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Pesquisa : D12.776.157.530.937.598.500 [Categoria DeCS]
Referências encontradas : 2221 [refinar]
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  1 / 2221 MEDLINE  
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[PMID]:29441965
[Au] Autor:Cai Z; Liu J; Bian H; Cai J; Guo X
[Ti] Título:MiR-455 enhances adipogenic differentiation of 3T3-L1 cells through targeting uncoupling protein-1.
[So] Source:Pharmazie;71(11):625-628, 2016 Nov 02.
[Is] ISSN:0031-7144
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:Accumulating evidence suggests that microRNAs (miRNAs) play an important role in regulating the pathways in adipose tissue that control processes such as adipogenesis, insulin resistance, and inflammation. Adipogenic differentiation of preadipocytes is a complex process regulated by various factors including miRNAs and cytokines. MiR-455 is a well-known miRNA that enhances adipogenesis. Uncoupling protein-1 (UCP-1), a heparinbinding growth factor, plays a negative role in adipogenesis. In this investigation, we demonstrate that UCP-1 is a target gene of miR-455 during adipogenic differentiation in 3T3-L1 preadipocytes. MiR-455 downregulates UCP-1 expression through interaction with a target site of miR-455 in the coding region of mouse UCP-1. The rare codons upstream of the target site regulate miR-455-induced translational knockdown of UCP-1, which provides more insight into the mechanism of adipogenic differentiation. Thus, these results suggest that the acceerative adipogenic effect of miR-455 in 3T3-L1 cells is due, at least in part, to suppression of UCP-1.
[Mh] Termos MeSH primário: Adipogenia/efeitos dos fármacos
Diferenciação Celular/efeitos dos fármacos
MicroRNAs/farmacologia
Proteína Desacopladora 1/efeitos dos fármacos
[Mh] Termos MeSH secundário: Células 3T3-L1
Tecido Adiposo/citologia
Tecido Adiposo/efeitos dos fármacos
Animais
Códon
Regulação para Baixo/efeitos dos fármacos
Técnicas de Silenciamento de Genes
Genes Reporter/genética
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Proteína Desacopladora 1/biossíntese
Proteína Desacopladora 1/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Codon); 0 (MIRN455 microRNA, mouse); 0 (MicroRNAs); 0 (Ucp1 protein, mouse); 0 (Uncoupling Protein 1)
[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:180215
[St] Status:MEDLINE
[do] DOI:10.1691/ph.2016.6734


  2 / 2221 MEDLINE  
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[PMID]:29351550
[Au] Autor:Rachid TL; Silva-Veiga FM; Graus-Nunes F; Bringhenti I; Mandarim-de-Lacerda CA; Souza-Mello V
[Ad] Endereço:Laboratory of Morphometry, Metabolism, and Cardiovascular Diseases, Biomedical Center, Institute of Biology, State University of Rio de Janeiro, Rio de Janeiro, Brazil.
[Ti] Título:Differential actions of PPAR-α and PPAR-ß/δ on beige adipocyte formation: A study in the subcutaneous white adipose tissue of obese male mice.
[So] Source:PLoS One;13(1):e0191365, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND AND AIMS: Obesity compromises adipocyte physiology. PPARs are essential to adipocyte plasticity, but its isolated role in the browning phenomenon is not clear. This study aimed to examine whether activation of PPAR-α or PPAR-ß/δ could induce beige cell depots in the subcutaneous white adipose tissue of diet-induced obese mice. MATERIAL AND METHODS: Sixty animals were randomly assigned to receive a control diet (C, 10% lipids) or a high-fat diet (HF, 50% lipids) for ten weeks. Then each group was re-divided to begin the treatments that lasted 4 weeks, totalizing six groups: C, C-α (C plus PPAR-α agonist, 2.5 mg/kg BM), C-ß (C plus PPAR-ß/δ agonist, 1 mg/kg BM), HF, HF-α (HF plus PPAR-α agonist), HF-ß (HF plus PPAR-ß/δ agonist). RESULTS: HF animals presented with overweight, glucose intolerance and subcutaneous white adipocyte hypertrophy. Both treatments significantly attenuated these parameters. Browning, verified by UCP1 positive beige cells and enhanced body temperature, was just observed in PPAR-α treated groups. PPAR-α agonism also elicited an enhanced gene expression of the thermogenesis effector UCP1, the beige-selective gene TMEM26 and the PRDM16, an essential gene for brown-like phenotype maintenance in the beige adipocytes when compared to their counterparts. The enhanced CIDEA and the reduced UCP1 gene levels might justify the white phenotype predominance after the treatment with the PPAR-ß/δ agonist. CONCLUSIONS: This work provides evidence that the PPAR-ß/δ agonist ameliorated metabolic disorders through enhanced beta-oxidation and better tolerance to glucose, whereas the PPAR-α agonism was confirmed as a promising therapeutic target for treating metabolic diseases via beige cell induction and enhanced thermogenesis.
