Polyunsaturated fatty acids, biotin

Biotin deficiency and the functional deficiency associated with lack of holo-carboxylase synthetase (Section 11.2.2.1), or biotinidase (Section 11.2.3.1), causes alopecia (hair loss) and a scaly erythematous dermatitis, especially around the body orifices. The dermatitis is similar to that seen in zinc and essential fatty acid deficiency and is commonly associated with Candida albicans infection. Histology of the skin shows an absence of sebaceous glands and atrophy of the hair follicles. The dermatitis is because of impaired metabolism of polyunsaturated fatty acids as a result of low activity of acetyl CoA carboxylase (Section 11.2.1.1). In biotin-deficient experimental animals, provision of supplements of long-chain 6 polyunsaturated fatty acids prevents the development of skin lesions (Mock et al., 1988a, 1988b Mock, 1991). 

Long-term regulation of acetyl-CoA carboxylase involves nutritional, hormonal (e.g., insulin, thyroxine), and other factors. In animals on high-carbohydrate diets, fat-free diets, choline deprivation, or vitamin B12 deprivation, the activity is enhanced. However, fasting, high intake of fat or of polyunsaturated fatty acids, and prolonged biotin deficiency leads to decreased activity. In diabetes, the enzyme activity is low, but insulin administration raises it to normal levels. 

Animals also depend on plants for essential organic molecules that they are unable to make. We call some of these molecules vitamins. Several vitamins, including niacin, riboflavin, pyridoxine, and biotin, are key players in catabolic and anabolic metabolism, and deficiencies in these vitamins have severe effects. Also, animals are incapable of synthesizing polyunsaturated fatty acids (fatty acids with more than one double bond). Polyunsaturated fatty acids are essential components of membrane lipids and must be obtained in the diet. So, the next time you have a salad, pay a tribute to photosynthesis. 

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