Fatty Liver Hemorrhagic Syndrome Research Articles

Fatty Liver-Hemorrhagic Syndrome Observed in Commercial Layers Fed Diets Containing Chelated Minerals

This study was originally conducted to determine the effect of various chloride levels and consumption of chelated versus non-chelated minerals on egg production and eggshell breaking strength. However, the focus of this report changed after fatty liver-hemorrhagic syndrome (FLHS) was observed in hens that consumed diets containing chelated minerals. No FLHS was observed in hens that consumed a diet that contained non-chelated minerals. Four hundred thirty-two 35-week-old commercial laying hens were housed in individual cages in groups of nine hens each. The treatments were factorially arranged (3 x 2) such that six experimental diets differing in chloride levels and in source of minerals were fed for six 28-day laying periods. A significantly higher mortality attributed to FLHS was observed in hens that consumed the diets having chelated minerals as compared with hens that consumed the diets with non-chelated minerals. No difference in mortality was observed among the hens fed the various chloride diets.

Effect of selected dietary antioxidants on fatty liver-haemorrhagic syndrome in laying hens.

1. Single comb White Leghorn hens of an inbred line highly susceptible to fatty liver haemorrhagic syndrome (FLHS) were fed supplemented dietary ascorbic acid (200 mg/kg), alpha-tocopherol (75 mg/kg), or L-cysteine (3 g/kg, and 6 g/kg) for 28 d in order to evaluate the potential therapeutic effect of these compounds against the disease. 2. Supplementation of ascorbic acid, alpha-tocopherol, or a low level of L-cysteine (3 g/kg) did not significantly affect any of the hepatic variables evaluated. Hepatic glutathione was not increased by the supplementation of dietary L-cysteine. 3. L-cysteine supplemented at a level of 6 g/kg decreased hepatic dry matter and fat contents without affecting the hepatic malondialdehyde or the liver haemorrhagic score. 4. Because one of the predisposing factors of FLHS is a high hepatic fat content it was concluded that dietary supplementation of L-cysteine (6 g/kg) may be useful in the prevention of the disease.

Effect of Dietary Protein and Selected Antioxidants on Fatty Liver Hemorrhagic Syndrome Induced in Japanese Quail

The effects of CP and antioxidants on fatty liver hemorrhagic syndrome (FLHS) in Japanese quail hens were studied. In Experiment 1, four treatments were arranged as a 2 × 2 factorial; dietary CP (18 or 24%) and reduced glutathione (GSH, 0 or 120 mg/kg diet) were the major variables, but cysteine and other amino acids were higher in the 24% CP diets. Negative control (NC1) and positive control (PC1) diets were also evaluated. In Experiment 2, the effects of vitamin E (VE) and GSH were evaluated in the presence and absence of adequate dietary sulfur amino acids. Negative control (NC2) and positive control (PC2) diets were used.In both experiments, liver hemorrhage was most severe in quail fed the diets that were formulated to induce hepatic steatosis and limit oxidant defense capability. Liver hemorrhage was least severe in quail fed the diets that were formulated to minimize liver lipid accumulation and support oxidant defenses. Histological evaluation of affected quail livers showed changes consistent with FLHS in chicken hens. In Experiment 1, neither CP concentration nor GSH supplementation influenced liver hemorrhage. In Experiment 2, liver hemorrhagic score was reduced from 3.8 to 2.7 (P ≤ .05) by adding VE to the basal diet The PC2 diet further depressed liver score to only 2.0 (P ≤ .05). The data clearly show that Japanese quail are susceptible to FLHS and indicate that a combination of lipotropic and antioxidant nutrients is protective against hemorrhage, even when lipogenic demands are maximized by feeding diets devoid of added fat.

Fatty Liver Hemorrhagic Syndrome in Hens Overfed a Purified Diet. Selected Enzyme Activities and Liver Histology in Relation to Liver Hemorrhage and Reproductive Performance ,

A nutritionally adequate, purified diet was developed and used in studies to characterize selected aspects of laying hens in which fatty liver hemorrhagic syndrome (FLHS) was induced by overfeeding. Hens consuming the diet ad libitum or intubated with the diet in quantities equivalent to usual daily energy intake maintained normal rates of lay, did not become obese, and did not develop liver hemorrhage. Overfed hens had a 33% incidence of FLHS, as indicated by the presence of severe liver hemorrhage score, and displayed the full range of symptoms associated with spontaneous outbreaks of FLHS, including definitive lesions of hepatic reticulin. Among four groups of hens clinically classified according to rates of liver hemorrhage and egg production, there were no differences noted in total liver fat, liver fat concentration, or final body weight. Liver hemorrhage was associated with the degree of induction of liver lipogenic accessory enzymes. Serum enzyme activities indicate that overfed hens, unlike the overfed goose, retain hepatocellular membrane integrity. Overfeeding caused altered reproductive performance in 72% of hens. Alterations included erratic laying, increased incidence of double ovulations, shell defects, follicular collapse, and oviduct involution. Pattern of lay preceding necropsy seemed to influence follicle weight at necropsy. The data presented re-emphasize the interdependence among liver, ovary, and oviduct function in the etiology of FLHS.

