Effects of L-carnitine and propionyl-L carnitine on glucose and fatty acid oxidation in myocytes from normal and diabetic rats

The present study was designed to evaluate effects of L-carnitine (LC) and its derivative propionyl-L-carnitine (PLC) on glucose and fatty acid metabolism under normal and diabetic conditions. LC and PLC increased the oxidation of long-chain fatty acid (palmitate) by 44% and 52% respectively, in normal myocytes (cont. 2.7 ± 0.33, LC 3.9 (0.37, PLC 4.1±0.43, p<0.001, 0.01 of LC & PLC vs cont.). PLC caused 66% increase of palmitate oxidation in diabetic cells (diab. 3.5 ±0.12, diab. + LPC 5.9 ( 0.25, p<0.001). LC had no effect on palmitate oxidation in these cells. PLC increased the oxidation of medium-chain fatty acid (octanoate) by 22% (cont. 13.1±0.7, PLC 16.8±1.37, p<0.001), while LC had no effect on its oxidation. PLC caused a significant 18% decrease of glucose oxidation in normal myocytes (cont. 2.5±0.08, PLC 1.9±0.3, p<0.01). The oxidation of glucose was not affected by LC in these cells. Both LC and PLC had no effect on glucose oxidation in diabetic myocytes. LC caused 65% increase in pyruvate dehydrogenase complex (PDH) activity in normal myocytes (cont 122.7±4.8, LC 203±27.3, p<0.01). Surprisingly, PLC had no effect on enzyme activity in these cells. Both LC and PLC increased PDH activity by 45-50% in diabetic myocytes (LC 104.6±13, LPC 107.8±18.8, p<0.01, 0.01 of LC & PLC vs diabetes). LC caused a significant 21 % decrease of [2-14C] pyruvate oxidation (cont. 25.75±2.63, LC 21.2±3.5, p<0.05), while PLC had no effect on its oxidation in normal myocytes. Both LC and PLC had no effect on [2-14C] pyruvate oxidation in diabetic myocytes. Different metabolic effects of these compounds are probably due to effects of the propionate group of PLC. The propionate moiety could increase anaplerotic pathways and reduce free CoA availability in the mitochondria.