Data/hora: 15/06/2024 14:16:59

Provedor de dados: | 42
País: | Brazil
Título: | A possible relationship between gluconeogenesis and glycogen metabolism in rabbits during myocardial ischemia
Autores: | AGUIAR,RAQUEL R. DE; VALE,DANIELA F.; SILVA,RENATO M. DA; MUNIZ,YOLANDA P.; ANTUNES,FERNANDA; LOGULLO,CARLOS; OLIVEIRA,ANDRÉ L.A.; ALMEIDA,ADRIANA J. DE.
Data: | 2017-09-01
Ano: | 2017
Palavras-chave: | Gene expression; Glycogen; Ischemia; Myocardium; Rabbit.
Resumo: | ABSTRACT Ischemia is responsible for many metabolic abnormalities in the heart, causing changes in organ function. One of modifications occurring in the ischemic cell is changing from aerobic to anaerobic metabolism. This change causes the predominance of the use of carbohydrates as an energy substrate instead of lipids. In this case, the glycogen is essential to the maintenance of heart energy intake, being an important reserve to resist the stress caused by hypoxia, using glycolysis and lactic acid fermentation. In order to study the glucose anaerobic pathways utilization and understand the metabolic adaptations, New Zealand white rabbits were subjected to ischemia caused by Inflow occlusion technique. The animals were monitored during surgery by pH and lactate levels. Transcription analysis of the pyruvate kinase, lactate dehydrogenase and phosphoenolpyruvate carboxykinase enzymes were performed by qRT-PCR, and glycogen quantification was determined enzymatically. Pyruvate kinase transcription increased during ischemia, followed by glycogen consumption content. The gluconeogenesis increased in control and ischemia moments, suggesting a relationship between gluconeogenesis and glycogen metabolism. This result shows the significant contribution of these substrates in the organ energy supply and demonstrates the capacity of the heart to adapt the metabolism after this injury, sustaining the homeostasis during short-term myocardial ischemia.
Tipo: | Info:eu-repo/semantics/article
Idioma: | Inglês
Identificador: | http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0001-37652017000401683
Editor: | Academia Brasileira de Ciências
Relação: | 10.1590/0001-3765201720160773
Formato: | text/html
Fonte: | Anais da Academia Brasileira de Ciências  v.89 n.3 2017
Fonte: | info:eu-repo/semantics/openAccess