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Experimental Thiamine DeficiencyNeuropathic and Mitochondrial Changes Induced in Rat Muscle
R. A. Pieter Kark, MD;
W. Jann Brown, MD;
V. Reggie Edgerton, PhD;
Susan F. Reynolds, PhD;
Gary Gibson, PhD
Arch Neurol. 1975;32(12):818-825.
Abstract
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• Whether pure thiamine deficiency produces a neuropathy in Mammalia is still debated. Rats were pair-fed synthetic diets with and without thiamine. When studied histochemically, soleus muscles from thiamine-deficient rats showed (1) small, angular fibers that had high NADH dehydrogenase activities; (2) a loss of 43% of type II (FOG) fibers; (3) decreased intensity of the reaction for βOHB dehydrogenase; and (4) fibers with subsarcolemmal collections resembling "raggedred" muscle. Electron microscopy revealed degeneration of some small myelin sheaths of distal and intramuscular nerves; atrophic, degenerating, hypoosmophilic muscle fibers in soleus and vastus medialis; and scattered muscle fibers with abnormal collections of deranged mitochondria accompanied by lipid droplets. These abnormalities, not found in control muscles, indicate that both motor neuropathy and mild mitochondrial changes, such as are seen in the "ragged-red" diseases, are induced by pure thiamine deficiency.
Author Affiliations
From the departments of neurology (Dr Kark), pathology (Dr Brown) biological chemistry (Dr Reynolds), and the Mental Retardation Program (Dr Kark, Dr Brown, Dr Gibson, and Dr Reynolds), the Reed Neurological Research Center (Dr Kark) and the Neuropsychiatric Institute, School of Medicine, and the Neuromuscular Research Laboratory, Department of Kinesiology (Dr Edgerton), UCLA.
Footnotes
Accepted for publication Nov 11, 1974.
Reprint requests to Reed Neurological Research Center, UCLA School of Medicine, 710 Westwood Plaza, Los Angeles, CA 90024 (Dr Kark).
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