scholarly journals Biotin deficiency and susceptibility to fatty liver and kidney syndrome in broiler chicks: reduced 6-phosphofructokinase (EC 2.7.1.11) activity but normal fructose 2,6-bisphosphate content in birds with hepatomegaly

1985 ◽  
Vol 54 (2) ◽  
pp. 535-543
Author(s):  
D. W. Bannister ◽  
D. I. Sales ◽  
Alison Lee
Keyword(s):  
Fatty Liver ◽  
Regulatory Mechanism ◽  
Bimodal Distribution ◽  
Broiler Chicks ◽  
Biotin Deficiency ◽  
Liver Size ◽  
Linear Discriminant ◽  
Body Weights ◽  
Liver And Kidney ◽  
Different Strains

1. In two separate experiments, using different strains, broiler chicks were reared on either a commercial-type chick mash (control) or a fatty liver and kidney syndrome (FLKS)-inducing diet.2. In Expt a, chicks were killed on day 29 and in Expt b, on day 32. Body-weights and liver weights were measured, and values from those given the control ration used to construct a hepatomegaly index by employing a variant of linear discriminant analysis.3. Application of the index to FLKS birds revealed a statistically significant bimodal distribution of liver size.4. The birds with enlarged livers (high index) also possessed metabolic abnormalities in that 6- phosphofructokinase (EC 2. 7. 1. 11; PFK-1) activity (measured at low substrate concentration) was depressed despite the presence of normal, or even slightly elevated fructose 2,6-bisphosphate concentration.5. This indicates the presence of an uncharacterized regulatory mechanism for PFK- 1 in FLKS-susceptible birds.

scholarly journals Metabolic changes associated with the occurrence of fatty liver and kidney syndrome in chicks

1978 ◽  
Vol 40 (2) ◽  
pp. 221-234 ◽  
Author(s):  
C. C. Whitehead ◽  
D. W Bannister ◽  
Maureen E. Cleland
Keyword(s):  
Lactate Dehydrogenase ◽  
Fatty Liver ◽  
Pyruvate Carboxylase ◽  
Liver Weight ◽  
High Plasma ◽  
Broiler Chicks ◽  
Plasma Lactate ◽  
Carboxylase Activity ◽  
Lactate Dehydrogenase Activity ◽  
Liver And Kidney

1. The changes in a number of metabolic measurements brought about by low-biotin diets associated with high and low incidences of fatty liver and kidney syndrome (FLKS) were studied in healthy 4-week-old broiler chicks.2. Liver pyruvate carboxylase (pyruvate: CO2 ligase (ADP); EC 6.4.1.1) activity was low in birds fed on a diet causing a high incidence of FLKS but the addition of fat or protein to this diet, to decrease the incidence of FLKS, increased enzyme activity.3. Liver weights, blood lactate concentrations, plasma lactate dehydrogenase (l-lactate:NAD oxidoreductase; EC 1.1.1.27) activities and values for C16:1:C18:0 fatty acid in liver, adipose tissue and plasma triglyceride were highest in birds fed on the high-FLKS diet and all measurements were negatively correlated with pyruvate carboxylase activity.4. Birds with high plasma lactate dehydrogenase activity or triglyceride C16:1:C18:0 values were the most likely to develop FLKS when fasted.5. There was no evidence that increased liver weight was associated with increased activities of certain other liver enzymes.6. It is concluded that FLKS occurs in birds with little or no hepatic gluconeogenic capacity via pyruvate carboxylase as a result of a dietary insufficiency of biotin but that the initiation of the syndrome is probably associated with the inhibition of other pathways of gluconeogenesis.

scholarly journals The development of a biotin deficiency in domestic fowl given wheat-based diets

