Abstract

L-carnitine a normal constituent of the body, in general, is expected to stimulate fatty acid oxidation and to regulate lipolysis. However, previous studies have demonstrated that carnitine administration is frequently ineffective for reducing obesity, possibly due to the difficulty in increasing carnitine concentrations in tissues by oral administation. This study demonstrated the relationship between carnitine and high-fat diet-included obesity in the C57BL/6J mouse model. An analysis of transcriptional regulation of the genes (ACS, CPT-1) and of serum lipid profiles, revealed that carnitine supplemented mice accumulated 3 times more carnitine in liver and 1.3 times more in muscle respectively than the mouse that fed a basal level. Particularly, L-carnitine supplementation could reduce the risk of obesity by reducing LDL concentrations in plasma. Extra dietary carnitine may improve the energetic status of muscle, thus protecting it against an energy depletion experienced by mice that fed high-fat diets. The current study suggests carnitine supplementation might increase fatty acid oxidation due to the increased CPT-1 activity, and resulted in decreased FAS (fatty acid synthase) activity in C57BL/6J mice.

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