Research Note: Relationship of Comb Color to Liver Appearance and Fat Content in Single Comb White Leghorn Laying Hens

A flock of commercial Single Comb White Leghorn laying hens, diagnosed as having Fatty Liver Hemorrhagic Syndrome (FLHS), was surveyed to ascertain the relationship between comb color and selected FLHS characteristics. Twenty-eight hens with and without pale combs were selected from 14 cages for paired comparisons. Hens with pale combs had a higher (P≤.05) liver score and relative liver weight than hens with normal combs. Differences were not detected in BW, comb weight, relative comb weight, liver fat, and plasma estrogen concentration. In flocks diagnosed with FLHS, comb appearance is associated with a higher incidence of FLHS.

Causes of mortality in chickens that regressed a Rous sarcoma virus-induced tumor.

Rous sarcomas were induced in 6-week-old chickens of several genetically different stocks: inbred lines C, 6(1), 6(3), and 7(2); crosses of inbred lines (6(3) X 7(2)) F4 and (6(1) X 15(1)) F2 X 6(1); and reciprocal crosses (15(1) X 100) F1 X 15(1) and (15(1) X 100) F1 X 100. The resulting tumors were scored for size six times during a 10-week period. Females that had completely regressed their sarcomas were placed in individual laying cages and examined weekly for reappearance of a tumor. After death, the probable cause was determined by necropsy. The major causes of death in the pooled sample of 49 females were fatty liver hemorrhagic syndrome (24.6%), reproductive disorder (14.2%), Marek's disease (12.2%), and lymphoid leukosis (6.1%). Elapsed time between tumor regression and death from any cause ranged from 21 days to 1930 days (5.3 years). One tumor recurred, this in a bird which eventually died with a massive sarcoma in the left wingweb and Rous metastasis in liver tissue. These data provide evidence of specific resistance to neoplastic disease.

Calcium and its Relationship to Excess Feed Consumption, Body Weight, Egg Size, Fat Deposition, Shell Quality, and Fatty Liver Hemorrhagic Syndrome ,

In Experiment 1, Hyline W36 caged hens were fed diets containing 1.7, 2.9, 3.5, and 4.1% calcium for 10 and 16 weeks. In Experiments 2 and 4, Dekalb XL and Hyline W36 pullets were fed diets containing 1.0, 1.7, and 3.75% calcium for 3 weeks (Exp. 2) or until 25 pullets from each group laid 7 eggs (Exp. 4). In Experiment 3 and 5, Dekalb and Hyline hens were fed diets containing 1.5 (Dekalb only), 1.75, 2.25, 2.75, and 3.75% calcium for 8 weeks. Criteria were liver, fat pad, egg and shell weights, egg specific gravity, production, feed consumption, liver fat and fatty acid composition, liver hemorrhage score, and body weight. As percent dietary calcium decreased, Hyline birds (Exp. 1, 4, and 5) had increased liver fat, body weight (except Exp. 4), and feed consumption, but egg specific gravity and shell weight decreased. Reduced dietary calcium levels had no effect on egg production in Experiment 1 but significantly reduced production in Experiment 5. Liver hemorrhage score significantly increased as percent dietary calcium decreased (Exp. 1). As dietary calcium decreased, Dekalb pullets (Exp. 2) had increased feed consumption, fat pad weight, and liver hemorrhage score. There was no increase in liver fat. However, in Dekalb hens (Exp. 3), feed consumption and egg production were significantly decreased as dietary calcium decreased. It is concluded that overconsumption caused by feeding pullets or hens inadequate calcium had no beneficial effect on egg size or egg production and, depending on strain, increased liver fat, liver hemorrhage score, body weight, and fat pad weight.

