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 biochemistry of fatty liver and kidney syndrome. Biotin-mediated restoration of hepatic gluconeogenesis in vitro and its relationship to pyruvate carboxylase activity

1976 ◽  
Vol 156 (1) ◽  
pp. 167-173 ◽  
Author(s):  
D W Bannister
Keyword(s):  
Fatty Liver ◽  
Nutrient Medium ◽  
Pyruvate Carboxylase ◽  
Control Valve ◽  
Protein Synthesis Inhibitors ◽  
Hepatic Gluconeogenesis ◽  
Carboxylase Activity ◽  
Liver And Kidney ◽  
Rate Limiting

Liver slices from chicks affected by the fatty liver and kidney syndrome display an extremely low extent of hepatic gluconeogenesis which is associated with decreased activities of certain rate-limiting gluconeogenic enzymes. Pyruvate carboxylase activity is particularly severely affected, being less than 4% of control values. Incubation of affected slices in a biotin-containing nutrient medium restores both gluconeogenesis and pyruvate carboxylase actiivity (the latter to approx. 35% of the control valve). Activities of the other enzymes studied were not greatly affected by this treatment. Restoration of gluconeogenesis did not occur if biotin was excluded from the nutrient medium, nor was it prevented by protein-synthesis inhibitors. It is concluded that the syndrome involves the lack of available biotin in the liver rather than suppression of apocarboxylase synthesis.

scholarly journals A biochemical explanation for the fatty liver and kidney syndrome of broilers: its alleviation by the short-term use of dietary fat

1977 ◽  
Vol 38 (3) ◽  
pp. 319-328 ◽  
Author(s):  
D. Balnave ◽  
R. B. Cumming ◽  
T. M. Sutherland
Keyword(s):  
Fatty Liver ◽  
Broiler Chickens ◽  
Specific Activity ◽  
Liver Lipid ◽  
Liver Weight ◽  
Atp Citrate Lyase ◽  
Commercial Diet ◽  
Meat Meal ◽  
Citrate Lyase ◽  
Liver And Kidney

1. Fatty liver and kidney syndrome (FLKS) was induced in young broiler chickens by giving them a diet composed principally of wheat and meat meal.2. FLKS resulted in reduced growth and increased liver weight; fasting for 18 h increased mortality, liver lipid and the specific activity of hepatic ATP-citrate lyase compared with birds fed on a commercial diet. The specific activities of hepatic fructose-l,6-diphosphate-l-phosphohydrolase and pyruvate carboxylase were reduced in birds suffering from FLKS and fasted for 18 h.3. Feeding of the FLKS-inducing diet supplemented with 150 g animal tallow/kg for 54 h considerably reduced mortality while restoring liver composition and enzyme activities towards those observed in birds fed a commercial diet. Investigations indicated that the glycerol component of the fat was not responsible for the observed responses.4. The present results suggest that in FLKS insufficiencies of biotin are induced in specific enzyme systems, but the syndrome may be alleviated without the use of supplementary biotin.5. The evidence indicates that, when stressed, birds affected by FLKS die from the hypoglycaemia occurring as a result of a reduced capacity for gluconeogenesis.

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 The activities and intracellular distribution of nicotinamide-adenine dinucleotide phosphate-malate dehydrogenase, phosphoenolpyruvate carboxykinase and pyruvate carboxylase in rat, guinea-pig and rabbit tissues

1975 ◽  
Vol 146 (2) ◽  
pp. 329-332 ◽  
Author(s):  
D E Saggerson ◽  
C J Evans
Keyword(s):  
Adipose Tissue ◽  
Guinea Pig ◽  
Malate Dehydrogenase ◽  
Pyruvate Carboxylase ◽  
Phosphoenolpyruvate Carboxykinase ◽  
Nicotinamide Adenine Dinucleotide Phosphate ◽  
Intracellular Distribution ◽  
Kidney Cortex ◽  
Carboxylase Activity ◽  
Liver And Kidney

1. Measurements are presented of the activity and intracellular distribution of phosphoenolypruvate carboxykinase, pyruvate carboxylase and NADP-malate dehydrogenase in rat, guinea-pig and rabbit liver and kidney cortex, together with previously obtained measurements of these enzymes in adipose tissue. 2. In all three tissues pyruvate carboxylase activity was greatest in the rat and lowest in the rabbit. 3. Guinea pig and rabbit were very similar to each other with respect to the extramitochondrial-mitochondrial distribution of phosphoenolpyruvate carboxykinase in all three tissues. 4. NADP-malate dehydrogenase was present in all three tissues in the rat, present in kidney cortex and adipose tissue in the guinea pig and absent from all tissues examines in the rabbit.

Interaction between chronic arsenic exposure via drinking water and plasma lactate dehydrogenase activity

2010 ◽  
Vol 409 (2) ◽  
pp. 278-283 ◽  
Author(s):  
Md. Rezaul Karim ◽  
Kazi Abdus Salam ◽  
Ekhtear Hossain ◽  
Khairul Islam ◽  
Nurshad Ali ◽  
...  
Keyword(s):  
Drinking Water ◽  
Lactate Dehydrogenase ◽  
Dehydrogenase Activity ◽  
Arsenic Exposure ◽  
Plasma Lactate ◽  
Lactate Dehydrogenase Activity ◽  
Chronic Arsenic Exposure
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