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Título : Impairment of glucose metabolism and energy transfer in the hypertriglyceridemic rat heart
Creador: Carvajal Aguilera, Karla Guadalupe
Nivel de acceso: Open access
Palabras clave : Hipertrigliceridemia
Metabolismo Energético
Fosforilación Oxidativa
Glucólisis
Consumo de Oxígeno
 Hypertriglyceridemia
Energy Metabolism
Oxidative Phosphorylation
Glycolysis
Oxygen Consumption
metabolismo energético
fosforilación oxidativa
glicolisis
consumo de oxígeno
función contráctil
hypertriglyceridemia
Energy metabolism
oxidative phosphorylation
glycolysis
oxygen consumption
contractile function
hypertriglyceridemia
Descripción : The metabolic pathways involved in ATP production in hypertriglyceridemic rat hearts were evaluated. Hearts from male Wistar rats with sugar-induced hypertriglyceridemia were perfused in an isolated organ system. Mechanical performance, oxygen uptake and beat rate were evaluated under perfusion with different oxidizable substrates. Age- and weight-matched animals were used as control. The hypertriglyceridemic (HTG) hearts showed a decrease in the mechanical work and slight diminution in the oxygen uptake when perfused with glucose, pyruvate or lactate. No differences were found when perfused with palmitate, octanoate or β-hydroxybutyrate. The glycolytic flux in HTG hearts was 2.4 times lower than in control hearts. Phosphofructokinase-I (PFK-I) was 16% decreased in HTG hearts, whereas pyruvate kinase activity did not change. The increased levels of glucose- 6-phosphate in HTG heart, suggested a flux limitation by the PFK-I. Pyruvate dehydrogenase in its active form (PDHa) diminished as well. The PDHa level in the HTG hearts was restored to control values by dichloroacetate; however, this addition did not significantly improve the mechanical performance. Levels of ATP and phosphocreatine as well as total creatine kinase activity and the MB fraction were significant lower in the HTG hearts perfused with glucose. The data suggested that supply of ATP by glucose oxidation did not suffice to support cardiac work in the HTG hearts; this impairment was exacerbated by the diminution of the creatine kinase system output. (Mol Cell Biochem 249: 157–165, 2003)
Colaborador(es) u otros Autores: Baños Guadalupe
Moreno Sánchez Rafael
Fecha de publicación : 2003
Tipo de publicación: Artículo
Formato: pdf
Identificador del Recurso : 10.1023/A:1024799025126
Fuente: Molecular And Cellular Biochemistry 249(1 y 2):157-165
URI : http://repositorio.pediatria.gob.mx:8180/handle/20.500.12103/2516
Idioma: spa
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