[Mh] Termos MeSH primário: Adipócitos Bege/efeitos dos fármacos
Obesidade/tratamento farmacológico
PPAR alfa/agonistas
PPAR delta/agonistas
PPAR beta/agonistas
[Mh] Termos MeSH secundário: Adipócitos Bege/metabolismo
Adipócitos Bege/patologia
Tecido Adiposo Branco/efeitos dos fármacos
Tecido Adiposo Branco/metabolismo
Tecido Adiposo Branco/patologia
Adiposidade/efeitos dos fármacos
Animais
Glicemia/metabolismo
Peso Corporal/efeitos dos fármacos
Tamanho Celular/efeitos dos fármacos
Dieta Hiperlipídica/efeitos adversos
Ingestão de Energia/efeitos dos fármacos
Expressão Gênica/efeitos dos fármacos
Intolerância à Glucose/tratamento farmacológico
Hiperinsulinismo/tratamento farmacológico
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Obesidade/metabolismo
Obesidade/patologia
Termogênese/efeitos dos fármacos
Proteína Desacopladora 1/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Blood Glucose); 0 (PPAR alpha); 0 (PPAR delta); 0 (PPAR-beta); 0 (Ucp1 protein, mouse); 0 (Uncoupling Protein 1)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180120
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0191365


  3 / 2221 MEDLINE  
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[PMID]:29317208
[Au] Autor:Xiao XH; Qi XY; Wang YD; Ran L; Yang J; Zhang HL; Xu CX; Wen GB; Liu JH
[Ad] Endereço:Department of Metabolism and Endocrinology, University of South China, Hengyang, 421001, Hunan Province, China.
[Ti] Título:Zinc alpha2 glycoprotein promotes browning in adipocytes.
[So] Source:Biochem Biophys Res Commun;496(2):287-293, 2018 02 05.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Recent studies have highlighted recruiting and activating brite adipocytes in WAT (so-called "browning") would be an attractive anti-obesity strategy. Zinc alpha2 glycoprotein (ZAG) as an important adipokine, is reported to ameliorate glycolipid metabolism and lose body weight in obese mice. However whether the body reducing effect mediated by browning programme remains unclear. Here, we show that overexpression of ZAG in 3T3-L1 adipocytes enhanced expression of brown fat-specific markers (UCP-1, PRDM16 and CIDEA), mitochondrial biogenesis genes (PGC-1α, NRF-1/2 and mtTFA) and the key lipid metabolism lipases (ATGL, HSL, CPT1-A and p-acyl-CoA carboxylase). Additionally, those effects were dramaticlly abolished by H89/SB203580, revealing ZAG-induced browning depend on PKA and p38 MAPK signaling. Overall, our findings suggest that ZAG is a candidate therapeutic agent against obesity via induction of brown fat-like phenotype in white adipocytes.
