• History of Biotin
    1901           Wildiers discovers that yeast requires a special growth factor which he names “bios”. Over the next 30 years, bios proves to be a mixture of essential factors, one of which – bios IIB – is biotin.
       
    1916 Bateman observes the detrimental effect of feeding high doses of raw egg white to animals.
       
    1927 Boas confirms the findings of dermatosis and hair loss in rats fed with raw egg white. She shows that this egg white injury can be cured by a “protective factor X” found in the liver.
       
    1931 György also discovers this factor in the liver and calls it vitamin H (from Haut, the German word for skin).
       
    1933 Allison and coworkers isolate a respiratory coenzyme – coenzyme R – that is essential for the growth of Rhizobium, a nitrogen-fixing bacterium found in leguminous plants.
       
    1935 Kögl and Tönnis extract a crystalline growth factor from dried egg yolk and suggest the name ‘biotin’.
       
    1940 György and his associates conclude that biotin, vitamin H and coenzyme R are identical. They also succeed in isolating biotin from the liver.
       
    1942 Kögl and his group in Europe and du Vigneaud and his associates in the USA establish the structure of biotin.
       
    1942 Sydenstricker and colleagues demonstrate the need for biotin in the human diet.
       
    1943 Total synthesis of biotin by Harris and colleagues in the USA.
       
    1949 Goldberg and Sternbach develop a technique for the industrial production of biotin.
       
    1956 Traub confirms the structure of biotin by X-ray analysis.
       
    1959 Lynen's group describes the biological function of biotin and paves the way for further studies on the carboxylase enzymes.
       
    1971 First description of an inborn error of biotin-dependent carboxylase metabolism by Gompertz and associates.
       
    1981 Burri and her colleagues show that the early infantile form of multiple carboxylase deficiency is due to a mutation affecting holocarboxylase synthetase activity.
       
    1993 Wolf and coworkers suggest that late-onset multiple carboxylase deficiency results from a deficiency in biotinidase activity.
  • Biotin General overview

    Biotin is necessary for cell growth, the production of fatty acids, and the metabolism of fats and amino acids. It plays a role in the citric acid cycle, which is the process by which biochemical energy is generated during aerobic respiration. Biotin not only assists in various metabolic reactions, but also helps to transfer carbon dioxide. It may also be helpful in maintaining a steady blood sugarlevel.[3]Biotin is often recommended as a dietary supplementfor strengthening hair and nails, though scientific data supporting this usage are weak.[4][5]As a consequence, biotin is found in many cosmetics and health products for the hair and skin.[6]

    Biotin deficiency is rare because, in general, intestinal bacteria produce biotin in excess of the body's daily requirements.[7]For that reason, statutory agencies in many countries, for example the USA[8]and Australia,[9]do not prescribe a recommended daily intake of biotin. However, a number of metabolic disordersexist in which an individual's metabolism of biotin is abnormal, such as deficiency in the holocarboxylase synthetase enzyme which covalently links biotin onto the carboxylase, where the biotin acts as a cofactor.[10]

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