Skip to main content
Journal cover image

Acetyl-L-carnitine deficiency as a cause of altered nerve myo-inositol content, Na,K-ATPase activity, and motor conduction velocity in the streptozotocin-diabetic rat.

Publication ,  Journal Article
Stevens, MJ; Lattimer, SA; Feldman, EL; Helton, ED; Millington, DS; Sima, AA; Greene, DA
Published in: Metabolism
July 1996

Defective metabolism of long-chain fatty acids and/or their accumulation in nerve may impair nerve function in diabetes by altering plasma or mitochondrial membrane integrity and perturbing intracellular metabolism and energy production. Carnitine and its acetylated derivatives such as acetyl-L-carnitine (ALC) promote fatty acid beta-oxidation in liver and prevent motor nerve conduction velocity (MNCV) slowing in diabetic rats. Neither the presence nor the possible implications of putative ALC deficiency have been definitively established in diabetic nerve. This study explored sciatic nerve ALC levels and the dose-dependent effects of ALC replacement on sciatic nerve metabolites, Na,K-ATPase, and MNCV after 2 and 4 weeks of streptozotocin-induced diabetes (STZ-D) in the rat. ALC treatment that increased nerve ALC levels delayed (to 4 weeks) but did not prevent nerve myo-inositol (MI) depletion, but prevented MNCV slowing and decreased ouabain-sensitive (but not -insensitive) ATPase activity in a dose-dependent fashion. However, ouabain-sensitive ATPase activity was also corrected by subtherapeutic doses of ALC that did not increase nerve ALC or affect MNCV. These data implicate nerve ALC depletion in diabetes as a factor contributing to alterations in nerve intermediary and energy metabolism and impulse conduction in diabetes, but suggest that these alterations may be differentially affected by various degrees of ALC depletion.

Duke Scholars

Published In

Metabolism

DOI

ISSN

0026-0495

Publication Date

July 1996

Volume

45

Issue

7

Start / End Page

865 / 872

Location

United States

Related Subject Headings

  • Sodium-Potassium-Exchanging ATPase
  • Sciatic Nerve
  • Rats, Wistar
  • Rats
  • Oxidation-Reduction
  • Ouabain
  • Neural Conduction
  • Motor Neurons
  • Male
  • Fatty Acids
 

Citation

APA
Chicago
ICMJE
MLA
NLM
Stevens, M. J., Lattimer, S. A., Feldman, E. L., Helton, E. D., Millington, D. S., Sima, A. A., & Greene, D. A. (1996). Acetyl-L-carnitine deficiency as a cause of altered nerve myo-inositol content, Na,K-ATPase activity, and motor conduction velocity in the streptozotocin-diabetic rat. Metabolism, 45(7), 865–872. https://doi.org/10.1016/s0026-0495(96)90161-4
Stevens, M. J., S. A. Lattimer, E. L. Feldman, E. D. Helton, D. S. Millington, A. A. Sima, and D. A. Greene. “Acetyl-L-carnitine deficiency as a cause of altered nerve myo-inositol content, Na,K-ATPase activity, and motor conduction velocity in the streptozotocin-diabetic rat.Metabolism 45, no. 7 (July 1996): 865–72. https://doi.org/10.1016/s0026-0495(96)90161-4.
Stevens MJ, Lattimer SA, Feldman EL, Helton ED, Millington DS, Sima AA, et al. Acetyl-L-carnitine deficiency as a cause of altered nerve myo-inositol content, Na,K-ATPase activity, and motor conduction velocity in the streptozotocin-diabetic rat. Metabolism. 1996 Jul;45(7):865–72.
Stevens, M. J., et al. “Acetyl-L-carnitine deficiency as a cause of altered nerve myo-inositol content, Na,K-ATPase activity, and motor conduction velocity in the streptozotocin-diabetic rat.Metabolism, vol. 45, no. 7, July 1996, pp. 865–72. Pubmed, doi:10.1016/s0026-0495(96)90161-4.
Stevens MJ, Lattimer SA, Feldman EL, Helton ED, Millington DS, Sima AA, Greene DA. Acetyl-L-carnitine deficiency as a cause of altered nerve myo-inositol content, Na,K-ATPase activity, and motor conduction velocity in the streptozotocin-diabetic rat. Metabolism. 1996 Jul;45(7):865–872.
Journal cover image

Published In

Metabolism

DOI

ISSN

0026-0495

Publication Date

July 1996

Volume

45

Issue

7

Start / End Page

865 / 872

Location

United States

Related Subject Headings

  • Sodium-Potassium-Exchanging ATPase
  • Sciatic Nerve
  • Rats, Wistar
  • Rats
  • Oxidation-Reduction
  • Ouabain
  • Neural Conduction
  • Motor Neurons
  • Male
  • Fatty Acids