[Mh] Termos MeSH primário: Adipócitos Marrons/metabolismo
Proteínas de Transporte/genética
Regulação da Expressão Gênica
Glicoproteínas/genética
Metabolismo dos Lipídeos/genética
[Mh] Termos MeSH secundário: Células 3T3-L1
Adipócitos Marrons/citologia
Adipócitos Marrons/efeitos dos fármacos
Animais
Proteínas Reguladoras de Apoptose/genética
Proteínas Reguladoras de Apoptose/metabolismo
Carbono-Carbono Ligases/genética
Carbono-Carbono Ligases/metabolismo
Carnitina O-Palmitoiltransferase/genética
Carnitina O-Palmitoiltransferase/metabolismo
Proteínas de Transporte/metabolismo
Proteínas Quinases Dependentes de AMP Cíclico/genética
Proteínas Quinases Dependentes de AMP Cíclico/metabolismo
Proteínas de Ligação a DNA/genética
Proteínas de Ligação a DNA/metabolismo
Glicoproteínas/metabolismo
Imidazóis/farmacologia
Isoquinolinas/farmacologia
Lipase/genética
Lipase/metabolismo
Camundongos
Fator 2 Relacionado a NF-E2/genética
Fator 2 Relacionado a NF-E2/metabolismo
Fator 1 Nuclear Respiratório/genética
Fator 1 Nuclear Respiratório/metabolismo
Coativador 1-alfa do Receptor gama Ativado por Proliferador de Peroxissomo/genética
Coativador 1-alfa do Receptor gama Ativado por Proliferador de Peroxissomo/metabolismo
Piridinas/farmacologia
Transdução de Sinais
Sulfonamidas/farmacologia
Fatores de Transcrição/genética
Fatores de Transcrição/metabolismo
Proteína Desacopladora 1/genética
Proteína Desacopladora 1/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (AZGP1 protein, mouse); 0 (Apoptosis Regulatory Proteins); 0 (Carrier Proteins); 0 (Cidea protein, mouse); 0 (DNA-Binding Proteins); 0 (Glycoproteins); 0 (Imidazoles); 0 (Isoquinolines); 0 (NF-E2-Related Factor 2); 0 (Nfe2l2 protein, mouse); 0 (Nrf1 protein, mouse); 0 (Nuclear Respiratory Factor 1); 0 (Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha); 0 (Ppargc1a protein, mouse); 0 (Prdm16 protein, mouse); 0 (Pyridines); 0 (Sulfonamides); 0 (Transcription Factors); 0 (Ucp1 protein, mouse); 0 (Uncoupling Protein 1); EC 2.3.1.21 (CPT1B protein, mouse); EC 2.3.1.21 (Carnitine O-Palmitoyltransferase); EC 2.7.11.11 (Cyclic AMP-Dependent Protein Kinases); EC 3.1.1.3 (Lipase); EC 3.1.1.3 (PNPLA2 protein, mouse); EC 6.4.- (Carbon-Carbon Ligases); EC 6.4.1.- (acyl-CoA carboxylase); M876330O56 (N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide); OU13V1EYWQ (SB 203580)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180214
[Lr] Data última revisão:
180214
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180111
[St] Status:MEDLINE


  4 / 2221 MEDLINE  
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[PMID]:29172481
[Au] Autor:Rebello CJ; Greenway FL; Johnson WD; Ribnicky D; Poulev A; Stadler K; Coulter AA
[Ad] Endereço:Pennington Biomedical Research Center , 6400 Perkins Road, Baton Rouge, Louisiana 70808, United States.
[Ti] Título:Fucoxanthin and Its Metabolite Fucoxanthinol Do Not Induce Browning in Human Adipocytes.
[So] Source:J Agric Food Chem;65(50):10915-10924, 2017 Dec 20.
[Is] ISSN:1520-5118
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Rodent studies suggest that the antiobesity effects of fucoxanthin relate to activation of brown fat and conversion of white adipocytes to the brown phenotype. To evaluate the browning effect in human adipocytes, we investigated the genes involved in browning and measured the oxygen consumption rate (OCR). Data were analyzed by one way ANOVA. Relative to control, fucoxanthinol (1 µM, 0.1 µM, 0.01 µM, 1 nM, 0.1 nM), the metabolite present in human plasma, stimulated lipolysis acutely (mean ± SEM: 4.2 ± 0.8, 3.1 ± 0.6, 4.1 ± 0.9, 3.8 ± 0.7, 3.8 ± 0.7, respectively, p < 0.01). There was no effect on OCR or the mRNA expression of UCP1, CPT-1ß, and GLUT4, the genes associated with browning of adipose tissue, when human adipocytes were treated with fucoxanthin or fucoxanthinol. -mRNA expression of PGC-1α, PPARα, PPARγ, PDK4, FAS, and the lipolytic enzymes was not significantly altered by fucoxanthinol treatment (p > 0.05). Thus, in human adipocytes, fucoxanthin and its metabolite do not stimulate conversion of white adipocytes to the brown phenotype.
