Biotin chicks

Riboflavin was found to be most responsible for the stimulation of rat growth, while vitamin B6 was needed to prevent a facial dermatitis or "rat pellagra." Pantothenic acid was especially effective in curing a chick dermatitis, while nicotinamide was required to cure human pellagra. Biotin was required for growth of yeast. 

Bioassay methods include the (1) rat and chick method (growth response after biotin deficiency) (2) microbiological with L arabinosus. Physicochemical methods make use of polarography. 

Fatty Liver and Kidney Syndrome in Biotin-Deficient Chicks... 

Bannister DW (1976b) Hepatic gluconeogenesis in chicks effect of biotin on gluconeogenesis in biotin-deficiency and fatty liver and kidney syndrome. Comparative Biochemistry and Physiology B 53, 575-9. 

Whitehead CC, Bannister DW, Evans AJ, Siller WG, and Wight PA (1976) Biotin deficiency and fattyliver and kidney syndrome in chicks given purified diets containing different fat and protein levels. British Journal of Nutrition 35, 115-25. 

Biotin is widely distributed in foods liver, milk, yeast, oilseeds and vegetables are rich sources. However, in some foods, much of the bound vitamin may not be released during digestion and hence may be imavailable. Studies with chicks and pigs have shown that the availability of biotin in barley and wheat is very low, whereas the biotin in maize and certain oilseed meals, such as soya bean meal, is completely available. 

In poultry, biotin deficiency causes reduced growth, dermatitis, leg bone abnormalities, cracked feet, poor feathering, and fatty liver and kidney syndrome (FLKS).This last condition, which mainly affects 2- to 5-week-old chicks, is characterised by a lethargic state with death frequently following within a few hours. On autopsy, the liver and kidneys, which are pale and swollen, contain abnormal depositions of lipid. 

A few years later egg-white injury in chicks was shown to be associated with a deficiency of biotin in the tissues, despite its abundance in the diet [145]. In the same year, avidin was isolated from egg-white and its ability to inactivate biotin in vitro was demonstrated [146]. Gyorgy and Rose [235] fed rats with avidin but only found very small amounts of biotin in the faeces until the faeces were steamed. Biotin was then released from the avidin-biotin complex. As the result of further experiments, it was concluded that the fundamental cause of egg-white injury is the unavailability of biotin due to its fixation to avidin, so that biotin is not absorbed from the intestinal tract and is excreted in the faeces [237]. A similar conclusion was reached by Sullivan and Nicholls [603] who showed that when egg-white is cooked, avidin is denatured and rendered incapable of binding biotin. Egg-white injury has been produced experimentally in man and can be cured by the administration of biotin [607]. In a recent study, Peters [497] reported that raw egg-white has a direct toxic effect which is not associated with its action in causing biotin deficiency. It would appear, therefore, that further studies on egg-white injury must be more closely associated with a critical analysis of the different components of egg-white. 

Dakshinamurti K and Mistry SP. Tissue and intracellular distribution of biotin- COOH in rats and chick. J. Biol. Chem. 238 294—296 (1963). 

Despite the appearance of nervous incoordination, there are no signs of damage to the central nervous system, but the muscles show signs of atrophy and in some regions there is necrosis of the fibers. In chicks Couch et al found that biotin deficiency caused shortening of the tibiotarsus, the distal end of which was bent posteriorly. The tarsometatarsus was also shortened, and the distal end was bent medially. In some chicks the wing bones were shortened also. 

Burt found that, in 236 tissue cultures of embryonic chick neuroblasts, spindle cells, and macrophages, biotin had no growth-stimulating properties. 

---