857 resultados para GLUCOSE METABOLISM


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Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)

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Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)

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Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)

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Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)

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Pós-graduação em Ciências da Motricidade - IBRC

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O Diabetes mellitus é uma desordem patológica de origem endócrina que provoca inúmeras alterações de ordem sistêmica. Tem sido considerado que o diabetes influencia na instalação e progressão da doença periodontal a exemplo da dificuldade cicatricial, mas também sofre influência da mesma, posto que o curso clínico da doença periodontal pode alterar o metabolismo da glicose e, conseqüentemente, dificultar o controle do diabetes. Desta forma, a estreita relação entre a doença periodontal e diabetes tem sido motivo de preocupação entre os cirurgiões-dentistas. O objetivo deste estudo foi avaliar a condição clinica do periodonto em indivíduos diabéticos tipo 2 e a necessidade de tratamento periodontal através do Registro Penodontal Simplificado (PSR), juntamente com análise laboratorial (HbAlc e Proteína C- reativa ultra-sensívelPCR). Dos 88 participantes do estudo, 5,69% apresentaram-se livres de doenças; 36,36% apresentaram-se com gengivite e 57,95% apresentaram-se com periodontite. No grupo dos indivíduos não diabéticos, 51,06% tiveram periodontite, enquanto 65,85% dos diabéticos apresentaram a doença. A doença periodontal apresentou-se mais grave na faixa etária de 60-69 anos (grupo controle) e 70-79 anos (grupo diabéticos). Todos os diabéticos apresentaram doença periodontal, e o escore 3 (50,34%) o mais prevalente. No grupo controle 89,36% apresentaram doença periodontal, e o escore 2 (31,25%) foi o mais prevalente. Apesar dos altos níveis de proteína C-reativa e de hemoglobina glicada, não houve associação com a gravidade da doença periodontal nos participantes do estudo.

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Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)

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Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)

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Metabolic syndrome (MetS) is often accompanied by pro-oxidative and pro-inflammatory processes. Lifestyle modification (LiSM) may act as primary treatment for these processes. This study aimed to elucidate influencing factors on changes of malondialdehyde (MDA) and C-reactive protein (CRP) concentrations after a LiSM intervention. Sixty subjects (53 yrs, 84% women) clinically approved to attend a 20 weeks LiSM-program were submitted to weekly nutritional counseling and physical activities combining aerobic (3 times/week) and resistance (2 times/week) exercises. Before and after intervention they were assessed for anthropometric, clinical, cardiorespiratory fitness test (CRF) and laboratory markers. Statistical analyses performed were multiple regression analysis and backward stepwise with p<0.05 and R(2) as influence index. LiSM was responsible for elevations in CRF, healthy eating index (HEI), total plasma antioxidant capacity (TAP) and HDL-C along with reductions in waist circumference measures and MetS (47-40%) prevalence. MDA and CRP did not change after LiSM, however, we observed that MDA concentrations were positively influenced (R(2)=0.35) by fasting blood glucose (β=0.64) and HOMA-IR (β=0.58) whereas CRP concentrations were by plasma gamma-glutamyltransferase activity (β=0.54; R(2)=0.29). Pro-oxidant and pro-inflammatory states of MetS can be attenuated after lifestyle modification if glucose metabolism homeostasis were recovered and if liver inflammation were reduced, respectively.

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Objective This study assessed early manifestations of metabolic syndrome determinants in patients submitted to hematopoietic stem cell transplantation. Methods Twenty-seven individuals participated in the study (20 with autologous and 7 with allogeneic hematopoietic stem cell transplantation). Anthropometric variables and biochemical indicators of lipid and glucose metabolism were determined before and 100 days after hematopoietic stem cell transplantation.Results The mean total cholesterol (p=0.086), very low density lipoprotein-cholesterol (p=0.069) and triglycerides (p=0.086) of all patients did not change significantly between the two study periods, but when the patients were separated by type of hematopoietic stem cell transplantation, triglycerides and very low density lipoprotein-cholesterol were close to the critical level of significance for individuals with allogeneic hematopoietic stem cell transplantation (p=0.060) and total cholesterol was significant in individuals with autologous hematopoietic stem cell transplantation (p=0.027). Anthropometric variables did not change significantly between before and 100 days after hematopoietic stem cell transplantation. Conclusion Metabolic syndrome risk factors may be associated with lipid metabolism in the early phase of allogeneic and autologous hematopoietic stem cell transplantation.