[Mh] Termos MeSH primário: Xantofilas/metabolismo
beta Caroteno/análogos & derivados
[Mh] Termos MeSH secundário: Adipócitos/efeitos dos fármacos
Adipócitos/metabolismo
Tecido Adiposo Marrom/citologia
Tecido Adiposo Marrom/efeitos dos fármacos
Tecido Adiposo Marrom/metabolismo
Transportador de Glucose Tipo 4/genética
Transportador de Glucose Tipo 4/metabolismo
Seres Humanos
Lipólise/efeitos dos fármacos
PPAR gama/genética
PPAR gama/metabolismo
Coativador 1-alfa do Receptor gama Ativado por Proliferador de Peroxissomo/genética
Coativador 1-alfa do Receptor gama Ativado por Proliferador de Peroxissomo/metabolismo
Proteína Desacopladora 1/genética
Proteína Desacopladora 1/metabolismo
Xantofilas/farmacologia
beta Caroteno/metabolismo
beta Caroteno/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Glucose Transporter Type 4); 0 (PPAR gamma); 0 (PPARGC1A protein, human); 0 (Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha); 0 (SLC2A4 protein, human); 0 (UCP1 protein, human); 0 (Uncoupling Protein 1); 0 (Xanthophylls); 01YAE03M7J (beta Carotene); 06O0TC0VSM (fucoxanthin); 7176-02-5 (fucoxanthinol)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180210
[Lr] Data última revisão:
180210
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171128
[St] Status:MEDLINE
[do] DOI:10.1021/acs.jafc.7b03931


  5 / 2221 MEDLINE  
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[PMID]:28452586
[Au] Autor:Ortega SP; Chouchani ET; Boudina S
[Ad] Endereço:a Department of Nutrition and Integrative Physiology and Division of Endocrinology , Metabolism and Diabetes and Program in Molecular Medicine, University of Utah School of Medicine , Salt Lake City , Utah , USA.
[Ti] Título:Stress turns on the heat: Regulation of mitochondrial biogenesis and UCP1 by ROS in adipocytes.
[So] Source:Adipocyte;6(1):56-61, 2017 01 02.
[Is] ISSN:2162-397X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Reactive oxygen species (ROS) production and oxidative stress (OS) in adipose tissue are associated with obesity and insulin resistance (IR). The nature of this relationship i.e., cause and effect or consequence has not been clearly determined. We provide evidence that elevated mitochondrial ROS generated by adipocytes from mice with diet-induced obesity (DIO) represents an adaptive mechanism that precipitates fatty acid oxidation, mitochondrial biogenesis, and mitochondrial uncoupling in an effort to defend against weight gain. Consistent with that, mice with adipocyte-specific deletion of manganese superoxide dismutase (MnSOD) exhibit increased adipocyte superoxide generation and are protected from weight gain and insulin resistance which otherwise develops in wild-type (WT) mice that consume an obesogenic diet. The defense mechanism displayed by MnSOD-deficiency in fat cells appears to be mediated by a dual effect of ROS on inefficient substrate oxidation through uncoupling of oxidative phosphorylation and enhanced mitochondrial biogenesis. The aim of this commentary is to summarize and contextualize additional evidence supporting the importance of mitochondrial ROS in the regulation of mitochondrial biogenesis and the modulation of uncoupling protein 1 (UCP1) expression and activation in both white and brown adipocytes.