Rapeseed induced liver haemorrhage, reticulolysis and biochemical changes in laying hens: the effects of feeding high and low glucosinolate meals

Rapeseed meal hepatosis was produced by feeding high and low glucosinolate meals as a source of protein (about 200 g kg-1 diet) but could not be distinguished histologically from fatty liver-haemorrhagic syndrome which occurred in birds on the control diet. Both types of meal increased haemorrhage, reticulolysis and lymphoproliferation in the liver, reduced the packed cell volume and caused thyroid enlargement. Haemorrhages emanated from ruptured intrahepatic portal veins, capillaries and sinusoids and were associated with degenerative changes in vessel walls. Haemorrhage and reticulin scores were correlated. Parenchymal necrosis occurred only around large haematomas and caused increased aspartate transaminase activity in the plasma. Both meals also caused hyperglycaemia and reduced the plasma triglyceride content. Only the high glucosinolate meal decreased egg production, caused liver enlargement and reduced the plasma urate level. The addition of myrosinase enhanced its effects on egg production and packed cell volume but did not increase its hepatotoxicity.

Lipid Alleviates Fatty Liver Hemorrhagic Syndrome

At 135% of control, Single Comb White Leghorn laying hens were force fed for 3 weeks, diets based on corn or wheat, the latter made isocaloric to the corn-based diet with either corn oil, corn starch, or wheat starch. The hens fed ad libitum received a corn-based diet. Force feeding the corn-based diet produced fatty liver hemorrhagic syndrome (FLHS) with scores averaging 3.3 where 1 = no hemorrhages and 5 = 25 or more hemorrhagic points per liver. Force feeding the wheat-based diet with corn starch, wheat starch, or corn oil resulted in scores of 3.1, 2.7, and 1.9, respectively. Only the latter score was significantly different from the score produced by force feeding the corn-based diet, which when fed ad libitum resulted in an average score of 1.3. Based on these data and the criteria of retained energy, weight gain, percent fat in liver, and plasma estradiol concentrations, we concluded that wheat-based diets with corn- or wheat-starch produce FLHS equivalent to that caused by diets based on corn. Lipid at 4% of the diet had an alleviating effect on FLHS.

Plasma Estradiol, Thyroid Hormones, and Liver Lipid Content in Laying Hens Fed Different Isocaloric Diets

Two experiments were conducted with laying hens fed a corn-soy basal diet or diets containing fish meal, distillers dried grains with solubles (DDGS) or torula yeast formulated to be isocaloric and isonitrogenous with the basal diet. One half of the hens were kept at a temperature range of 13–24° and the other half at 24–35° for 49 days in experiment 2. Liver lipid content was significantly lower in hens fed DDGS (experiment 1) and DDGS or fish meal (experiment 2) than in hens fed the corn-soy basal diet, but it was not influenced by environmental temperature. Feeding DDGS or fish meal reduced lipoprotein lipase activity in adipose tissue. High temperature reduced plasma estradiol level but not thyroid hormone levels. Plasma estradiol in the hens fed DDGS or fish meal (experiment 1) and DDGS, fish meal or torula yeast (experiment 2) and plasma thyroxine and triiodothyronine in hens fed the DDGS or fish meal at 24–35° in experiment 2 were significantly lower than that of hens fed the corn-soy basal diet. Significant correlations were observed between liver lipid content and plasma estradiol or thyroxine concentrations. These findings show that plasma estrogen and thyroxine levels were influenced by diet composition and that these hormones have a close relation to induction of fatty livers in laying hens.environmental temperature fatty liver fatty liver-hemorrhagic syndrome liver lipid lipoprotein lipase plasma estradiol plasma thyroxine

The Relationship of Plasma Estradiol and Progesterone Levels to the Fatty Liver Hemorrhagic Syndrome in Laying Hens ,

The relationship of plasma estradiol and progesterone levels to fatty liver-hemorrhagic syndrome (FLHS) was studied with three groups of 9 White Leghorn hens per group. One group was fed ad libitum; the other two groups were force-fed at 120% and 135% of their own pre-experimental daily feed intake. Force-feeding for 3 weeks produced FLHS. The average FLHS score was 1.6 for control, 3.7 for 120% force-fed, and 4.5 for 135% force-fed. The average liver fat contents were 31.3%, 75.1%, and 76.8% (dry matter basis), respectively. Plasma estradiol averaged 165 pg/ml in the control group and 194 and 247 pg/ml in groups force-fed at 120% and 135%, respectively. The correlation coefficient between plasma estradiol and FLHS was .72 (P<.01). No significant differences in plasma progesterone were obtained among the control and force-fed groups. The data indicate that high endogenous estrogen levels are associated with FLHS.