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Fundação de Apoio à Pesquisa do Estado de São Paulo (FAPESP)

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Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)

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The molecular integration of nutrient-and pathogen-sensing pathways has become of great interest in understanding the mechanisms of insulin resistance in obesity. The double-stranded RNA-dependent protein kinase (PKR) is one candidate molecule that may provide cross talk between inflammatory and metabolic signaling. The present study was performed to determine, first, the role of PKR in modulating insulin action and glucose metabolism in physiological situations, and second, the role of PKR in insulin resistance in obese mice. We used Pkr(-/-) and Pkr(+/+) mice to investigate the role of PKR in modulating insulin sensitivity, glucose metabolism, and insulin signaling in liver, muscle, and adipose tissue in response to a high-fat diet. Our data show that in lean Pkr(-/-) mice, there is an improvement in insulin sensitivity, and in glucose tolerance, and a reduction in fasting blood glucose, probably related to a decrease in protein phosphatase 2A activity and a parallel increase in insulin-induced thymoma viral oncogene-1 (Akt) phosphorylation. PKR is activated in tissues of obese mice and can induce insulin resistance by directly binding to and inducing insulin receptor substrate (IRS)-1 serine307 phosphorylation or indirectly through modulation of c-Jun N-terminal kinase and inhibitor of kappa B kinase beta. Pkr(-/-) mice were protected from high-fat diet-induced insulin resistance and glucose intolerance and showed improved insulin signaling associated with a reduction in c-Jun N-terminal kinase and inhibitor of kappa B kinase beta phosphorylation in insulin-sensitive tissues. PKR may have a role in insulin sensitivity under normal physiological conditions, probably by modulating protein phosphatase 2A activity and serine-threonine kinase phosphorylation, and certainly, this kinase may represent a central mechanism for the integration of pathogen response and innate immunity with insulin action and metabolic pathways that are critical in obesity. (Endocrinology 153:5261-5274, 2012)

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The effects of a moderate electrical stimulation on superoxide and nitric oxide production by primary cultured skeletal muscle cells were evaluated. The involvement of the main sites of these reactive species production and the relationship between superoxide and nitric oxide production were also examined. Production of superoxide was evaluated by cytochrome c reduction and dihydroethidium oxidation assays. Electrical stimulation increased superoxide production after 1?h incubation. A xanthine oxidase inhibitor caused a partial decrease of superoxide generation and a significant amount of mitochondria-derived superoxide was also observed. Nitric oxide production was assessed by nitrite measurement and by using 4,5-diaminofluorescein diacetate (DAF-2-DA) assay. Using both methods an increased production of nitric oxide was obtained after electrical stimulation, which was also able to induce an increase of iNOS content and NF-?B activation. The participation of superoxide in nitric oxide production was investigated by incubating cells with DAF-2-DA in the presence or absence of electrical stimulation, a superoxide generator system (xanthinexanthine oxidase), a mixture of NOS inhibitors and SOD-PEG. Our data show that the induction of muscle contraction by a moderate electrical stimulation protocol led to an increased nitric oxide production that can be controlled by superoxide generation. The cross talk between these reactive species likely plays a role in exercise-induced maintenance and adaptation by regulating muscular glucose metabolism, force of contraction, fatigue, and antioxidant systems activities. J. Cell. Physiol. 227: 25112518, 2012. (c) 2011 Wiley Periodicals, Inc.

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Aims: NADPH oxidase (NOX) is a known source of superoxide anions in phagocytic and non-phagocytic cells. In this study, the presence of this enzyme in human pancreatic islets and the importance of NADPH oxidase in human beta-cell function were investigated. Main methods and key findings: In isolated human pancreatic islets, the expression of NADPH oxidase components was evidenced by real-time PCR (p22(PHOX), p47(PHOX) and p67(PHOX)), Western blotting (p47(PHOX) and p67(PHOX)) and immunohistochemistry (p47(PHOX), p67(PHOX) and gp91(PHOX)). Immunohistochemistry experiments showed co-localization of p47(PHOX), p67(PHOX) and gp91(PHOX) (isoform 2 of NADPH oxidase-NOX2) with insulin secreting cells. Inhibition of NADPH oxidase activity impaired glucose metabolism and glucose-stimulated insulin secretion. Significance: These findings demonstrate the presence of the main intrinsic components of NADPH oxidase comprising the NOX2 isoform in human pancreatic islets, whose activity also contributes to human beta-cell function. (C) 2012 Elsevier Inc. All rights reserved.