Nutritional and metabolic aspects of fatty liver disease in poultry

Summary There are two metabolic disorders of major commercial importance in poultry that involve the occurrence of fatty deposits in the liver. Fatty Liver and Kidney Syndrome (FLKS) affects young birds and the main manifestations, lipid infiltrations into liver and many other organs, are apparently secondary effects of the primary lesion that lies in carbohydrate metabolism. Although several nutritional and environmental factors influence FLKS, the main factor is the vitamin, biotin. In the absence of an adequate supply of biotin, the hepatic activity of pyruvate carboxylase, a biotin-dependent enzyme, becomes so low that gluconeogenesis in the liver via pyruvate becomes negligible. When the bird is then subject to a mild stress and 1or short term fasting, liver glycogen reserves become rapidly depleted and a progressive hypoglycaemia develops that ultimately proves fatal. Supplementing diets with adequate amounts of biotin can prevent the syndrome. Fatty Liver Haemorrhagic Syndrome (FLHS) is brought about by an excessive accumulation of fat in the livers of adult hens which weakens the cellular structure of the liver and allows fatal haemorrhaging to occur. The aetiology of the syndrome is not clear, but a major factor is an excessive intake of dietary energy. However, Me involvement of hormonal and toxicological factors, as well as other nutritional factors, is also possible.     

Clinical signs of fatty liver and kidney syndrome in broilers and their alleviation by the short‐term use of biotin or animal tallow

1. Birds affected by fatty liver and kidney syndrome (FLKS) had elevated concentrations of serum Na⁺, K+, lactate, pyruvate and uric acid and reduced concentrations of serum HCO‐₃ and glucose.

2. Short‐term treatment with biotin or animal tallow reduced the mortality from FLKS and prevented the clinical signs.

3. Lactic acidosis may be a major factor contributing to the mortality and physical symptoms observed in birds affected by FLKS. The lactic acidosis and the hypoglycaemia observed in FLKS are due primarily to an accumulation of pyruvate as a result of an insufficiency of biotin for normal pyruvate carboxylase activity.     

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.     

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.     

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.     

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).     

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.     

不同生物素水平对北京鸭前期生长性能影响及后期缺乏症观察

选用体重相近的1日龄雄性北京鸭512只,随机分成8组,每组8个重复,每个重复8只鸭。研究不同生物素水平对1~14日龄北京鸭生长性能的影响,以及进行后期生物素缺乏症的观察。结果表明:提高日粮中生物素水平,1~14日龄北京鸭日采食量和日增重也随之提高(P<0.05),料重比没有改善(P<0.05)。以日增重为衡量指标,通过直线折线模型分析,初步确定生物素适宜添加水平为0.186 mg/kg。北京鸭生物素缺乏症病变依次表现:眼部>羽毛>腿部>肝脏,伴发脂肪肝肾综合症(FLKS)。     

Biotin deficiency and liver metabolism in relation to fatty liver and kidney syndrome

1. Varying degrees of biotin deficiency were induced by adding freeze‐dried, raw egg white to the diet of broiler chicks. Aspects of liver metabolism were studied with reference to fatty liver and kidney syndrome.

2. Mortality was low with 11 .8 g egg white/kg diet, or less, but with 17.7 g/kg or more, mortality was very high. High mortality was observed with less than 0.33 μg biotin/g liver.

3. Associated with low concentrations of liver biotin were substantial increases in liver weight and lipid content in starved birds. The increased liver lipid content was not observed in birds fed ad libitum.

4. The increased liver lipid content in biotin‐deficient, starved birds was not reflected in the specific activities of hepatic lipogenic enzymes or hepatic lipogenesis in vivo measured by the incorporation of tritium from ³H‐labelled water into liver lipid.

5. Biotin deficiency affected the specific activities of the biotin‐requiring enzymes, pyruvate carboxylase and acetyl CoA carboxylase, differently; the latter was unaffected whereas the former decreased concomitantly with liver biotin concentration.     

A syndrome of dental abnormalities of sheep: II. The pathology and radiology

Histological and radiographic examination of 23 ewe heads has revealed that mandibular osteopathy is a feature of the ovine dental abnormality syndrome described by Bruère et al.⁽³⁾ The bone changes consisted of excessive irregular remodelling of bone with osteoporosis. Developmental faults were also demon-strated. The most dramatic of these were dentigerous cysts involving unerupted permanent incisors, although malposition-ing of permanent incisors was also observed.

A histological feature of the excessive incisor wear was chronic pulpitis, perhaps a. result of the rate of wear exceeding the rate at which protective secondary dentine could be de-posited in the pulp cavity.

A number of nutritional deficiencies is known to cause gener-alised osteoporosis. Recognition of the osteopathy described here thus supports the clinical evidence of Bruère et al.⁽³⁾ that a nutritional disorder could be a major factor in the pathogenesis of this syndrome.     

Zollinger‐Ellison Syndrome in a cat

Summary

Zollinger‐Ellison Syndrome in a 12‐year old castrated male European Shorthair cat is described. The clinical symptoms were vomiting, weight loss, listlessness and alternating diarrhoea and obstipation.

An endocrine tumour near the pancreatic duct had metastasised to the liver. Many duodenal ulcers were present. Immunohistochemistry revealed cells positive for gastrin and neuronspecific enolase (NSE) scattered throughout the tumour.     

