SODIUM PIVALATE REDUCES CARDIAC CARNITINE CONTENT AND INCREASES GLUCOSE-OXIDATION WITHOUT AFFECTING CARDIAC FUNCTIONAL-CAPACITY

This study determined how selected cardiac functional, metabolic, and contractile properties were impacted by sodium pivalate, a compound wh ich creates a secondary carnitine deficiency. Young male rats received either sodium pivalate (20 mM, PIV) or sodium bicarbonate (20mM, CONT R) in their drinking water. After 11-12 weeks cardiac function and glu cose oxidation rates were measured in isolated, perfused working heart preparations. Hearts were also analyzed for carnitine content; activi ties of hexokinase (HK), citrate synthase (CS), and B-hydroxyacyl CoA dehydrogenase (HOAD); and myosin isoenzyme distribution. Sodium pivala te treatment significantly reduced cardiac carnitine content and incre ased glucose oxidation but did not alter cardiac functional capacity. HK activity was increased in the PIV group (p < 0.05), and HOAD activi ty decreased (p < 0.05). CS activity and myosin isoform distribution ( V1 > 85%) remained unchanged. These results demonstrate that pivalate treatment of this duration and the accompanying carnitine deficiency s hifts cardiac substrate utilization without compromising cardiac funct ional capacity.