[Mh] Termos MeSH primário: Adipócitos/metabolismo
Espécies Reativas de Oxigênio/metabolismo
Superóxido Dismutase/metabolismo
Proteína Desacopladora 1/metabolismo
[Mh] Termos MeSH secundário: Adipócitos/efeitos dos fármacos
Animais
Metabolismo Energético/efeitos dos fármacos
Camundongos
Mitocôndrias/efeitos dos fármacos
Proteínas Mitocondriais/metabolismo
Biogênese de Organelas
Estresse Oxidativo/fisiologia
Superóxido Dismutase/deficiência
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Mitochondrial Proteins); 0 (Reactive Oxygen Species); 0 (Uncoupling Protein 1); EC 1.15.1.1 (Superoxide Dismutase)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171216
[Lr] Data última revisão:
171216
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170429
[St] Status:MEDLINE
[do] DOI:10.1080/21623945.2016.1273298


  6 / 2221 MEDLINE  
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[PMID]:29054764
[Au] Autor:Li C; Li J; Xiong X; Liu Y; Lv Y; Qin S; Liu D; Wei R; Ruan X; Zhang J; Xu L; Wang X; Chen J; Zhang Y; Zheng L
[Ad] Endereço:Laboratory of Chinese Herbal Pharmacology, Oncology Center, Renmin Hospital, Hubei University of Medicine, Shiyan 442000, China; Laboratory of Medicinal Plant, School of Basic Medicine, Hubei University of Medicine, Shiyan 442000, China.
[Ti] Título:TRPM8 activation improves energy expenditure in skeletal muscle and exercise endurance in mice.
[So] Source:Gene;641:111-116, 2018 Jan 30.
[Is] ISSN:1879-0038
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Skeletal muscle serving as the major organ is responsible for energy expenditure and exercise endurance, which directly influence cardiometabolic risk factors. Transient receptor potential melastatin 8 (TRPM8), a Ca -permeable non-selective cation channel, plays vital roles in the regulation of various cellular functions. It has been reported that TRPM8 activation enhanced the energy metabolism of adipocytes. However, the involvement of TRPM8 in the energy metabolism of skeletal muscle remains unexplored. Our data revealed that TRPM8 was expressed in cultured C2C12 myocytes. Menthol treatment increased uncoupling protein 1 (UCP1) and peroxisome proliferator-activated receptor-γ coactivator 1α (PGC1α) expression in C2C12 myotubes through TRPM8 activation. Moreover, dietary menthol upregulated the expression of UCP1 and PGC1α in skeletal muscle of mice. In addition, dietary menthol enhanced exercise endurance and reduced blood lactic acid and triglycerides through TRPM8 activation. It is concluded that dietary menthol improves energy metabolism and exercise endurance by increasing UCP1 and PGC1α in skeletal muscles, suggesting dietary menthol might be a novel therapeutic approach for cardiometabolic diseases management and prevention.
[Mh] Termos MeSH primário: Metabolismo Energético/fisiologia
Mentol/farmacologia
Músculo Esquelético/metabolismo
Coativador 1-alfa do Receptor gama Ativado por Proliferador de Peroxissomo/biossíntese
Resistência Física/fisiologia
Canais de Cátion TRPM/metabolismo
Proteína Desacopladora 1/biossíntese
[Mh] Termos MeSH secundário: Animais
Linhagem Celular
Ativação Enzimática
Ácido Láctico/sangue
Camundongos
Camundongos Endogâmicos C57BL
Mitocôndrias/metabolismo
Consumo de Oxigênio/efeitos dos fármacos
Triglicerídeos/sangue
Regulação para Cima/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha); 0 (TRPM Cation Channels); 0 (TRPM8 protein, mouse); 0 (Triglycerides); 0 (Ucp1 protein, mouse); 0 (Uncoupling Protein 1); 1490-04-6 (Menthol); 33X04XA5AT (Lactic Acid)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171128
[Lr] Data última revisão:
171128
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171022
[St] Status:MEDLINE


  7 / 2221 MEDLINE  
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[PMID]:28938440
[Au] Autor:Larson KR; Russo KA; Fang Y; Mohajerani N; Goodson ML; Ryan KK
[Ad] Endereço:Department of Neurobiology, Physiology, and Behavior, College of Biological Sciences, University of California, Davis, Davis, California 95616.
[Ti] Título:Sex Differences in the Hormonal and Metabolic Response to Dietary Protein Dilution.
[So] Source:Endocrinology;158(10):3477-3487, 2017 Oct 01.
