Fatty acids are not an important fuel for coronary microvascular endothelial cells

Abstract

The metabolism by coronary microvascular endothelial cells (CMEC) of the heart typical substrates palmitate and lactate was compared to that of glucose and glutamine. Confluent cultures of CMEC were used. Palmitate oxidation was saturable and independent of the exogenous albumin concentration. Palmitate, 300 microM, lactate, 1 mM, and glutamine, 0.5 mM, were oxidized to 35, 46, and 56 nmol CO2/h x mg protein. These oxidation rates were decreased by 80, 66, and 48% in presence of 5 mM glucose. The largest energy yield was obtained by glycolytic breakdown of glucose. Glucose, 5 mM, was degraded to lactate by 99%, and oxidized in the Krebs cycle by only 0.04%. 1% was catabolized via the hexose monophosphate pathway. The rate of glucose oxidation in the Krebs cycle could be 30-fold increased by the uncoupler 2,4-dinitrophenol, 30 microM. At concentrations lower than 1 mM the amount of glucose oxidized in the Krebs cycle also grew, indicating existence of the Crabtree effect. The energy demand of CMEC seems to be of the same order as that of the arrested heart.

Evidence for vesicles that mediate long-chain fatty acid uptake by human microvascular endothelial cells

“…However, thorough analysis revealed that LCFA metabolism does not play a major role in HMEC, as Ͼ75% of intracellular oleate remained unmetabolized within 10 min. This concurs with Spahr et al (47), who showed that coronary microvascular endothelial cells do not depend on fatty acids as energy source. Nagelkerke et al (5) describe that native oleate is almost instantaneously transferred from For these assays, HMEC-1 cell monolayers were incubated in serum-free medium with 173 mol/oleate plus [ 3 H]oleate tracer bound to 173 mol/l albumin for 10 min.…”

Changes in Human Endothelial Cell Energy Metabolic Capacities during in vitro Cultivation. The Role of “Aerobic Glycolysis” and Proliferation

“…The presence of mitochondrial pathways indicated that ATP-supply of EC by "aerobic glycolysis" can be supported or partially replaced by respiration. In coronary EC, palmitate, lactate or glutamine are oxidized, particularly if no extracellular glucose is present [22]. Correspondingly, we found increasing activities of the mitochondrial enzymes HOADH and ICDH in HUVEC during proliferation, but their maximum activities are considerably lower than that of PFK.…”

“…Coronary EC from rats degrade 99% of glucose to lactate even under aerobic conditions but they are able to oxidize glutamine, lactate or fatty acids as well [21,22]. Furthermore, Loike et al discovered that HUVEC contain phosphocreatine and express creatine kinase (CK) [23] while Culic et al (1997) did not find phosphocreatine in porcine EC [24].…”

Angiogenesis revisited – role and therapeutic potential of targeting endothelial metabolism

“…1), oxidative pathways only contribute a small portion of the total ATP production (Culic et al, 1997;De Bock et al, 2013b;Quintero et al, 2006;Spahr et al, 1989). This implies that the flux through the electron transport chain is kept in check.…”