Bacterial endotoxins and the pathogenesis of fatty liver—haemorrhagic syndrome in the laying hen

A high energy maize diet produced a higher incidence of fatty liver-haemorrhagic syndrome than a low energy barley diet when the diets were fed during the summer. The triglyceride content of the liver increased with the liver haemorrhage score and in hens with the highest scores there was evidence of hepatic hyperplasia. They also had high activities of aspartate transaminase and cholinesterase in the plasma and a low activity of sorbitol dehydrogenase. There was no increase in plasma endotoxin levels as the syndrome developed or any significant variation in these levels with the haemorrhage score, the triglyceride content of the liver or plasma enzyme activities. It was concluded that the steatosis does not impair the ability of the liver to inactivate endotoxins of enteric bacteria and that these toxins are not involved in the pathogenesis of the syndrome.

Induction of Fatty Liver-Hemorrhagic Syndrome in Laying Hens by Exogenous b-Estradiol

SUMMARY Intramuscular administration of exogenous fp-estradiol (E2) every 4 or 5 days (5.0 or 7.5 mg E2/kg body weight) induced fatty liver-hemorrhagic syndrome (FLHS) in both Rhode Island Red (RIR) and White Leghorn (WL) hens. RIR hens exhibited ataxia and opisthotonus, and 30% died from hepatic hemorrhage within 14 days. No WL birds similarly treated for 32 days died or showed neurologic disorder, thereby indicating a major breed difference in response to exogenous E2. Liver lipid, incidence of liver hemorrhage, and plasma volume increased as a direct result of Eo injection. Inclusion of 6% oat hulls in the diet significantly (P < .05) reduced the magnitude of these physiological responses.

The response of liver enzymes to feed restriction and subsequent ad lib. feeding in the laying hen.

1. The effects of restricted feeding, and ad lib. feeding following food restriction, on hepatic carbohydrate and lipid metabolism in the laying hen were studied. 2. The birds were allocated to four groups and given either 92, 84 or 75 g/d or allowed ad lib. access to food. 3. Food restriction significantly reduced liver total lipid content compared with ad lib.-fed control birds and this was reflected in reduced hepatic lipogenic enzyme activities. 4. When birds from the restricted regimens were allowed free access to food they initially consumed more food than the control group but after 2 weeks of ad lib. feeding the food consumptions of the birds in all the groups were similar. 5. Concomitant with the increase in food intake there were also increases in liver lipid content and hepatic lipogenic enzyme activities. After 18 d of ad lib. feeding these measurements were similar in the previously restricted birds and the ad lib.-fed control group. 6. Despite these effects on lipid metabolism, food restrictio, and the subsequent release from food restriction, had no significant effects on the specific activities of the glycolytic enzymes examined. 7. Although there were large increases in liver lipid content following release from feed restriction no birds died from, or showed any of the symptoms of, fatty liver-haemorrhagic syndrome. This suggests that, in the absence of any other factor which may be involved in the syndrome, these high liver lipid contents were not, alone, sufficient to cause FLHS. The results also indicate that free access to food following food restriction is unlikely to be a major factor in initiating the syndrome.

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.

Comparison of Fish Meal and Soybean Meal in the Prevention of Fatty Liver-Hemorrhagic Syndrome in Caged Layers

TWO experiments, of five weeks each, were designed to study the effect of protein source and level of dietary protein on hepatic and plasma lipids and incidence of liver hemorrhagein caged laying hens.Experiment 1 compared equicaloric (3.1 kcal/g) and isonitrogenous (12.5%) corn-fish meal and corn-soybean diets. An equicaloric 16.5% protein corn-soybean diet was included to assess the effect of dietary protein level. Fatty Iiver-hemorrhagic syndrome was induced under ad libitum feeding in birds fed the corn-soybean diet. The corn-fish meal diet reduced (P<.05) liver weight, hepatic and plasma lipids, and incidence of liver hemorrhage. Significant effects due to the level of dietary protein were not detected. No concomitant changes in egg production, egg weight, or body weight were observed. Plasma estrogen was lower (P<.01) in birds fed the corn-fish meal diet when compared to those fed the corn-soybean diet. Liver lipid was positively correlated (r = .83; P<.025) with plasma estrogen.Influence of dietary protein source was reevaluated in Experiment 2 and the effect of adding selenium (0.3 mg/kg as Na2 SeO3) or a combination of trace elements (As, Br, Cr, F, Mo, Ni, Sn, V) to the corn-soybean diet on liver lipid accumulation examined. Results with respect to dietary protein source were similar to the previous experiment. Neither selenium nor the combination of trace elements had a significant effect on hepatic and plasma lipids. Adding selenium to the corn-soybean diet reduced incidence of liver hemorrhage to the same level as that observed with the corn-fish meal diet.

