A possible relationship between gluconeogenesis and glycogen metabolism in rabbits during myocardial ischemia

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 shortterm myocardial ischemia.

Energy Metabolism in Exercise-Induced Physiologic Cardiac Hypertrophy

“…It was found that the glycogen accumulation in the perfused heart of exercise training adapted mice ( Riehle et al., 2014 ) may be due to the increased glucose uptake stimulated by insulin ( Jensen and Richter, 2012 ). The cardiac glycogen is a potential source of myocardial energy ( Aguiar et al., 2017 ), and glycogen resynthesis after exercise contributes to glucose homeostasis. Recent studies have manifested that cardiac-specific expression of a kinase-deficient 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase transgene lowered glycolytic rate and regulated the expression of genes known to promote cardiac growth ( Boström et al., 2010 ; Bezzerides et al., 2016 ; Gibb et al., 2017 ).…”

Impaired tricarboxylic acid cycle flux and mitochondrial aerobic respiration during isoproterenol induced myocardial ischemia is rescued by bilobalide

“…Myocardial ischemia (MI) is a major threat to human health worldwide and there is an urgent need to study its pathogenesis and treatment [ 1 ]. MI is a metabolic disorder characterized by enhanced glycolysis, inhibition of glucose aerobic oxidation, and reduced ATP production [ [2] , [3] , [4] ]. Therefore, myocardial energy metabolism is an important target for the prevention and treatment of MI.…”