Fatty Liver and Kidney Syndrome in Chicks II. Biochemical Role of Biotin

Abstract

The role of biotin-dependent enzymes in the fatty liver and kidney syndrome of young chicks was studied. Under conditions of a marginal deficiency of dietary biotin, the level of biotin in the liver has differing effects on the activities of two biotin-dependent enzymes, pyruvate carboxylase and acetyl-CoA carboxylase. The activity of acetyl-CoA carboxylase is increased, but when the dietary deficiency of biotin produces biotin levels which are below o· 8 p,g/g of liver, the activity of pyruvate carboxylase may be insufficient to completely metabolize pyruvate via gluconeogenesis. There is an increase in liver size and in the activities of enzymes involved in alternate pathways for the removal of pyruvate. Blood lactate accumulates and there is increased synthesis of fatty acids, and an accumulation of palmitoleic acid; these steps are accomplished by increased activities of at least the following enzymes: acetyl-CoA carboxylase, malate dehydrogenase (decarboxylating) (NADP+) and the desaturase enzyme. When the biotin level is below 0·35 p,g/g of liver and the chick is subjected to a stress, physiological defence mechanisms of the chick may be inadequate to maintain homeostasis and they finally collapse, resulting in accumulation of triacylglycerol in the liver and blood; the chick is unable to maintain blood glucose levels and death occurs, often only a few hours after the imposition of the stress.

Influences of biotin deficiency and dietary trans-fatty acids on tissue lipids in chickens

“…Suboptimal biotin nutriture coupled with other nutritional and environmental stresses has been implicated in fatty liver and kidney syndrome (FLKS) which can cause high mortality in commercial flocks of meat-type chickens (Hood et al 1976). The symptoms of FLKS differ from classical biotin deficiency in that the onset is sudden and death is rapid (within 24 h), but this condition is responsive to biotin supplementation (Bannister, 1976).…”

Tissue depletion of biotin in chickens and the development of deficiency lesions and the fatty liver and kidney syndrome

“…It may be that there is a homeostatic mechanism that endeavours to maintain plasma concentrations, thus ensuring supply of the vitamin to tissues for essential functions. Further, plasma and tissue concentrations of the vitamin were unaffected by starvation; a result that can also be inferred from Hood et al (1976).…”

“…The discrepancies in the literature presumably relate to the age of the bird or period of time that liver reserves of biotin have been depleted prior to the occurrence or inducement of FLKS. Hood et al (1976) suggested that chickens with liver biotin concentrations below 0.8 ßg/g are vulnerable to the development of FLKS although these authors and others (Pearce & Balnave, 1978;Balnave & Pearce, 1979) have shown that chicks dying from FLKS usually have liver biotin concentrations below 0.35 //g/g. Similar liver biotin concentrations were also found in this study.…”

“…The most obvious, is the failure of many birds dying from FLKS to exhibit signs of classical biotin deficiency. This has led to the view that FLKS results from a marginal biotin deficiency, yet liver concentrations of biotin in birds succumbing to FLKS is extremely low (Hood et al, 1976). In many previous studies of biotin deficiency and the incidence of FLKS, tissue concentrations of biotin were not reported.…”

Biological significance and development of practical synthesis of biotin

“…The dangerous effects of chickens and pigs are cured by supplementation of biotin as a feed additive. [75][76][77] Biotin-dependent multiple carboxylase defects in man are known to occur because of mutation of holocarboxylase 78 or biotinidase, which are much less common than in poultries. 79 Biotin deficiency may trigger teratogenesis.…”