Some aspects of lipid metabolism in fatty liver and kidney syndrome in chicks.

Various aspects of lipid metabolism were examined in broiler chicks affected with fatty liver and kidney syndrome (FLKS). Plasma free fatty acid concentrations were invariably elevated. Plasma triglyceride concentrations were increased amounts of triglyceride-rich lipoproteins. Lipoprotein lipase activity in adipose tissue was considerably reduced, but in heart tissue the enzyme activity was increased. Hepatic lipogenesis was reduced. Rates of oxidation of palmitic and succinic acids by liver, heart and kidney were normal. The increased oxidation rate of palmitic acid following the addition of carnitine was also normal. These findings indicate that elevated blood lipid levels are likely to be an important factor contributing to the development of fatty deposition, particularly in extrahepatic tissues.     

Evidence for a lesion in carbohydrate metabolism in fatty liver and kidney syndrome in chicks.

Liver and kidney slices from chicks affected with fatty liver and kidney syndrome (FLKS) were incubated in vitro with a variety of non-carbohydrate precursors and their ability to form glucose was studied. The results show that the affected liver was unable to form significant quantities of glucose from the precursors (gluconeogenesis). Glycogen breakdown was also drastically reduced because the tissue was almost devoid of this carbohydrate store. Blood chemistry revealed no evidence of overall liver malfunction but reflected the consequences of lack of gluconeogenesis. In contrast, kidney gluconeogenic activity was significantly higher than in the controls, suggesting an attempt by this organ to offset the reduced hepatic capability. Attempts to restore activity in vitro were made by adding known cofactors of gluconeogenesis. Asmall but significant improvement resulted from addition of biotin to liver slices.     

Aspects of lipid and carbohydrate metabolism, dietary biotin and fatty liver and kidney syndrome in broilers.

Two experiments were performed to investigate the biochemical changes associated with FLKS. A diet reported to induce FLKS was fed with or without supplementary biotin to broilers. In experiment 1 various stresses were applied to the birds. 2. In experiment 1 mortality from FLKS was 6% and in experiment 2 nil. Stress had little effect on the induction of the syndrome. 3. There were no significant differences due to diet in any of the variables examined in apparently normal birds. 4. Birds affected by FLKS showed the typical changes of increased liver and kidney weights and lipid contents but hepatic enzyme activities did not differ significantly from those of normal birds except that malate dehydrogenase (decarboxylating) (NADP) activity was significantly decreased. 5. Despite the low content of biotin in the unsupplemented diet (57 mug/kg) liver biotin content was not low in birds fed on this diet. 6. The results suggest that the incidence of FLKS is not related solely to dietary biotin content.     

The histopathology of fatty liver and kidney syndrome in chicks.

Studies of the general histopathology of the fatty liver and kidney syndrome in chickens have shown abnormal accumulations of the lipid in a variety of organs but no degenerative or inflammatory reactions. Lipid was found in some skeletal muscles, alimentary tract, autonomic ganglia, central nervous system and pineal gland as well as in the liver, kidney and heart. Small amounts of lipid were sometimes seen in the exocrine pancreas, adrenal medulla and epithelium of the thyroid follicles. Lipid deposits in the liver were primarily associated with the hepatic structural unit. The glycogen content of the hepatic cell was reduced. The lipid-metabolising gastrocnemius muscle contained abnormal amounts of lipid but this did not apply to the carbohydrate-metabolising pectoralis major muscle. The thymus did not contain excessive lipid but was significantly smaller in affected than in control birds of similar ages. There was loss of tinctorial distinction between the cortex and medulla of the adrenal gland associated with decreased basophilia of the latter region. Many of these morphological changes can be correlated with previously reported biochemical findings and they are discussed in relation to the hyperlipaemia and hypoglycaemia which characterise the disease.     

Involvement of biotin in the fatty liver and kidney syndrome of broilers

Experiments were conducted with caged broilers using diets containing 79% wheat and 20% meat meal. In the first experiment an outbreak of fatty liver and kidney syndrome (FLKS) occurred. Mortality was prevented, and subsequent growth rate was improved, by a single oral dose of a mixture of water‐soluble vitamins. A similar but less concentrated mixture successfully controlled a field outbreak of FLKS and lowered overall mortality.

In further experiments, it was shown that a deficiency of biotin was the main contributing factor in causing FLKS. With these wheat‐meat meal diets biotin concentrations of up to 120 μg/kg diet were associated with FLKS mortality but when the biotin concentration was raised to 145 μg/kg diet growth was maximised and mortality due to FLKS eliminated. There was also evidence that the concentration of biotin levels in breeder diets may affect the incidence of FLKS in their progeny.     

Lactate administration and fatty liver and kidney syndrome development in biotin-deficient chicks.

