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

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.

1985 ◽  
Vol 54 (2) ◽  
pp. 535-543
Author(s):  
D. W. Bannister ◽  
D. I. Sales ◽  
Alison Lee

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.


1975 ◽  
Vol 34 (1) ◽  
pp. 83-90 ◽  
Author(s):  
D. Balnave

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.


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

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.


2016 ◽  
Vol 3 (5) ◽  
pp. 143
Author(s):  
Fatemeh Almasi ◽  
Mozafar Khazaei ◽  
Shima Chehrei ◽  
Ali Ghanbari

Non-alcoholic fatty liver induces many complications to the liver tissue and also serum related parameters. Medicinal plants are the safe therapeutic strategy for the treatment of diseases. In this regards, the present study was conducted to evaluate the effect of Tribulus terrestris L. (Zygophyllales: Zygophyllaceae) extract on non-alcoholic fatty liver in rats. In this experimental study, thirty male Wistar rats were divided into five groups (n = 6). Animals in experimental groups were received high fructose diet (70%) (HDF) daily alone or in combined with daily intraperitoneal injection of 500, 700 and 1,000 mg/kg extract of T. terrestris. Control group of rats was feed with standard chow. The serum levels of biomarkers of liver and serum lipid profiles were assessed, also histopathological examination of liver tissue done. Data were analyzed using One-way ANOVA method followed by Tukey’s post-hoc multiple comparison test and P < 0.05 was considered statistically significant. There were significant improvements for biomarkers of liver tissue (P < 0.05) and serum lipid profiles (P < 0.01) in the HFD-fed rats that were treated with T. terrestris extract compare to HFD-fed group. In addition, accumulation of lipids in hepatocytes was significantly reduced in the HFD-fed + extract administrated groups in comparison to HFD-fed rats (P < 0.01). T. terrestris extract has protective effects against non-alcoholic fatty liver by changing biomarkers of liver tissue, serum lipid profiles and histopathological anomalies of liver tissue, to normal range.


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