[Is] ISSN:1945-7170
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Consumption of a low-protein, high-carbohydrate diet induces a striking increase in circulating fibroblast growth factor-21 (FGF21), which is associated with improved cardiometabolic health and increased longevity. Increased lifespan during this dietary protein "dilution" has been explained by resource-mediated trade-offs between reproduction and survival, such that fecundity is optimized at a greater relative intake of proteins/carbohydrates. The magnitude of this trade-off is thought to be sex-dependent. In this study, we tested the hypothesis that metabolic responses to dietary protein dilution are likewise dependent on sex. We maintained age-matched adult male and female C57BL/6J mice on isocaloric diets containing 22% fat and differing in the ratio of protein/carbohydrate. The normal protein (NP) control diet contained 18% protein and 60% carbohydrate by kcal. The protein diluted (PD) diet contained 4% protein and 74% carbohydrate. Consistent with previous reports, PD males gained less weight and less fat than did normal protein controls and exhibited both improved glucose tolerance and decreased plasma lipids. In contrast, these metabolic benefits were absent among age-matched females maintained on the same diets. Likewise, whereas circulating FGF21 was increased up to 66-fold among PD male mice, this was substantially blunted among female counterparts. Sex differences in energy balance, glucose control, and plasma FGF21 were reversed upon ovariectomy. Collectively, our findings support that female mice are relatively less sensitive to the metabolic improvements observed following dietary protein dilution. This is accompanied by blunted circulating levels of FGF21 and requires an intact female reproductive system.
[Mh] Termos MeSH primário: Glicemia/metabolismo
Dieta com Restrição de Proteínas
Carboidratos da Dieta
Proteínas na Dieta
Fatores de Crescimento de Fibroblastos/metabolismo
Metabolismo dos Lipídeos
Ganho de Peso
[Mh] Termos MeSH secundário: Animais
Composição Corporal
Ingestão de Energia
Metabolismo Energético
Feminino
Teste de Tolerância a Glucose
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Ovariectomia
Coativador 1-alfa do Receptor gama Ativado por Proliferador de Peroxissomo/genética
RNA Mensageiro/metabolismo
Receptor Tipo 1 de Fator de Crescimento de Fibroblastos/genética
Fatores Sexuais
Transcriptoma
Proteína Desacopladora 1/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Blood Glucose); 0 (Dietary Carbohydrates); 0 (Dietary Proteins); 0 (Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha); 0 (Ppargc1a protein, mouse); 0 (RNA, Messenger); 0 (Ucp1 protein, mouse); 0 (Uncoupling Protein 1); 0 (fibroblast growth factor 21); 62031-54-3 (Fibroblast Growth Factors); EC 2.7.10.1 (Fgfr1 protein, mouse); EC 2.7.10.1 (Receptor, Fibroblast Growth Factor, Type 1)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171016
[Lr] Data última revisão:
171016
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170923
[St] Status:MEDLINE
[do] DOI:10.1210/en.2017-00331


  8 / 2221 MEDLINE  
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[PMID]:28917655
[Au] Autor:Hu Z; Chen M; Zhou H; Tharakan A; Wang X; Qiu L; Liang S; Qin X; Zhang Y; Wang W; Xu Y; Ying Z
[Ad] Endereço:Department of Endocrinology, The People's Hospital of Zhengzhou University (Henan Provincial People's Hospital), Zhengzhou, Henan 450003, China; Department of Medicine Cardiology Division, University of Maryland School of Medicine, Baltimore, MD 21201, USA. Electronic address: huziying828@126.com.
[Ti] Título:Inactivation of TNF/LT locus alters mouse metabolic response to concentrated ambient PM .
[So] Source:Toxicology;390:100-108, 2017 Sep 01.
[Is] ISSN:1879-3185
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Exposure to ambient fine particulate matter (PM ) is associated with increased cardiometabolic morbidity and mortality. This is widely believed to be attributable to PM exposure-induced pulmonary and subsequent systemic inflammation. Tumor necrosis factor alpha (TNFα), lymphotoxin α (LTα), and lymphotoxin ß (LTß) are three homologous pro-inflammatory cytokines, each with both unique and redundant activities in inflammation. Their role in PM exposure-induced inflammation and adverse cardiometabolic effects has to be determined. METHODS AND RESULTS: LTα/TNFα/LTß triple-knockout (TNF/LT KO) and wildtype (WT) mice were exposed to concentrated ambient PM (CAP) for 5 months. Lung pathological analysis revealed that TNF/LT deficiency reduced CAP exposure-induced pulmonary inflammation. However, glucose homeostasis assessments showed that TNF/LT deficiency significantly aggravated CAP exposure-induced glucose intolerance and insulin resistance. Consistent with glucose homeostasis assessments, CAP exposure significantly increased the body weight and adiposity of TNF/LT KO but not WT mice. In contrast to its body weight effects, CAP exposure reduced food intake of WT but not TNF/LT KO mice. On the other hand, CAP exposure induced marked fat droplet accumulation in brown adipose tissues of WT mice and significantly decreased their uncoupling protein 1 (UCP1) expression, and these effects were markedly exacerbated in TNF/LT KO mice. CONCLUSION: The present study suggests that TNF/LT deficiency influences PM exposure-induced response of energy metabolism through alterations in both food intake and energy expenditure.
