scholarly journals Interrelationships between biotin, choline and other B-vitamins and the occurrence of fatty liver and kidney syndrome and sudden death syndrome in broiler chickens

1982 ◽  
Vol 48 (1) ◽  
pp. 177-184 ◽  
Author(s):  
C. C. Whitehead ◽  
C. J. Randall
Keyword(s):  
Sudden Death ◽  
Fatty Liver ◽  
Broiler Chickens ◽  
Dietary Supplementation ◽  
B Vitamins ◽  
Sudden Death Syndrome ◽  
Post Mortem ◽  
Deficient Diet ◽  
Liver And Kidney ◽  
B Vitamin

1. Addition of supplemental choline to a biotin-deficient diet decreased the biotin status of chicks and increased mortality from fatty liver and kidney syndrome (FLKS).2. Mortality was also increased by dietary supplementation with a mixture of other B-vitamins, excluding biotin, and was highest when the choline and B-vitamin supplements were combined.3. The occurrence of sudden death syndrome (SDS) was unaffected by dietary biotin concentration.4. A previously unreported condition was observed in which birds died showing post-mortem signs characteristic of both FLKS and SDS and whose occurrence was related to the biotin status of the chicks.

EFFECTS OF DIETARY ASPIRIN (ACETYLSALICYLIC ACID) ON THE INCIDENCE OF SUDDEN DEATH SYNDROME AND THE GENERAL PERFORMANCE OF BROILER CHICKENS

1983 ◽  
Vol 63 (2) ◽  
pp. 469-471 ◽  
Author(s):  
F. G. PROUDFOOT ◽  
H. W. HULAN
Keyword(s):  
Growth Rate ◽  
Sudden Death ◽  
Deleterious Effect ◽  
Broiler Chickens ◽  
Dietary Supplementation ◽  
Sudden Death Syndrome ◽  
The Other ◽  
Reduced Body ◽  
Body Weights ◽  
Overall Mortality

A total of 2400 broiler chickens were used in four experiments to estimate the effects of using 0.04, 0.08 and 0.16% aspirin (ASA) as dietary supplements. Not only did the ASA dietary supplementation have no significant (P < 0.05) beneficial effect on the incidence of sudden death syndrome but it also had a deleterious effect on overall mortality which was significant (P < 0.01) in two of the four experiments. Furthermore, the addition of ASA at 0.16% to the diet resulted in reduced body weights which were significant at P < 0.05 in two experiments and at P < 0.10 in the other two experiments. Key words: Aspirin, sudden death syndrome, broiler chickens, growth rate

Diet, total plasma homocysteine concentrations and mortality rates in broiler chickens

2003 ◽  
Vol 83 (3) ◽  
pp. 601-604 ◽  
Author(s):  
S. E. Samuels
Keyword(s):  
Cardiovascular Disease ◽  
Sudden Death ◽  
Broiler Chickens ◽  
Independent Risk Factor ◽  
Total Mortality ◽  
Mortality Rates ◽  
Plasma Homocysteine ◽  
Sudden Death Syndrome ◽  
Total Plasma ◽  
Elevated Plasma

The aim of this study was to determine if total plasma homocysteine (HCY) concentrations and mortality rates due to ascites syndrome and (AS) sudden death syndrome (SDS) in broiler chickens could be lowered by diet. Elevated plasma HCY is an independent risk factor for cardiovascular disease in humans. A total of 828 day-old male broiler chickens (Arbor Acre) were fed, for 6 wk, either a basal practical diet or one supplemented with excess vitamins B6 and B12, folic acid and betaine to stimulate the degradation of HCY. The supplemented diet decreased plasma HCY by 17% (P < 0.05; n = 16 per diet). Total mortality due to AS and SDS was 18% lower in the supplemented diet but this difference was not statistically significant. Key words: Homocysteine, folate, chickens, cardiovascular disease, ascites, sudden death syndrome

Role of cardiac hypoxia in the pathogenesis of sudden death syndrome in broiler chickens – A metabolic and molecular study