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.     

IMPORTANCE OF ACUTE DEATH SYNDROME IN MORTALITIES IN BROILER CHICKEN FLOCKS

SUMMARY A survey of the weekly causes of mortality was carried out in a flock of 64,000 broiler chickens in Western Australia. Some 6.86% of the flock died or was culled in the period from day-old to slaughter and were examined post mortem. The most important cause of death, acute death syndrome (ADS) (36%), occurred during all weeks of production and 74% of affected birds were male. A comparison of liver biotin content made between 120 ADS-affected birds and 60 clinically normal flockmates established that the biotin status of ADS-affected birds was adequate.     

蛋鸡脂肪肝出血综合征的病因研究进展

蛋鸡脂肪肝出血综合征(FLHS)是一种代谢性疾病,营养、内分泌、遗传和环境等因素都可影响其发生。日粮中能量过高或蛋白不足是诱发FLHS的主要因素,能量、蛋白来源也影响FLHS的发生。日粮中脂肪酸来源影响FLHS的发生,动物性脂肪较易引起FLHS,适量添加植物油可降低肝脏脂肪含量。雌激素水平升高可引起肝脏脂肪含量增加,与FLHS存在一定的量效关系。甲状腺素和孕酮可降低肝脏脂肪含量,防止出血发生。FLHS易感品系UCD-3蛋鸡肯定了遗传因素对该病的影响。空间不充足或必要活动受限制,导致能量过剩是FLHS发生的重要诱因。肝脏脂肪沉积并不总是引起肝脏出血,脂质过氧化物分解生成大量脂质自由基引起细胞损伤,可能是肝脏脂肪含量升高导致出血的分子机制。     

Aspects of metabolism related to the occurrence of skin lesions in biotin‐deficient chicks

1. Chicks were fed on biotin‐deficient low‐ and high‐protein diets supplemented with increasing concentrations of biotin.

2. Biotin deficiency decreased hepatic activity of pyruvate carboxylase [EG 6.4.1.1] but activity of acetyl‐CoA carboxylase [EG 6.4.1.2] was comparatively unaffected.

3. Increasing dietary protein increased the severity of biotin deficiency as assessed by skin lesions and decreased plasma biotin concentrations.

4. The severity of the skin lesions over all the treatments was most closely related to plasma biotin concentration.     

Facteurs de risque nutritionnels de la pathologie hépatique dans les troupeaux bovins laitiers en France

Nutritional risk factors for liver damage were surveyed in Black-Pied French dairy herds using serum glutamic dehydrogenase and gamma glutamyl transferase levels to monitor liver dysfunction.

The 34 herds chosen were free of parasitic liver injuries. Feeding systems, nutritional blood parameters and production characteristics are analyzed. Two risk factors appeared to be involved in hepatic injury: feeding of fresh rape (Brassica napus) and high levels of serum urea (≥6.64 mmol/L) associated with grass pasture or dietary nonprotein nitrogen with corn silage.

     

LOW ALPHA-TOCOPHEROL LEVELS IN LIVERS OF WEANER SHEEP WITH NUTRITIONAL MYOPATHY

SUMMARY Outbreaks of ovine weaner nutritional myopathy occurring in the southwest of Western Australia outside the recognised selenium-responsive areas have been investigated. One hundred and five sheep died in 3 outbreaks following 5 months grazing cereal stubble paddocks. Liver selenium and glutathione peroxidase activities, measured as an index of biological availability of dietary selenium, indicated that the selenium status of the animals was probably adequate. A comparison of liver selenium and α-tocopherol concentrations and glutathione peroxidase activity was made with both selenium supplemented sheep and sheep affected with selenium-responsive nutritional myopathy. In all cases investigated in this study liver α-tocopherol levels in affected animals were low and this may be important in the aetiology of this myopathy.     

家禽脂肪酸代谢及其在禽蛋中的沉积和营养调控

在肝脏中载脂蛋白作用下,内源合成或外源获取的脂肪酸以甘油三酯的形式同胆固醇及其他脂类组装形成极低密度脂蛋白(VLDL)。VLDL经血液循环到达卵巢,穿过卵母细胞外层屏障后,经卵母细胞受体介导的内吞作用进入卵母细胞发生沉积。而机体的营养状况或饲粮中营养成分的改变可通过影响脂肪酸的从头合成或VLDL结构直接或间接影响禽蛋中脂肪酸的最终沉积。本文阐述了家禽体内脂肪酸的来源、转运与沉积过程,并探讨了脂肪酸代谢及其在禽蛋中沉积的营养调控。     

A survey of "normal" broiler mortality in East Anglia.

A survey of routine mortality was carried out on six different broiler sites. A total of 535 individual post mortem examinations was carried out. The chief cause of mortality on all six sites was colisepticaemia. Fatty liver and kidney syndrome caused significant loss on three of the six sites and on three of them a low incidence of an oedema syndrome was of interest. Salmonella senftenberg was isolated during the first four weeks from the intestines of chickens from five of the six sites but on none of them was this occurrence associated with any manifestations of disease. The vaccination procedures against Newcastle disease and infectious bronchitis were not producing adequate immunity against a possible challenge by a virulent virus of either although the administration of the vaccines appeared to be causing stress sufficiently severe to be one of the factors predisposing to a high incidence of colisepticaemia.