Navegando por Palavras-chave "Hepatic Metabolism"

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    Participação Do Receptor B1 De Cininas No Metabolismo Hepático De Gllcose
    (Universidade Federal de São Paulo (UNIFESP), 2017-05-30) Gregnani, Marcos Antonio Fernandes Da Silva [UNIFESP]; Araujo, Ronaldo De Carvalho [UNIFESP]; Universidade Federal de São Paulo (UNIFESP)
    Objective: To analyze Kinin 81 receptor participation in hepatic rnetabolisrn using maximal exercise test as strategy. Methods: 81 KO and WT mice was submited to maximal test protocol in treadmill in conditions "feeding" and "fasting". Measures of glycemia was done in basal state and during exercise protocol, as well after a challenge with piruvate to induce gluconeogenesis. Also, we done a measure of urinary glucose excretion after a big injection with these compound. In ex vivo analysis, we evaluated hepatic glycogen content, enzymatic activity of citrate synthase, tecidual oxygen consumption, and gene expression of proteins involved with glucose metabolism. Results: The 81 KO mice presented reduced performance in exercise protocol, coupled a reduced glycemic response in fed state, this phenotype was absent in fasting state.Furthermore,81 KO has a reduced glucose urinary excretion, and a reduced content of hepatic glycogen. The enzymes that are responsible for synthesis and degradation of glycogen has upregulated expression in 81 KO mice. Which respect to regulation of glucose flux inside hepatocytes, the enzyme glucose-6-phospatase, involved in gluconeogenesis presented a reduction in fed state. In addition, PPARalpha and two targets genes of these protein was also reduced, suggesting a modulation directed to glycolysis. This data was corroborated by a increassd rate of oxigen consumption in 81 KO mice in hepatic tissue, whereas there was not differences in muscle. It was observed also a increased expression of 82 kinin receptor in 81 knockout mice. Conclusion: The 81 kinin receptor seems able to modulate maximal exercise tolerance and this outcomes probably are related to his hepatic activity. In this tissue 81 kinin receptor can be able to maintain a equilibrated distribution in between glycolisis and glycogenesis, having a important role in glycemic homeostasis in fed state. These effects seems to be mediated by transcription factor PPAR-alpha and your target genes. Its translates in a global frame of adaptations that resu s in increased 02 consumption in hepatic tissue, negatively influencing glycogen 5 esis, en resulting in poor performance in acute maximal exercise.