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

Plasma homocysteine is decreased in the hypothyroid rat

2000 ◽  
Vol 78 (7) ◽  
pp. 565-570 ◽  
Author(s):  
René L Jacobs ◽  
Lori M Stead ◽  
Margaret E Brosnan ◽  
John T Brosnan
Keyword(s):  
Cardiovascular Disease ◽  
Thyroid Hormone ◽  
Independent Risk Factor ◽  
Hormone Replacement ◽  
Plasma Homocysteine ◽  
Total Plasma ◽  
Thyroid Hormone Replacement ◽  
Cystathionine Beta Synthase ◽  
Osmotic Pumps ◽  
Hypothyroid Patients

Recent clinical studies have indicated that plasma homocysteine was significantly increased in hypothyroid patients. Since hyperhomocysteinemia is an independent risk factor for cardiovascular disease we investigated homocysteine metabolism in hypothyroid rats. Hypothyroidism was induced in one study by addition of propylthiouracil (PTU) to the drinking water for 2 weeks. In a second study, thyroidectomized and sham-operated rats were used with thyroid hormone replacement via mini-osmotic pumps. Unlike the human hypothyroid patients, both groups of hypothyroid rats exhibited decreased total plasma homocysteine (30% in PTU rats, 50% in thyroidectomized rats) versus their respective controls. Thyroid replacement normalised homocysteine levels in the thyroidectomized rat. Increased activities of the hepatic trans-sulfuration enzymes were found in both models of hypothyroidism. These results provide a possible explanation for the decreased plasma homocysteine concentrations. The hypothyroid rat cannot be used as a model to study homocysteine metabolism in hypothyroid patients.Key words: homocysteine, cystathionine beta-synthase, cystathionine gamma-lyase, thyroid hormone.

EFFECT OF DIETARY TAURINE SUPPLEMENTATION ON SUDDEN DEATH SYNDROME IN BROILER CHICKENS

1989 ◽  
Vol 69 (2) ◽  
pp. 509-512 ◽  
Author(s):  
G. L. CAMPBELL ◽  
H. L. CLASSEN
Keyword(s):  
Body Weight ◽  
Sudden Death ◽  
Key Words ◽  
Broiler Chickens ◽  
Total Mortality ◽  
Sudden Death Syndrome ◽  
Taurine Supplementation ◽  
Gain Ratio

Dietary taurine supplementation (0, 0.05, 0.10, or 0.20%) was examined as a means of reducing sudden death syndrome (SDS) in male broiler chickens (624 per treatment) raised to market weight. Total mortality and sudden death syndrome were lower for broilers fed taurine-supplemented diets. The feed-to-gain ratio from 3 to 6 wk decreased linearly with increasing dietary taurine while taurine addition had no effect on 3-wk or 6-wk body weight, or feed-to-gain ratio from 0 to 3 wk. Key words: Sudden death syndrome, taurine, broiler chickens

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.

scholarly journals Homocysteine and vitamins in cardiovascular disease

1998 ◽  
Vol 44 (8) ◽  
pp. 1833-1843 ◽  
Author(s):  
Donald W Jacobsen
Keyword(s):  
Cardiovascular Disease ◽  
Folic Acid ◽  
Vascular Endothelium ◽  
Intervention Studies ◽  
Genetic Mutation ◽  
Plasma Homocysteine ◽  
Total Plasma ◽  
Homocysteine Concentration ◽  
Atherothrombotic Disease ◽  
Lines Of Evidence

Abstract On the basis of recent retrospective and prospective studies, it is now widely accepted that increased total plasma homocysteine is a risk factor for cardiovascular disease. Impaired enzyme function as a result of genetic mutation or deficiency of the essential B vitamins folic acid, B12, and B6 can lead to hyperhomocysteinemia. Oxidized forms of homocysteine account for 98–99% of total plasma homocysteine. Although there is uncertainty as to whether increased homocysteine is causal or merely a proxy for cardiovascular disease, several lines of evidence suggest that it may play a role in atherothrombotic disease. Homocysteine appears to alter the anticoagulant properties of endothelial cells to a procoagulant phenotype. Mildly increased homocysteine causes dysfunction of the vascular endothelium. Folic acid effectively lowers homocysteine concentration in the plasma. Intervention studies are urgently needed to determine if lowering homocysteine is effective in decreasing the morbidity and mortality of cardiovascular disease.

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 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

Pathogenic Mechanisms of Trimethylamine N-Oxide-induced Atherosclerosis and Cardiomyopathy

2021 ◽  
Vol 19 ◽  
Author(s):  
Youjing Zheng ◽  
Jia-Qiang He
Keyword(s):  
Cardiovascular Disease ◽  
Dairy Products ◽  
Cardiovascular Events ◽  
Independent Risk Factor ◽  
Prognostic Index ◽  
Strong Relationship ◽  
Clinical Findings ◽  
Direct Effects ◽  
Elevated Plasma ◽  
Potential Biomarker

: Trimethylamine N-oxide (TMAO) is a gut microbiota metabolite derived from trimethylamine-containing nutrient precursors such as choline, L-carnitine, and betaine, which are rich in many vegetables, fruits, nuts, dairy products, and meats. An increasing number of clinical studies have demonstrated a strong relationship between elevated plasma TMAO levels and adverse cardiovascular events. It is commonly agreed that TMAO acts as both an independent risk factor and a prognostic index for patients with cardiovascular disease. Although most animal (mainly rodent) data support the clinical findings, the mechanisms by which TMAO modulates the cardiovascular system are still not well understood. In this context, we provide an overview of the potential mechanisms underlying TMAO-induced cardiovascular disease at the cellular and molecular levels, with a focus on atherosclerosis. We also address the direct effects of TMAO on cardiomyocytes (a new and under-researched area) and finally propose TMAO as a potential biomarker and/or therapeutic target for diagnosis and treatment of patients with cardiovascular disease.

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