Energy substrate preference and metabolic flexibility in quiescent and oxytocin-stimulated human myometrial cells.

The uterus requires energy for sustained contractility during labor to deliver the fetus and diminish the risk of postpartum hemorrhage. Our objective was to define energy requirements and assess metabolic flexibility in myometrial cells, with and without oxytocin to stimulate myometrial contractility. Our data show that myometrial cells rely on oxidative phosphorylation during quiescence and, when treated with oxytocin, can adapt to higher energy demands by shifting to glycolysis. Treatment with mitochondrial oxidation inhibitors revealed that basal oxygen consumption rate decreased when treated with the glucose oxidation inhibitor UK5099 but not the long-chain fatty acid oxidation inhibitor etomoxir or the glutamine oxidation inhibitor BPTES. In oxytocin-treated myometrial cells, this decrease was also observed upon BPTES treatment in addition to UK5099, suggesting that contractile myometrial cells can also utilize glutamine. Functionally, myometrial contractility was significantly reduced by UK5099 but not etomoxir, further indicating dependence on glucose utilization.