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American Journal of Clinical Nutrition, Vol 51, 853-858, Copyright © 1990 by The American Society for Clinical Nutrition, Inc
ORIGINAL RESEARCH COMMUNICATIONS |
VK Proud, WB Rizzo, JW Patterson, GS Heard and B Wolf
Department of Human Genetics, Medical College of Virginia, Richmond 23298-0033.
Full-thickness biopsies of haired and alopecic skin of biotin-deficient rats had less subcutaneous fat and showed lipophilic follicular plugging, vascular engorgement, epidermal hyperplasia, and abnormal keratinization. Mean activities of the three mitochondrial biotin- dependent carboxylases in the skin of biotin-deficient animals were reduced to 3-18% of control whereas the cytosolic enzyme, acetyl-CoA carboxylase, was reduced only to 38-61%. The total fatty acid content of haired and alopecic skin of deficient rats was 30% of those in the corresponding skin sites of control animals. Skin from deficient rats contained less of several long-chain fatty acids (16:0, 16:1, 18:0, 18:1, and 18:2) and more very-long-chain fatty acid, particularly 24:1 and 26:1. These alterations in fatty acids in biotin-deficient rats suggest that the skin findings in biotin and biotinidase deficiencies in humans may be due to similar fatty acid changes.
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