Fatty Liver Syndrome in Laying Hens—An Attempt to Review

SummaryFatty Liver Syndrome (FLS), also described as Fatty Liver Haemorrhagic Syndrome (FLHS), is a metabolic disorder in laying hens, characterised by an excessive accumulation of fat, with an aberrant fatty-acid composition in the liver. The liver structure is affected and numerous capillary bleedings (haemorrhages), varying in size, may be observed in the liver tissue. Mortality generally remains on a low level and is caused by a fatal internal bleeding due to a rupture of the liver capsule in hens still producing. Egg production may fall with 30 per cent with a few weeks.The accumulation of fat in the liver is probably a consequence of a too intensive “de novo” synthesis of fat from carbohydrates. Factors, frequently mentioned as the causes of FLS, are either energetic overconsumption, or breeding on a high egg production level. The surplus of energy available, resulting from overconsumption and possibly inducing an intensified “de novo” synthesis of fat, may be reinforced by the restricted movement of hens in batteries and by high temperatures.A common method to control FLS is raising the concentration of lipotropic compounds (choline, inositol, vit. B12, vit. E) in the diet. A number of successful treatments with this method, especially in the field, have been reported. The recovery was not always complete however, fall backs have been reported and also negative results, especially in experiments under controlled circumstances. This must therefore not be regarded as a reliable and adequate control measure.Reduction of the energy intake, either by feed restriction, or by lowering the ME-content of the diet, seems a more reliable method to reduce the liver fat content. In several experiments this method was a success. A similar effect may be obtained by offering the hens more opportunity to move.A number of trials have indicated, that an increase of the fat content in the diet may favourably effect the liver fat content, especially if fats, rich in linoleic acid, are used. As the physiological background of this phenomenon is not known yet and this method has not been tested on FLS in the field, more research on this point is required.

Effects of rapeseed meal on laying hens (Gallus domesticus) in relation to fatty liver-haemorrhagic syndrome and egg taint

Fatty liver-haemorrhagic syndrome (FLHS) occurred in the controls and was modified in hens that received a diet containing 10 per cent rapeseed meal. This diet increased the extent and severity of the hepatic haemorrhage without affecting the reticulin content of the liver but decreased the body weight and liver lipid levels and so weakened the correlation between these parameters and haemorrhage score found in FLHS. Plasma aspartate transaminase and beta-glucuronidase activities tended to increase with the score. The rapeseed meal diet also produced thyroid hypertrophy and since this was greater in the hens that produced tainted eggs and was positively correlated with the trimethylamine (TMA) content of the eggs it was postulated that rapeseed meal goitrogens may be involved as secondary factors in producing the disturbance in TMA metabolism that causes the egg taint. This abnormality was associated with a reduction in the soluble protein content of the liver, which reflected a decrease in TMA oxidase activity, but was not related to hepatic haemorrhage, steatosis or reticulolysis, or to lipid levels and the activities of lysosomal enzymes and transaminases in the plasma.

Environmental temperature as a factor in the aetiology of fatty liver-haemorrhagic syndrome in the fowl

Unidirectional air flow isolators were used to house laying hens at 13 degrees C, 18--30 degrees C and 29 degrees C. Their diet was formulated to provide 2655 k cal metabolisable energy/kg and 142 g crude protein/kg. Groups were killed for examination at the age of 35 and 45 weeks. Sub-clinical FLHS occurred in all isolators but in the case of the younger hens appeared to be more prevalent at 29 degrees C than at 13 degrees C. Both the triglyceride and the glycogen content of the liver were higher at 29 degrees C despite a reduction in food intake. The free fatty acid level in the plasma was lower, probably as a consequence of reduced lipolysis. Liver haemorrhage was associated with an increase in plasma aspartate transaminase activity. It was concluded that an interaction between environmental temperature and the energy balance is not the only factor involved in the aetiology of FLHS and maybe of secondary importance, and that there is a pathogenic relationship between hepatic steatosis and haemorrhage.

Pathological and biochemical observations on subclinical cases of fatty liver-haemorrhagic syndrome in the fowl

A high incidence of subclinical fatty liver-haemorrhagic syndrome (FLHS) was found in three flocks of laying hens in which deaths from FLHS had occurred. There was so significant difference between the affected hens and the remainder of the block in egg production or quality, but the former were more obese and had higher concentrations of lipids in their livers, suggesting a pathogenic relationship between hepatic steatosis and haemorrhage. Soluble protein tended to accumulate with the fat in the livers. Reticulolysis had occurred in over half the haemorrhagic livers examined. Histological examination and DNA estimations provided no evidence of generalised hyperplasia. From the composition of the liver lipids it was concluded that the steatosis resulted mainly from an increase in lipogenesis from dietary carbohydrate. Lipid levels in the plasma were weakly correlated with those in the liver. No change was detected in the plasma protein pattern.