1975 ◽  
Vol 34 (1) ◽  
pp. 83-90 ◽  
Author(s):  
D. Balnave
Keyword(s):  
Fatty Liver ◽  
Domestic Fowl ◽  
Body Weight Gain ◽  
Physical Symptoms ◽  
Metabolic Effects ◽  
Hepatic Enzyme ◽  
Meat And Bone Meal ◽  
Bone Meal ◽  
Biotin Deficiency ◽  
Liver And Kidney

1. Studies were done of the possible development of a biotin deficiency in domestic fowl of various ages as a result of feeding with diets composed mainly of wheat, and meat-and-bone meal. The degree of deficiency was estimated from physical symptoms, liver and kidney composition and hepatic enzyme activities.2. Only a mild biotin deficiency developed in 3-week-old chickens and no adverse metabolic effects were found for chickens reared to 7 or 15 weeks of age or maintained for 9 months in lay on these diets, which were suspected of producing fatty liver and kidney disease in young chickens. At 3 weeks of age the deficiency was more severe the heavier the strain of chicken and the greater the rate of body-weight gain.3. The present results question the supposition that biotin deficiency is the sole factor responsible for the development of fatty liver and kidney syndrome in young chickens.

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

1976 ◽  
Vol 29 (6) ◽  
pp. 429 ◽  
Author(s):  
RL Hood ◽  
A RJohnson ◽  
AC Fogerty ◽  
Judith A Pearson
Keyword(s):  
Fatty Liver ◽  
Pyruvate Carboxylase ◽  
Acetyl Coa Carboxylase ◽  
Defence Mechanisms ◽  
Acetyl Coa ◽  
Liver Size ◽  
Glucose Levels ◽  
Blood Glucose Levels ◽  
Liver And Kidney

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.

scholarly journals Biotin Deficiency and the Development of the Fatty Liver and Kidney Syndrome in Chickens: An Ultrastructural Study

1977 ◽  
Vol 30 (2) ◽  
pp. 57
Author(s):  
Joan M Bain
Keyword(s):  
Fatty Liver ◽  
Ultrastructural Study ◽  
Liver Tissue ◽  
Normal Tissue ◽  
Adrenal Glands ◽  
Biotin Deficiency ◽  
Liver And Kidney ◽  
Different Levels

The structure of the tissue from the liver, kidneys, pancreas and adrenal glands of 4-week-old chickens showing symptoms of the fatty liver and kidney syndrome (FLKS) was compared with that of normal tissue and related to the amount of biotin present in the liver tissue. These birds were reared with different levels of dietary biotin and were stressed by removal of food before being killed. Birds with less than 1�5 pg biotin/g liver were considered to be deficient in biotin. In the stressed birds the severity of FLKS increased with decreasing levels of biotin.

scholarly journals Biotin deficiency and fatty liver and kidney syndrome in chicks given purified diets containing different fat and protein levels

1976 ◽  
Vol 35 (1) ◽  
pp. 115-125 ◽  
Author(s):  
C. C. Whitehead ◽  
D. W. Bannister ◽  
A. J. Evans ◽  
W. G. Siller ◽  
P. A. L. Wight
Keyword(s):  
Fatty Acids ◽  
Fatty Acid Composition ◽  
Fatty Acid ◽  
Free Fatty Acid ◽  
Fatty Liver ◽  
Acid Composition ◽  
Plasma Glucose ◽  
Biotin Deficiency ◽  
Protein Levels ◽  
Liver And Kidney