[Mh] Termos MeSH primário: Inativação Gênica
Transtornos do Metabolismo de Glucose/induzido quimicamente
Linfotoxina-alfa/deficiência
Linfotoxina-beta/deficiência
Obesidade/induzido quimicamente
Material Particulado/toxicidade
Pneumonia/prevenção & controle
Fator de Necrose Tumoral alfa/deficiência
[Mh] Termos MeSH secundário: Tecido Adiposo Marrom/efeitos dos fármacos
Tecido Adiposo Marrom/metabolismo
Tecido Adiposo Marrom/fisiopatologia
Tecido Adiposo Branco/efeitos dos fármacos
Tecido Adiposo Branco/metabolismo
Tecido Adiposo Branco/fisiopatologia
Adiposidade/efeitos dos fármacos
Animais
Biomarcadores/sangue
Glicemia/efeitos dos fármacos
Glicemia/metabolismo
Ingestão de Alimentos/efeitos dos fármacos
Metabolismo Energético/efeitos dos fármacos
Genótipo
Transtornos do Metabolismo de Glucose/genética
Transtornos do Metabolismo de Glucose/metabolismo
Insulina/sangue
Resistência à Insulina
Gotículas Lipídicas/efeitos dos fármacos
Gotículas Lipídicas/metabolismo
Linfotoxina-alfa/genética
Linfotoxina-beta/genética
Camundongos Endogâmicos C57BL
Camundongos Knockout
Obesidade/genética
Obesidade/metabolismo
Obesidade/fisiopatologia
Tamanho da Partícula
Fenótipo
Pneumonia/induzido quimicamente
Pneumonia/genética
Pneumonia/metabolismo
Fatores de Tempo
Fator de Necrose Tumoral alfa/genética
Proteína Desacopladora 1/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (Blood Glucose); 0 (Insulin); 0 (Ltb protein, mouse); 0 (Lymphotoxin-alpha); 0 (Lymphotoxin-beta); 0 (Particulate Matter); 0 (Tumor Necrosis Factor-alpha); 0 (Ucp1 protein, mouse); 0 (Uncoupling Protein 1)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171023
[Lr] Data última revisão:
171023
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170918
[St] Status:MEDLINE


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[PMID]:28851749
[Au] Autor:Dore R; Levata L; Gachkar S; Jöhren O; Mittag J; Lehnert H; Schulz C
[Ad] Endereço:Department of Internal Medicine ICenter of Brain, Behavior and Metabolism (CBBM), University of Lübeck, Lübeck, Germany.
[Ti] Título:The thermogenic effect of nesfatin-1 requires recruitment of the melanocortin system.
[So] Source:J Endocrinol;235(2):111-122, 2017 Nov.
