farmacologia
Citocromo P-450 CYP2E1/genética
Fígado/efeitos dos fármacos
Síndrome Metabólica/tratamento farmacológico
[Mh] Termos MeSH secundário: Animais
Citocromo P-450 CYP2E1/metabolismo
Dissulfiram/farmacologia
Radicais Livres/antagonistas & inibidores
Radicais Livres/metabolismo
Regulação da Expressão Gênica
Glicogênio/metabolismo
Cobaias
Fígado/enzimologia
Fígado/patologia
Masculino
Síndrome Metabólica/induzido quimicamente
Síndrome Metabólica/enzimologia
Síndrome Metabólica/patologia
Estresse Oxidativo/efeitos dos fármacos
Protaminas
Pirazóis/farmacologia
Quercetina/farmacologia
ATPase Trocadora de Sódio-Potássio/genética
ATPase Trocadora de Sódio-Potássio/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cytochrome P-450 CYP2E1 Inhibitors); 0 (Free Radicals); 0 (Protamines); 0 (Pyrazoles); 83LCM6L2BY (fomepizole); 9005-79-2 (Glycogen); 9IKM0I5T1E (Quercetin); EC 1.14.13.- (Cytochrome P-450 CYP2E1); EC 3.6.3.9 (Sodium-Potassium-Exchanging ATPase); TR3MLJ1UAI (Disulfiram)
[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:171212
[St] Status:MEDLINE
[do] DOI:10.15407/ubj88.02.098


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[PMID]:29253016
[Au] Autor:Knudsen JG; Gudiksen A; Bertholdt L; Overby P; Villesen I; Schwartz CL; Pilegaard H
[Ad] Endereço:Section for Cell Biology and Physiology, Department of Biology, University of Copenhagen, Copenhagen, Denmark.
[Ti] Título:Skeletal muscle IL-6 regulates muscle substrate utilization and adipose tissue metabolism during recovery from an acute bout of exercise.
[So] Source:PLoS One;12(12):e0189301, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:An acute bout of exercise imposes a major challenge on whole-body metabolism and metabolic adjustments are needed in multiple tissues during recovery to reestablish metabolic homeostasis. It is currently unresolved how this regulation is orchestrated between tissues. This study was undertaken to clarify the role of skeletal muscle derived interleukin 6 (IL-6) in the coordination of the metabolic responses during recovery from acute exercise. Skeletal muscle specific IL-6 knockout (IL-6 MKO) and littermate Control mice were rested or ran on a treadmill for 2h. Plasma, skeletal muscle, liver and adipose tissue were obtained after 6 and 10h of recovery. Non-exercised IL-6 MKO mice had higher plasma lactate and lower plasma non-esterified fatty acids than Controls. The activity of pyruvate dehydrogenase in the active form was, in skeletal muscle, higher in IL-6 MKO mice than Controls in non-exercised mice and 6h after exercise. IL-6 MKO mice had lower glucose transporter 4 protein content in inguinal adipose tissue (WAT) than Control in non-exercised mice and 10h after treadmill running. Epididymal WAT hormone sensitive lipase phosphorylation and inguinal WAT mitogen activated kinase P38 phosphorylation were higher in IL-6 MKO than Control mice 6h after exercise. These findings indicate that skeletal muscle IL-6 may play an important role in the regulation of substrate utilization in skeletal muscle, basal and exercise-induced adaptations in adipose tissue glucose uptake and lipolysis during recovery from exercise. Together this indicates that skeletal muscle IL-6 contributes to reestablishing metabolic homeostasis during recovery from exercise by regulating WAT and skeletal muscle metabolism.
[Mh] Termos MeSH primário: Tecido Adiposo/metabolismo
Interleucina-6/metabolismo
Músculo Esquelético/metabolismo
Condicionamento Físico Animal
[Mh] Termos MeSH secundário: Animais
Glicemia/metabolismo
Glucose/metabolismo
Glicogênio/metabolismo
Homeostase
Fígado/metabolismo
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Fosforilação
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Blood Glucose); 0 (Interleukin-6); 0 (interleukin-6, mouse); 9005-79-2 (Glycogen); IY9XDZ35W2 (Glucose)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180108
[Lr] Data última revisão:
180108
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171219
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0189301