Two experiments were carried out to determine whether administration of lactate to biotin-deficient chicks induced fatty liver and kidney syndrome (FLKS). 2. The results suggest that increased serum lactate concentrations are a consequence of the syndrome rather than a contributory factor in its incidence. 3. The increase in liver lipids of birds affected by FLKS was not associated with an increase in the specific activity of the hepatic lipogenic enzyme acetyl CoA carboxylase accept when birds developed FLKS spontaneously in experiment 2. 4. Some biotin-deficient chicks did not show physical symptoms of deficiency although mean liver biotin concentrations were low (0.31 microgram/g liver).     

The effects of choline and inositol on hepatic lipid metabolism and the incidence of the fatty liver and kidney syndrome in broilers.

1. Diets high in wheat and low in protein (18%) produced 5 to 6% mortality from fatty liver and kidney syndrome (FLKS) in broiler chicks whereas there were no deaths from FLKS in birds fed on a maize/barley diet containing 20% protein. 2. Supplementation of the wheat-based diets with choline or inositol (2-5 g additive/kg diet) did not affect the incidence of FLKS or liver lipid metabolism. 3. The wheat-based diet did not significantly affect the activities of hepatic lipogenic enzymes suggesting that hepatic lipid biosynthesis is not a cause of the syndrome. 4. The biotin contents of the wheat and maize/barley diets were little different, which may suggest that factors other than this are implicated in FLKS.     

Carbohydrate absorption by chicks affected with the fatty liver and kidney syndrome.

Chicks with fatty liver and kidney syndrome (FLKS) were given oral doses of one of the following test solutions: water, glucose, maltose, starch. Plasma glucose concentration was measured during the four subsequent hours. All FLKS-affected chicks were hypoglycaemic before treatment. Although in some cases plasma glucose concentration increased slightly in the FLSK-chicks given water alone, significantly greater increases were invariably observed following the administration of carbohydrate to sick birds. Results obtained from dietary experiments in which starch was replaced by glucose in a ration causing high mortality from the syndrome revealed no beneficial effect due to the substitution. It was concluded that FLKS does not involve any major impairmant of carbohydrate digestion or absorption.     

The involvement of biotin in preventing the fatty liver and kidney syndrome in chicks.

Three experiments were carried out to investigate the involvement of vitamins in the fatty liver and kidney syndrome. The compounds studied, singly and in combination, were thiamin, riboflavin, nicotinic acid, pyridoxine, pantothenic acid, biotin, folic acid vitamin B12, ascorbic acid, choline and inositol and of these, only biotin prevented the syndrome. The minimum levels of supplemental dietary biotin required to prevent mortality varied from 0-05 to 0-15 mg/kg, depending on the diet. These levels were higher than the amounts required for maximum liveweight.     

鸡脂肪肝出血综合征发生过程中脂质代谢与血清甲状腺激素水平变化

探讨血清甲状腺激素水平与鸡脂肪肝出血综合征（FLHs）发生之间的关系。选用14日龄青脚麻鸡160只,按体质量随机分为对照组和FLHS组。对照组饲喂基础日粮,FLHs组饲喂高脂日粮（基础日粮＋10％牛油）的同时肌肉注射苯甲酸雌二醇（剂量为2．4mg／kg,每周3次,共3周）,试验期为28d。结果显示,试验期间,FLHS组鸡的体温明显降低;28和42日龄时,FLHS组鸡的平均体质量与平均采食量均显著高于对照组（P〈0．05或P〈10．01）;皮下脂肪厚度、肌间脂肪宽度、肝指数、肝脂率、皮脂率、腹脂率升高;血清TG、TC和LDL—C浓度均显著高于对照组（P〈0．05或P％0．01）,而血清HDL—C浓度均显著低于对照组（P〈0．01）;血清T3、T4和FT3水平降低,特别在试验后期降低更明显,而血清FT4水平变化不显著;同时FLHS组血清TP、ALB和PA浓度均比对照组有所提高。结果提示,FLHS可引起血清甲状腺激素水平的下降,而甲状腺激素水平的下降进一步造成脂质代谢紊乱,参与了鸡FLHS的发生。     

Changes in plasma lipid and glucose levels during the onset of fatty liver and kidney syndrome in chics

Plasma glucose, free fatty acid and triglyceride levels were measured during the onset of fatty liver and kidney syndrome in chicks. Intial studies indicated that behavioural and clinical changes characteristically associated with the syndrome were observed only during the 24 h preceding death. A more detailed examination of the blood changes was made on fasted birds. Typically, affected birds could be distinguished from healthy fasted birds by a hypoglycaemia which developed within 2.5 h of the removal of food, and a slightly higher and more sustained elevation of free fatty acid levels. Triglyceride values were not generally different from those found in normal birds. Although moderate to large amounts of lipid were occasionally observed in the kidneys of healthy fasted birds, only in affected birds was significant lipid infiltration of the kidneys associated with a similar level of lipid infiltration of the liver. In extreme cases death from fatty liver and kidney syndrome could occur within 4 h of the removal of food.