[Is] ISSN:1479-6805
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Nesfatin-1 is a bioactive polypeptide expressed both in the brain and peripheral tissues and involved in the control of energy balance by reducing food intake. Central administration of nesfatin-1 significantly increases energy expenditure, as demonstrated by a higher dry heat loss; yet, the mechanisms underlying the thermogenic effect of central nesfatin-1 remain unknown. Therefore, in this study, we sought to investigate whether the increase in energy expenditure induced by nesfatin-1 is mediated by the central melanocortin pathway, which was previously reported to mediate central nesfatin-1´s effects on feeding and numerous other physiological functions. With the application of direct calorimetry, we found that intracerebroventricular nesfatin-1 (25 pmol) treatment increased dry heat loss and that this effect was fully blocked by simultaneous administration of an equimolar dose of the melanocortin 3/4 receptor antagonist, SHU9119. Interestingly, the nesfatin-1-induced increase in dry heat loss was positively correlated with body weight loss. In addition, as assessed with thermal imaging, intracerebroventricular nesfatin-1 (100 pmol) increased interscapular brown adipose tissue (iBAT) as well as tail temperature, suggesting increased heat production in the iBAT and heat dissipation over the tail surface. Finally, nesfatin-1 upregulated pro-opiomelanocortin and melanocortin 3 receptor mRNA expression in the hypothalamus, accompanied by a significant increase in iodothyronine deiodinase 2 and by a nonsignificant increase in uncoupling protein 1 and peroxisome proliferator-activated receptor gamma coactivator-1 alpha mRNA in the iBAT. Overall, we clearly demonstrate that nesfatin-1 requires the activation of the central melanocortin system to increase iBAT thermogenesis and, in turn, overall energy expenditure.
[Mh] Termos MeSH primário: Proteínas de Ligação ao Cálcio/metabolismo
Proteínas de Ligação a DNA/metabolismo
Melanocortinas/metabolismo
Proteínas do Tecido Nervoso/metabolismo
Termogênese/fisiologia
[Mh] Termos MeSH secundário: Animais
Biomarcadores
Proteínas de Ligação ao Cálcio/genética
Proteínas de Ligação a DNA/genética
Orelha
Hipotálamo/metabolismo
Masculino
Hormônios Estimuladores de Melanócitos/farmacologia
Proteínas do Tecido Nervoso/genética
RNA Mensageiro/genética
RNA Mensageiro/metabolismo
Ratos
Ratos Wistar
Receptores de Melanocortina/antagonistas & inibidores
Receptores de Melanocortina/genética
Receptores de Melanocortina/metabolismo
Cauda
Proteína Desacopladora 1/genética
Proteína Desacopladora 1/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (Calcium-Binding Proteins); 0 (DNA-Binding Proteins); 0 (Melanocortins); 0 (Nerve Tissue Proteins); 0 (RNA, Messenger); 0 (Receptors, Melanocortin); 0 (Ucp1 protein, rat); 0 (Uncoupling Protein 1); 0 (nucleobindin); 168482-23-3 (SHU 9119); 9002-79-3 (Melanocyte-Stimulating Hormones)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170925
[Lr] Data última revisão:
170925
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170831
[St] Status:MEDLINE
[do] DOI:10.1530/JOE-17-0151


  10 / 2221 MEDLINE  
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[PMID]:28842500
[Au] Autor:Chouchani ET; Kazak L; Spiegelman BM
[Ad] Endereço:From the Dana-Farber Cancer Institute, Harvard Medical School and.
[Ti] Título:Mitochondrial reactive oxygen species and adipose tissue thermogenesis: Bridging physiology and mechanisms.
[So] Source:J Biol Chem;292(41):16810-16816, 2017 Oct 13.
[Is] ISSN:1083-351X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Brown and beige adipose tissues can catabolize stored energy to generate heat, relying on the principal effector of thermogenesis: uncoupling protein 1 (UCP1). This unique capability could be leveraged as a therapy for metabolic disease. Numerous animal and cellular models have now demonstrated that mitochondrial reactive oxygen species (ROS) signal to support adipocyte thermogenic identity and function. Herein, we contextualize these findings within the established principles of redox signaling and mechanistic studies of UCP1 function. We provide a framework for understanding the role of mitochondrial ROS signaling in thermogenesis together with testable hypotheses for understanding mechanisms and developing therapies.
[Mh] Termos MeSH primário: Tecido Adiposo Marrom/metabolismo
Espécies Reativas de Oxigênio/metabolismo
Transdução de Sinais
Termogênese
Proteína Desacopladora 1/metabolismo
[Mh] Termos MeSH secundário: Adipócitos/metabolismo
Animais
Seres Humanos
Oxirredução
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Reactive Oxygen Species); 0 (UCP1 protein, human); 0 (Uncoupling Protein 1)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171020
[Lr] Data última revisão:
171020
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170827
[St] Status:MEDLINE
[do] DOI:10.1074/jbc.R117.789628



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