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[PMID]:28747486
[Au] Autor:Chalvon-Demersay T; Even PC; Chaumontet C; Piedcoq J; Viollet B; Gaudichon C; Tomé D; Foretz M; Azzout-Marniche D
[Ad] Endereço:UMR Nutrition Physiology and Ingestive Behavior, AgroParisTech, INRA, Paris-Saclay University, Paris, France.
[Ti] Título:Modifying the Dietary Carbohydrate-to-Protein Ratio Alters the Postprandial Macronutrient Oxidation Pattern in Liver of AMPK-Deficient Mice.
[So] Source:J Nutr;147(9):1669-1676, 2017 09.
[Is] ISSN:1541-6100
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Hepatic AMP-activated kinase (AMPK) activity is sensitive to the dietary carbohydrate-to-protein ratio. However, the role of AMPK in metabolic adaptations to variations in dietary macronutrients remains poorly understood. The objective of this study was to determine the role of hepatic AMPK in the adaptation of energy metabolism in response to modulation of the dietary carbohydrate-to-protein ratio. Male 7-wk-old wild-type (WT) and liver AMPK-deficient (knockout) mice were fed either a normal-protein and normal-carbohydrate diet (NP-NC; 14% protein, 76% carbohydrate on an energy basis), a low-protein and high-carbohydrate diet (LP-HC; 5% protein, 85% carbohydrate), or a high-protein and low-carbohydrate diet (HP-LC; 55% protein, 35% carbohydrate) for 3 wk. During this period, after an overnight fast, metabolic parameters were measured and indirect calorimetry was performed in mice during the first hours after refeeding a 1-g calibrated meal of their own diet in order to investigate lipid and carbohydrate metabolism. Knockout mice fed an LP-HC or HP-LC meal exhibited 24% and 8% lower amplitudes in meal-induced carbohydrate and lipid oxidation changes. By contrast, knockout mice fed an NP-NC meal displayed normal carbohydrate and lipid oxidation profiles. These mice exhibited a transient increase in hepatic triglycerides and a decrease in hepatic glycogen. These changes were associated with a 650% higher secretion of fibroblast growth factor 21 (FGF21) 2 h after refeeding. The consequences of hepatic AMPK deletion depend on the dietary carbohydrate-to-protein ratio. In mice fed the NP-NC diet, deletion of AMPK in the liver led to an adaptation of liver metabolism resulting in increased secretion of FGF21. These changes possibly compensated for the absence of hepatic AMPK, as these mice exhibited normal postprandial changes in carbohydrate and lipid oxidation. By contrast, in mice fed the LP-HC and HP-LC diets, the lack of adjustment in liver metabolism in knockout mice resulted in a metabolic inflexibility, leading to a reduced amplitude of meal-induced changes in carbohydrate and lipid oxidation.
[Mh] Termos MeSH primário: Proteínas Quinases Ativadas por AMP/metabolismo
Metabolismo dos Carboidratos
Carboidratos da Dieta/administração & dosagem
Proteínas na Dieta/administração & dosagem
Metabolismo dos Lipídeos
Fígado/efeitos dos fármacos
Período Pós-Prandial
[Mh] Termos MeSH secundário: Proteínas Quinases Ativadas por AMP/deficiência
Adaptação Fisiológica
Animais
Dieta
Dieta com Restrição de Carboidratos
Dieta com Restrição de Proteínas
Carboidratos da Dieta/metabolismo
Carboidratos da Dieta/farmacologia
Gorduras na Dieta/metabolismo
Proteínas na Dieta/metabolismo
Proteínas na Dieta/farmacologia
Metabolismo Energético/efeitos dos fármacos
Jejum
Fatores de Crescimento de Fibroblastos/metabolismo
Glicogênio/metabolismo
Fígado/metabolismo
Masculino
Refeições
Camundongos Knockout
Oxirredução
Triglicerídeos/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Dietary Carbohydrates); 0 (Dietary Fats); 0 (Dietary Proteins); 0 (Triglycerides); 0 (fibroblast growth factor 22, mouse); 62031-54-3 (Fibroblast Growth Factors); 9005-79-2 (Glycogen); EC 2.7.11.31 (AMP-Activated Protein Kinases)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171215
[Lr] Data última revisão:
171215
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170728
[St] Status:MEDLINE
[do] DOI:10.3945/jn.117.250803


