Fatty Liver and Kidney Syndrome in Biotin Deficient Chicks

Birds are especially sensitive to biotin deficiency, at least partly because their intestinal flora make little or no contribution to biotin intake. This is of considerable commercial importance with intensively reared poultry. In adult birds, biotin deficiency does not affect egg production, but does reduce the amount of biotin in the eggs, thus impairing embryonic development. In severe deficiency, the hatchability of the eggs can fall to near zero.

In young chicks, biotin deficiency is associated with the fatal fatty liver and kidney syndrome. Apparently healthy chicks 3 to 5 weeks old become lethargic, then sink onto the sternum and become motionless, dying within 6 to 10hours of the onset of the condition. Postmortem examination shows enlarged liver and kidneys, with extensive fatty infiltration, but none of the classical skin and feather signs of biotin deficiency. The syndrome can be induced with only a moderate degree of biotin deficiency if the birds are maintained on a high-carbohydrate, low-fat and low-protein diet; a mild stress, such as short-term fasting, will then induce the syndrome in up to 20% of the birds. Supplementing the diet with biotin prevents the problem.

Gluconeogenesis is severely impaired in birds suffering from the fatty liver and kidney syndrome; the administration of biotin rapidly restores gluconeogenesis to normal, by activating apopyruvate carboxylase. The affected animals also have impaired glucose 6-phosphatase and phosphoenolpyruvate carboxykinase activity, but increased hepatic activity of acetyl CoA carboxylase and malate dehydrogenase, with increased desaturation of long-chain fatty acids.

The problem is thus obviously not simply one of biotin deficiency, although supplementary biotin will alleviate the condition.

Birds fed the high-carbohydrate, low-fat, low-protein diet show more marked hypoglycemia on fasting than do controls, and modest hyperglycemia on refeeding. The cause of death in response to modest stress is believed to be acute hypoglycemia because of the impairment of hepatic gluconeogenesis; birds fed the same diet that do not succumb are believed to have a compensatory increase in renal gluconeogenesis, and hence are more resistant to the effects of food deprivation (Bannister, 1976a, 1976b; Whitehead et al., 1976). Cot Death Cot death, or Sudden Infant Death Syndrome, when an apparently healthy child dies suddenly, and from no apparent cause, has some similarities with the fatty liver and kidney syndrome in birds. It has been suggested that it may result from marginal biotin deficiency, together with a precipitating metabolic stress.

There is circumstantial evidence to support this suggestion, because the liver content of biotin is lower in infants who have died from cot death than in infants who have died from known causes. By parallel with the fatty liver and kidney syndrome, it has been suggested that a modest metabolic stress, such as a mild fever, causes a higher requirement for gluconeogenesis than can be met, resulting in acute hypoglycemia. There are rapid postmortem changes in blood and tissue glucose, so it is unlikely that there can be any direct evidence to support this suggestion (Johnson et al., 1980; Heard et al., 1983).

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