1. The occurrence of biotin deficiency and fatty liver and kidney syndrome (FLKS) in chicks was studied using a 2 × 2 × 2 × 2 factorial-design experiment in which the variables were dietary biotin, fat and protein, and starvation.2. The severity of biotin deficiency, using growth retardation and severity of dermal lesions as criteria, was least when the low-biotin diet also contained low levels of fat and protein. Addition of fat or protein increased the severity of the deficiency. Tissue fatty acid composition was affected by biotin deficiency only in those birds given the low-protein, low-fat diet. The main change was an increase in the ratio, 16:1 fatty acids:18:0 fatty acids. Plasma glucose and free fatty acid levels in non-fasted birds were unaffected by the dietary variables.3. Mortality from FLKS with the diet containing low biotin, fat and protein levels was 52% at 28 d, but was reduced or eliminated when the dietary level of any of these ingredients was increased.4. Starvation considerably increased the incidence of FLKS in the period immediately after fasting, and also affected plasma glucose and free fatty acid concentrations. Liver fatty acid composition indicated an increase in the proportion of 18:0 at the expense of 16:1 and 18:1, irrespective of diet, except when the bird developed FLKS, when 16:1 and 18:1 concentrations increased in proportion, at the expense of 18:0.5. The relationship between biotin deficiency and FLKS, and a possible mechanism for the induction of FLKS by starvation are discussed.

Effect of Riboflavin Deficiency on the Metabolism of Oxypurines in Chicks

1971 ◽  
Vol 49 (12) ◽  
pp. 1059-1062 ◽  
Author(s):  
S. T. Chou
Keyword(s):  
Uric Acid ◽  
Acid Synthesis ◽  
Xanthine Dehydrogenase ◽  
Broiler Chicks ◽  
Uric Acid Concentration ◽  
Riboflavin Deficiency ◽  
Deficient Diet ◽  
High Incidence ◽  
Liver And Kidney ◽  
Riboflavin Deficient

Day-old broiler chicks of both sexes were used in three experiments to determine the effect of riboflavin deficiency on oxypurine metabolism catalyzed by xanthine dehydrogenase, a riboflavin-containing enzyme. Chicks fed a riboflavin-deficient diet (1.38 mg/kg) for 3 weeks exhibited depressed growth and a high incidence of curled-toe paralysis (higher than 80%) as compared to control chicks (15.1 mg riboflavin per kilogram diet; no incidence of curled-toe paralysis). In addition, the precursors of uric acid, hypoxanthine and/or xanthine, accumulated in the liver and kidney of deficient chicks showing curled-toe paralysis. These observations show that dietary riboflavin being incorporated into xanthine dehydrogenase is essential for oxypurine metabolism. Moreover in the chick, the liver and the kidney may be important sites of uric acid synthesis. The low uric acid concentration in the plasma of the deficient chicks appeared to be indicative of a disturbance in uric acid synthesis in the liver and kidney.

scholarly journals Paradoxical Regulation of Biotin Utilization in Brain and Liver and Implications for Inherited Multiple Carboxylase Deficiency

2004 ◽  
Vol 279 (50) ◽  
pp. 52312-52318 ◽  
Author(s):  
Diana Pacheco-Alvarez ◽  
R. Sergio Solórzano-Vargas ◽  
Roy A. Gravel ◽  
Rafael Cervantes-Roldán ◽  
Antonio Velázquez ◽  
...  
Keyword(s):  
High Dose ◽  
Mrna Levels ◽  
Holocarboxylase Synthetase ◽  
Biotin Deficiency ◽  
Multiple Carboxylase Deficiency ◽  
Regulatory Impact ◽  
Normal Metabolism ◽  
Liver And Kidney ◽  
Essential Function ◽  
The Brain

Holocarboxylase synthetase (HCS) catalyzes the biotinylation of five carboxylases in human cells, and mutations of HCS cause multiple carboxylase deficiency (MCD). Although HCS also participates in the regulation of its own mRNA levels, the relevance of this mechanism to normal metabolism or to the MCD phenotype is not known. In this study, we show that mRNA levels of enzymes involved in biotin utilization, including HCS, are down-regulated during biotin deficiency in liver while remaining constitutively expressed in brain. We propose that this mechanism of regulation is aimed at sparing the essential function of biotin in the brain at the expense of organs such as liver and kidney during biotin deprivation. In MCD, it is possible that some of the manifestations of the disease may be associated with down-regulation of biotin utilization in liver because of the impaired activity of HCS and that high dose biotin therapy may in part be important to overcoming the adverse regulatory impact in such organs.

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