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Research Article Free access | 10.1172/JCI118621

Primary preventive and secondary interventionary effects of acetyl-L-carnitine on diabetic neuropathy in the bio-breeding Worcester rat.

A A Sima, H Ristic, A Merry, M Kamijo, S A Lattimer, M J Stevens, and D A Greene

Department of Pathology, University of Michigan Medical Center, Ann Arbor, 48109, USA.

Find articles by Sima, A. in: PubMed | Google Scholar

Department of Pathology, University of Michigan Medical Center, Ann Arbor, 48109, USA.

Find articles by Ristic, H. in: PubMed | Google Scholar

Department of Pathology, University of Michigan Medical Center, Ann Arbor, 48109, USA.

Find articles by Merry, A. in: PubMed | Google Scholar

Department of Pathology, University of Michigan Medical Center, Ann Arbor, 48109, USA.

Find articles by Kamijo, M. in: PubMed | Google Scholar

Department of Pathology, University of Michigan Medical Center, Ann Arbor, 48109, USA.

Find articles by Lattimer, S. in: PubMed | Google Scholar

Department of Pathology, University of Michigan Medical Center, Ann Arbor, 48109, USA.

Find articles by Stevens, M. in: PubMed | Google Scholar

Department of Pathology, University of Michigan Medical Center, Ann Arbor, 48109, USA.

Find articles by Greene, D. in: PubMed | Google Scholar

Published April 15, 1996 - More info

Published in Volume 97, Issue 8 on April 15, 1996
J Clin Invest. 1996;97(8):1900–1907. https://doi.org/10.1172/JCI118621.
© 1996 The American Society for Clinical Investigation
Published April 15, 1996 - Version history
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Abstract

The abnormalities underlying diabetic neuropathy appear to be multiple and involve metabolic neuronal and vasomediated defects. The accumulation of long-chain fatty acids and impaired beta-oxidation due to deficiencies in carnitine and/or its esterified derivatives, such as acetyl-L-carnitine, may have deleterious effects. In the present study, we examined, in the diabetic bio-breeding Worcester rat, the short- and long-term effects of acetyl-L-carnitine administration on peripheral nerve polyols, myoinositol, Na+/K+ -ATPase, vasoactive prostaglandins, nerve conduction velocity, and pathologic changes. Short-term prevention (4 mo) with acetyl-L-carnitine had no effects on nerve polyols, but corrected the Na+/K+ -ATPase defect and was associated with 63% prevention of the nerve conduction defect and complete prevention of structural changes. Long-term prevention (8 mo) and intervention (from 4 to 8 mo) with acetyl-L-carnitine treatment normalized nerve PGE(1) whereas 6-keto PGF(1-alpha) and PGE(2) were unaffected. In the prevention study, the conduction defect was 73% prevented and structural abnormalities attenuated. Intervention with acetyl-L-carnitine resulted in 76% recovery of the conduction defect and corrected neuropathologic changes characteristic of 4-mo diabetic rats. Acetyl-L-carnitine treatment promoted nerve fiber regeneration, which was increased two-fold compared to nontreated diabetic rats. These results demonstrate that acetyl-L-carnitine has a preventive effect on the acute Na+/- K+_ATPase defect and a preventive and corrective effect on PGE1 in chronically diabetic nerve associated with improvements of nerve conduction velocity and pathologic changes.

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