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December 1975

Experimental Thiamine Deficiency: Neuropathic and Mitochondrial Changes Induced in Rat Muscle

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.

Arch Neurol. 1975;32(12):818-825. doi:10.1001/archneur.1975.00490540062008

• 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.

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