Assessment of Biotin Nutritional Status

The plasma concentration of the biotin does not provide a sensitive index of stams, at least partly because there is increased renal reabsorption of the vitamin as intake falls. Urinary excretion of biotin and its metabolites is more sensitive, but may be confounded by changes in biotin excretion caused by glucocorticoid hormones (McMahon, 2002). There are three sensitive markers of stams (Mock, 1999)  

The activity of propionyl CoA carboxylase in lymphocytes falls, and the activation of the apoenzyme on incubation with biotin rises, in patients receiving total parenteral nutrition before there is any change in the plasma concentration of biotin (Velazquez et al., 1990). In experimental animals, the activity of lymphocyte propionyl CoA carboxylase falls early during biotin depletion, at the same time as the activity of the hepatic enzyme. There is not the expected increase in urinary excretion of hydroxypropionic acid, presumably because propionyl CoA carboxylase is not rate-limiting for propionate metabolism (Mock and Mock, 2002). 

Reduced activity of methylcrotonyl CoA carboxylase (Section 11.2.1.4) results in the formation and excretion of 3-hydroxy-isovaleric acid in experimental biotin depletion, significant amounts of 3-hydroxy-isovaleric acid are excreted at the same time as the excretion of biotin and bisnorbiotin falls, before there is any change in the plasma concentration of biotin (Mock et al., 1997). 

As a result of impaired activity of acetyl CoA and propionyl CoA carboxylases, there are changes in the fatty acid composition of lipids in the lymphocytes of biotin-deficient rats. There is an increase in the proportion of long-chain fatty acids (C22 0 to C30 0) and odd-carbon fatty acids (Cl 5 0 to C29 0), with a decrease in the proportion of unsaturated fatty acids and the ratio of ds-vaccenic acid (C18 l )9) palmitoleic acid (C16 lft)6), which is indicative of impaired elongation and desaturation of fatty acids (Liu et al., 1994). 

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