2021 ◽  
Author(s):  
Pegah Safaei ◽  
Gholamhossein Khadjeh ◽  
Mohammad Reza Tabandeh ◽  
Keramat Asasi
Keyword(s):  
Sudden Death ◽  
Cardiac Muscle ◽  
Internal Control ◽  
Broiler Chickens ◽  
Sudden Death Syndrome ◽  
Pyruvate Dehydrogenase Kinase ◽  
Cardiac Insufficiency ◽  
Monocarboxylate Transporter ◽  
Pcr Analysis ◽  
Glucose Transporter 1

AbstractSudden death syndrome (SDS) is an economically important disorder in broiler chickens with unknown aetiology. The aim of the present study was to evaluate the metabolic and molecular alterations related to hypoxia in the myocardium of broiler chickens with SDS. Samples from the cardiac muscle of internal control broiler chickens (ICs) (n = 36) and chickens having died of SDS (n = 36) were obtained during the rearing period. The activities of lactate dehydrogenase (LDH) and creatine phosphokinase (CPK) and the concentration of lactate were measured in the cardiac tissue using available commercial kits. The expression of hypoxia-inducing factor 1α (HIF1α), glucose transporter 1 (GLUT1), pyruvate dehydrogenase kinase 4 (PDHK4) and monocarboxylate transporter 4 (MCT4) genes was determined in the myocardium by real-time PCR analysis. The results showed the elevation of lactate level and activities of LDH and CPK in the cardiac muscle of SDS-affected chickens compared with the IC birds (P < 0.05). The cardiac muscle expression of HIF1α, MCT4 and GLUT1 genes was increased, while the PDHK4 mRNA level was decreased in the SDS-affected group compared to those in the IC chickens (P < 0.05). Our results showed that metabolic remodelling associated with hypoxia in the cardiac tissues may have an important role in the pathogenesis of cardiac insufficiency and SDS in broiler chickens.

THE EFFECTS OF DIETARY MICRONUTRIENT, FAT AND PROTEIN COMPONENTS IN PELLETED FEEDS ON THE INCIDENCE OF SUDDEN DEATH SYNDROME AND OTHER TRAITS AMONG MALE BROILER CHICKENS

1984 ◽  
Vol 64 (1) ◽  
pp. 159-164 ◽  
Author(s):  
F. G. PROUDFOOT ◽  
H. W. HULAN ◽  
K. B. McRAE
Keyword(s):  
Sudden Death ◽  
Key Words ◽  
Soybean Meal ◽  
Dietary Protein ◽  
Broiler Chickens ◽  
Sudden Death Syndrome ◽  
Canola Meal ◽  
Protein Supplements ◽  
Protein Components

Three experiments involving 11 600 male broiler chickens sought to determine if the pelleting process affects the dietary micronutrient, fat and protein components to increase the incidence of sudden death syndrome. Processed dietary micronutrient and fat components were not significantly associated with an increase in sudden death syndrome among broiler chickens. In one of the experiments, the incidence of sudden death syndrome was reduced (P < 0.01) when the dietary protein supplements (soybean meal, canola meal and fishmeal) bypassed the pelleting process. Key words: Sudden death syndrome, broiler chickens, feed pelleting, fat, micronutrients, protein supplements

scholarly journals Research Note: Effect of Feed Restriction on Feed Efficiency and Incidence of Sudden Death Syndrome in Broiler Chickens

1988 ◽  
Vol 67 (7) ◽  
pp. 1102-1104 ◽  
Author(s):  
VICTORIA A. BOWES ◽  
R.J. JULIAN ◽  
STEVEN LEESON ◽  
TANYA STIRTZINGER
Keyword(s):  
Sudden Death ◽  
Feed Efficiency ◽  
Broiler Chickens ◽  
Sudden Death Syndrome ◽  
Research Note ◽  
Feed Restriction

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 Effect of Dietary Lactate and Glucose on the Incidence of Sudden Death Syndrome in Male Broiler Chickens

1990 ◽  
Vol 69 (9) ◽  
pp. 1529-1532 ◽  
Author(s):  
J.P. JACOB ◽  
R. BLAIR ◽  
E.E. GARDINER
Keyword(s):  
Sudden Death ◽  
Broiler Chickens ◽  
Sudden Death Syndrome

