Decreased Maternal Cardiac Glucose Oxidation
Taking One for the Fetus
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During pregnancy, there are several coordinated and dynamic maternal adaptations that take place to meet the demands of the growing and developing fetus. This includes significant physiological, endocrine, and metabolic adaptations that produce a diabetogenic state of progressive insulin resistance.1,2 It is thought that these metabolic adaptations occur so that nutrients, such as glucose, are conserved and directed toward the fetus to sustain its constant nutritional and oxygen requirements. Pregnancy is also associated with significant physiological remodeling of the cardiovascular system, which includes increases in ventricular wall mass, ventricular hypertrophy, myocardial contractility, and cardiac compliance.1,2 These cardiac adaptations combined with an increase in heart rate and cardiac output further ensure the optimization of nutrient and oxygen delivery to the growing fetus. Although the maternal cardiovascular and metabolic adaptations that allow for optimal nutrient delivery to the fetus during pregnancy are well understood, one particular area where knowledge is lacking in pregnancy relates to maternal cardiac energy metabolism profiles. Because pregnancy results in an increased maternal cardiac hypertrophy, and both physiological and pathophysiological cardiac hypertrophy are associated with several alterations in myocardial energy metabolism,3,4 it is likely that pregnancy-associated cardiac hypertrophy is also accompanied by altered myocardial metabolism. In support of this, in this issue of Circulation Research, Liu et al5 provide evidence that the cardiac hypertrophy associated with late pregnancy is associated with reductions in myocardial glucose oxidation rates and increases in fatty acid oxidation rates (Figure).
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