Biotin status

H Baker. Assessment of biotin status clinical implications. Ann N Y Acad Sci 477 129-132, 1985. 

Dietary deficiency of biotin sufficient to cause clinical signs is extremely rare in human beings, although it may be a problem in intensively reared poultry. However, there is increasing evidence that suboptimal biotin status may be relatively common, despite the fact that the vitamin is widely distributed in many foods, is synthesized by intestinal flora, and there is an efficient mechanism for conserving biotin after the catabolism of biotin-containing enzymes. 

Mock DM (1999) Biotin status which are valid indicators and how do we know Journal... 

Mock NI, Malik MI, Stumbo PJ, Bishop WP, and Mock DM (1997) Increased urinary excretion of 3-hydroxyisovaleric acid and decreased urinary excretion of biotin are sensitive early indicators of decreased biotin status in experimental biotin deficiency. American Journal of Clinical Nutrition 65, 951-8. 

Velazquez A, Zamudio S, Baez A, Murguia-Corral R, Rangel-Peniche B, and Carrasco A (1990) Indicators of biotin status a study of patients on prolonged total parenteral nutrition. European Journal of Nutrition 44,11-16. 

Mock, D. M-, Stadier, D. D., Stratton, S. and Mock, N. I. (1997b). Biotin status assessed longitudinally in pregnant women. /. Nutr. 127, 710-716. 

Baker, H., 1985. Assessment of biotin status—clinical implications. Annals of the New York Academy of Sciences. 447 129-132. 

Human milk is the primary agent for infant nutriture and thereby guides the composition of manufactured infant formula and milk substitutes. The reported concentration of biotin in human milk is variable with lactation (and unfortunately between analytical methods), but is more than sufficient to supply the newborn infant with the RDI of 5-6pg/day, as evidenced by the absence of reported deficiency syndromes in breast-fed babies. Interestingly, most biotin in milk is present in a free form and therefore unbound with any macromolecules. As expected, when milk is separated into its fat and aqueous fractions, the water-soluble biotin is found predominantly in the skim-milk phase. Biotin has some lipophilidty and so a small percentage is carried into the cream as part of the fat-globule membrane. The total concentration of human milk is not large and somewhat similar to bovine milk. With respect to breast milk substitutes, it is necessary to ensure the biotin status remains comparable, thus international guidelines recommend 0.4-2.4pg/100 kJ of reconstituted or ready-to-feed infant formula. 

There is sparse information on the biotin status in patients on AEDs. Krause et at. (1988) reported that over 80% of the patients were at risk of biotin deficiency. The biotin levels were influenced by the inducer AEDs and not VPA. 

The Food and Nutrition Board of the US National Research Council has released adequate intakes for infants, adults and pregnant women (Mock 2004 National Research Council 1989 Yates et al. 1998). These recommendations (Table 43.1) refer to studies assuming that, with a daily dose of 60 pg of biotin, adults on parenteral nutrition declared they were symptom-free for six months and with diets supplying 28 2pg/day, no inadequate biotin status was observed. The dietary biotin intake in Western populations has been estimated to be 35-70 pg per day (143-287 nmoles per day). 

A negative correlation between deficient biotin status and blood lipid concentrations was found in rats (Marshall et al. 1976) as well as in humans (Marshall et al. 1980). A decrease in plasma lipids was observed in human healthy volunteers within 30 min of absorption of 100 mg of biotin infusion. It was shown that oral biotin supplementation affected plasma lipid concentrations. The administration of 5 mg/day of biotin decreased hypercholesterolemia in atherosclerosis and hyperlipidemia patients (Dukusova and Krivoruchenko 1972). A 15 mg/day treatment by biotin for 28 days decreased hypertriglyceridemia of subjects whose triacylglycerol concentrations were more than 25% above the normal of 1.8mmol/L (Baez-Saldana 2004). 

To allow estimation of human biotin requirements and evaluation of potential deleterious efiects of marginal degrees of biotin deficiency, indicators of biotin status need to be determined and validated. Several explored directions include serum concentrations and urinary excretion rates of biotin and biotin metabolites, activities of the biotin-dependent decarboxylases in peripheral blood mononuclear cells, and urinary excretion rates of 3-hydroxy-isovaleric acid 3-methylcrotonyl glycine and 2-methylcitric acid. 

D. M., 2010. Quantitative measurement of plasma 3-hydroxyisovaleryl carnitine by LC-MS/MS as a novel biomarker of biotin status in humans. Analytical Chemistry. 82 4140-4144. 

Marshall, M.W., Haubrich, M., Washington, V.A., Chang, M.W., Young, C.W., Wheeler, M.A., 1976. Biotin status and lipid metabolism in adult obese hypercholesterolemic inbred rats. Nutritional Metabolism. 20 41-61. 

Coggeshall JC, Heggers IP, Robson MC, and Baker H. Biotin status and plasma glucose levels in diabetics. Ann. NY Acad. Sci. 447 389-392 (1985). 

Determination of biotin levels in the blood and urinary excretion levels of biotin both provide evidence of biotin status in human Ereings. 

Studies have been conducted on diabetic humans and rats that support an effect of biotin status on carbohydrate metabolism. Genes studied include glu-cokinase, phosphoenolpyruvate carboxykinase (PEPCK), and expression of the asialoglycoprotein receptor on the surface of hepatocytes. The effect of biotin status on PEPCK expression was particularly striking when diabetic rats were compared to nondiabetic rats. However, most studies have been performed on rats in which metabolic pathways have been perturbed prior to administration of biotin. Thus, the role of biotin in regulation of these genes during normal biotin status remains to be elucidated. 

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