  9 / 20862 MEDLINE  
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[PMID]:29049322
[Au] Autor:Brandt N; Dethlefsen MM; Bangsbo J; Pilegaard H
[Ad] Endereço:The August Krogh Club, Section for Cell Biology and Physiology, Department of Biology, University of Copenhagen, Universitetsparken 13, Copenhagen Ø, Denmark.
[Ti] Título:PGC-1α and exercise intensity dependent adaptations in mouse skeletal muscle.
[So] Source:PLoS One;12(10):e0185993, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The aim of the present study was to examine the role of PGC-1α in intensity dependent exercise and exercise training-induced metabolic adaptations in mouse skeletal muscle. Whole body PGC-1α knockout (KO) and littermate wildtype (WT) mice performed a single treadmill running bout at either low intensity (LI) for 40 min or moderate intensity (MI) for 20 min. Blood and quadriceps muscles were removed either immediately after exercise or at 3h or 6h into recovery from exercise and from resting controls. In addition PGC-1α KO and littermate WT mice were exercise trained at either low intensity (LIT) for 40 min or at moderate intensity (MIT) for 20 min 2 times pr. day for 5 weeks. In the first and the last week of the intervention period, mice performed a graded running endurance test. Quadriceps muscles were removed before and after the training period for analyses. The acute exercise bout elicited intensity dependent increases in LC3I and LC3II protein and intensity independent decrease in p62 protein in skeletal muscle late in recovery and increased LC3II with exercise training independent of exercise intensity and volume in WT mice. Furthermore, acute exercise and exercise training did not increase LC3I and LC3II protein in PGC-1α KO. In addition, exercise-induced mRNA responses of PGC-1α isoforms were intensity dependent. In conclusion, these findings indicate that exercise intensity affected autophagy markers differently in skeletal muscle and suggest that PGC-1α regulates both acute and exercise training-induced autophagy in skeletal muscle potentially in a PGC-1α isoform specific manner.
[Mh] Termos MeSH primário: Músculo Esquelético/metabolismo
Coativador 1-alfa do Receptor gama Ativado por Proliferador de Peroxissomo/metabolismo
Condicionamento Físico Animal
[Mh] Termos MeSH secundário: Animais
Epinefrina/sangue
Feminino
Glicogênio/metabolismo
Masculino
Camundongos
Camundongos Knockout
Coativador 1-alfa do Receptor gama Ativado por Proliferador de Peroxissomo/genética
Fosforilação
RNA Mensageiro/metabolismo
Reação em Cadeia da Polimerase em Tempo Real
Reação em Cadeia da Polimerase Via Transcriptase Reversa
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (PPARGC1A protein, human); 0 (Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha); 0 (RNA, Messenger); 9005-79-2 (Glycogen); YKH834O4BH (Epinephrine)
[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:171020
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0185993


  10 / 20862 MEDLINE  
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[PMID]:28951248
[Au] Autor:Li R; Zhu LN; Ren LQ; Weng JY; Sun JS
[Ad] Endereço:Tianjin Key Laboratory of Animal and Plant Resistance, College of Life Science, Tianjin Normal University, Tianjin, People's Republic of China.
[Ti] Título:Molecular cloning and characterization of glycogen synthase in Eriocheir sinensis.
[So] Source:Comp Biochem Physiol B Biochem Mol Biol;214:47-56, 2017 Dec.
[Is] ISSN:1879-1107
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Glycogen plays an important role in glucose and energy homeostasis at cellular and organismal levels. In glycogen synthesis, glycogen synthase (GS) is a rate-limiting enzyme catalysing the addition of α-1,4-linked glucose units from (UDP) -glucose to a nascent glycogen chain using glycogenin (GN) as a primer. While studies on mammalian liver GS (GYS2) are numerous, enzymes from crustaceans, which also use glycogen and glucose as their main energy source, have received less attention. In the present study, we amplified full-length GS cDNA from Eriocheir sinensis. Tissue expression profiling revealed the highest expression of GS in the hepatopancreas. During moulting, GS expression and activity declined, and glycogen levels in the hepatopancreas were reduced. Recombinant GS was expressed in Escherichia coli Rosetta (DE3), and induction at 37°C or 16°C yielded EsGS in insoluble inclusion bodies (EsGS-I) or in soluble form (EsGS-S), respectively. Enzyme activity was measured in a cell-free system containing glucose-6-phosphate (G6P), and both forms possessed glycosyltransferase activity, but refolded EsGS-I was more active. Enzyme activity of both GS and EsGS-I in the hepatopancreas was optimum at 25°C, which is coincident with the optimum growth temperature of Chinese mitten crab, and higher (37°C) or lower (16°C) temperatures resulted in lower enzyme activity. Taken together, the results suggest that GS may be important for maintaining normal physiological functions such as growth and reproduction.
[Mh] Termos MeSH primário: Proteínas de Artrópodes/genética
Braquiúros/enzimologia
Glicogênio Sintase/genética
Glicogênio/biossíntese
Hepatopâncreas/enzimologia
[Mh] Termos MeSH secundário: Sequência de Aminoácidos
Animais
Proteínas de Artrópodes/metabolismo
Sítios de Ligação
Braquiúros/genética
Braquiúros/crescimento & desenvolvimento
Clonagem Molecular
Escherichia coli/genética
Escherichia coli/metabolismo
Expressão Gênica
Glucose-6-Fosfato/metabolismo
Glucosiltransferases/metabolismo
Glicogênio Sintase/metabolismo
Glicoproteínas/metabolismo
Hepatopâncreas/crescimento & desenvolvimento
Corpos de Inclusão/química
Cinética
Muda/genética
Especificidade de Órgãos
Filogenia
Ligação Proteica
Domínios e Motivos de Interação entre Proteínas
Proteínas Recombinantes/genética
Proteínas Recombinantes/metabolismo
Alinhamento de Sequência
Homologia de Sequência de Aminoácidos
Especificidade por Substrato
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Arthropod Proteins); 0 (Glycoproteins); 0 (Recombinant Proteins); 0 (glycogenin); 56-73-5 (Glucose-6-Phosphate); 9005-79-2 (Glycogen); EC 2.4.1.- (Glucosyltransferases); EC 2.4.1.11 (Glycogen Synthase)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171030
[Lr] Data última revisão:
171030
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170928
[St] Status:MEDLINE



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