Autophagy regulates whitefly–symbiont metabolic interactions

2021 ◽  
Author(s):  
Yan-Bin Wang ◽  
Ce Li ◽  
Jin-Yang Yan ◽  
Tian-Yu Wang ◽  
Ya-Lin Yao ◽  
...  
Keyword(s):  
Amino Acid ◽  
Essential Amino Acid ◽  
Critical Role ◽  
Dietary Supplementation ◽  
B Vitamins ◽  
Host Cells ◽  
Cellular Mechanisms ◽  
Essential Nutrients ◽  
Metabolic Interactions ◽  
B Vitamin

Nutritional symbionts are restricted to specialized host cells called bacteriocytes in various insect orders. These symbionts can provide essential nutrients to the host. However, the cellular mechanisms underlying the regulation of these insect–symbiont metabolic associations remain largely unclear. The whitefly, Bemisia tabaci MEAM1, hosts Portiera and Hamiltonella bacteria in the same bacteriocyte. In this study, the induction of autophagy by chemical treatment and gene silencing decreased symbiont titers, and essential amino acid (EAA) and B vitamin contents. In contrast, the repression of autophagy in bacteriocytes via Atg8 silencing increased symbiont titers, and amino acid and B vitamin contents. Furthermore, dietary supplementation with non-EAAs or B vitamins alleviated autophagy in whitefly bacteriocytes, elevated TOR (target of rapamycin) expression and increased symbiont titers. TOR silencing restored symbiont titers in whiteflies after dietary supplementation with B vitamins. These data suggest that Portiera and Hamiltonella evade autophagy of the whitefly bacteriocytes by activating the TOR pathway via providing essential nutrients. Taken together, we demonstrated that autophagy plays a critical role in regulating the metabolic interactions between the whitefly and two intracellular symbionts. Therefore, this study reveals that autophagy is an important cellular basis for bacteriocyte evolution and symbiosis persistence in whiteflies. The whitefly symbiosis unravels the interactions between cellular and metabolic functions of bacteriocytes. Importance Nutritional symbionts, which are restricted to specialized host cells called bacteriocytes, can provide essential nutrients for many hosts. However, the cellular mechanisms of regulation of animal–symbiont metabolic associations have been largely unexplored. Here, using the whitefly- Portiera / Hamiltonella endosymbiosis, we demonstrate autophagy regulates the symbiont titers, and thereby alters the essential amino acid and B vitamin contents. For persistence in the whitefly bacteriocytes, Portiera and Hamiltonella alleviate autophagy by activating the TOR (target of rapamycin) pathway through providing essential nutrients. Therefore, we demonstrate that autophagy plays a critical role in regulating the metabolic interactions between the whitefly and two intracellular symbionts. This study also provides insight into the cellular basis of bacteriocyte evolution and symbiosis persistence in the whitefly. The mechanisms underlying the role of autophagy in whitefly symbiosis could be widespread in many insect nutritional symbioses. These findings provide new avenue for whitefly control via regulating autophagy in the future.

scholarly journals The post mortem diagnosis of fatal hypoglycaemia using the fatty liver and kidney syndrome of chicks as a model

1982 ◽  
Vol 47 (2) ◽  
pp. 235-241 ◽  
Author(s):  
D. W. Bannister ◽  
Iris E. O'Neill ◽  
C. C. Whitehead
Keyword(s):  
Fatty Liver ◽  
Plasma Glucose ◽  
Vitreous Humour ◽  
Hepatic Glycogen ◽  
Time Of Death ◽  
Post Mortem ◽  
Liver And Kidney

1. The concentrations of vitreous humour and plasma glucose were closely correlated in both healthy and fatty liver and kidney syndrome-affected chicks at time of death.2. The values of vitreous humour glucose and lactate decreased rapidly after death, such that they were not reliable indicators of the presence of hypoglycaemia immediately ante mortem.3. Hepatic glycogen was extremely low in fatty liver and kidney syndrome-affected birds, whereas significant quantities remained in healthy birds up to at least 24 hpost mortem.

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