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Active transport of carnitine into skeletal muscle

H. Houston Merritt Clinical Research Center for Muscular Dystrophy and Related Diseases, Columbia University College of Physicians and Surgeons, and the Neurological Institute of the Presbyterian Hospital, New York.

Skeletal muscle carnitine concentration exceeds plasma carnitine concentration. To determine whether this concentration gradient is maintained by active transport we studied rat soleus and extensor digitorum longus muscles. Observations consistent with the existence of an active transport mechanism were that the soleus accumulated carnitine linearly for 3 hours of incubation to exceed a distribution ratio of 1; the temperature coefficient for carnitine accumulation between 33° C and 43° C was 2.0; anaerobic incubation reduced carnitine accumulation by 30 percent; and the rate of carnitine accumulation was saturated at high substrate concentrations and competitively inhibited by y-butyrobetaine. The K_m for carnitine of the carnitine transport mechanism of the soleus muscle was 0.259 mM and of the extensor digitorum longus muscle, 0.585 mM. The greater affinity of the soleus transport mechanism may explain the difference in carnitine transport by red and white muscle in intact animals. A defect in active transport of carnitine may be involved in the pathogenesis of some human myopathies characterized by excessive lipid storage and in diphtheritic cardiomyopathy.

Dr. Willner's address is Department of Neurology, College of Physicians and Surgeons of Columbia University, Neurological Institute, 710 West 168th Street, New York, NY 10032.

This study was supported by center grants from NINCDS (NS-117766-01) and the Muscular Dystrophy Association.

Dr. Willner is the recipient of a postdoctoral fellowship from the Muscular Dystrophy Association.

Accepted for publication August 18, 1977.

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