High metabolic substrate load induces mitochondrial dysfunction in rat skeletal muscle microvascular endothelial cells

The influence of glucose and palmitic acid (PA) on mitochondrial respiration and emission of hydrogen peroxide (H2O2) was determined in skeletal muscle‐derived microvascular endothelial cells. Measurements were assessed in intact and permeabilized (cells treated with 0.025% saponin) low passage endothelial cells with acute‐or prolonged (3 days) incubation with regular (1.7 mM) or elevated (2.2 mM) PA concentrations and regular (5 mM) or elevated (11 mM) glucose concentrations. In intact cells, acute incubation with 1.7 mM PA alone or with 1.7 mM PA + 5 mM glucose (p
This study investigated and compared the impact of glucose and palmitic acid on mitochondrial respiration and emission of hydrogen peroxide measured simultaneously in low passage microvascular endothelial cells derived from rat skeletal muscle. The study shows for the first time that acute and prolonged lipid availability and prolonged hyperglycemia, as seen in lifestyle‐related diseases, lower mitochondrial respiration and enhance hydrogen peroxide emission in primary microvascular endothelial cells.