Effect of Different Levels of Supplemental Yeast on Body Weight, Thyroid Hormone Metabolism and Lipid Profile of Broiler Chickens

As there is a possibility that Se influences the growth of animals via thyroid hormone metabolism, the following three experiments were undertaken in order to determine the effects of dietary Se on growth, skeletal muscle protein turnover and thyroid hormone status in broiler chickens. Broiler chickens were raised on a Se-deficient diet until 12 d of age and then used for the experiments. In Experiment 1, twenty-eight birds were randomly assigned to four groups and fed purified diets with the following amounts of Se supplementation: 0·0, 0·1, 0·3 and 0·5 mg Se/kg diet. Dietary Se supplementation significantly increased plasma 3,5,3′-triiodothyronine (T3) concentration and improved growth, while plasma thyroxine (T4) concentration was decreased. In Experiment 2, twenty-eight birds were assigned to four groups and fed either a Se-deficient diet or a Se-supplemented diet (0·3 mg Se/kg diet) with or without the supplementation of iopanoic acid, a specific inhibitor of 5′-deiodinase (5 mg/kg diet). The growth was promoted and feed efficiency was improved by dietary Se supplementation as was also observed in Experiment 1. However, this effect of Se was halted by iopanoic acid supplementation. Hepatic 5′-deiodinase activity was elevated by Se and inhibited by iopanoic acid. In Experiment 3, birds were fed on the following diets to show that Se influences growth of birds via thyroid hormone metabolism: Se-deficient diet, Se-supplemented diets (0·1 and 0·3 mg/kg) and T3 supplemented diets (0·1 and 0·3 mg/kg diet). Lower dietary T3 supplementation (0·1 mg/kg diet) resulted in growth promotion similar to Se supplementation, while higher level of T3 caused growth depression. Furthermore, it was observed that the rate of skeletal muscle protein breakdown tended to be increased by Se similarly to the effect of T3. In conclusion, it was shown in the present study that Se deficiency depresses growth of broilers by inhibiting hepatic 5′-deiodinase activity which causes lower plasma T3 concentration.

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Thyroid function in rats with iodine deficiency is not further impaired by concurrent, marginal zinc deficiency

British Journal Of Nutrition ◽

10.1079/bjn19930150 ◽

1993 ◽

Vol 70 (2) ◽

pp. 585-592 ◽

Cited By ~ 6

Author(s):

John G. G. Smit ◽

Daan Van Der Heide ◽

Gerrit Van Tintelen ◽

Anton C. Beynen

Keyword(s):

Body Weight ◽

Thyroid Hormone ◽

Thyroid Function ◽

Body Weight Gain ◽

Male Rats ◽

Zn Deficiency ◽

Hormone Metabolism ◽

Thyroid Hormone Metabolism ◽

Marginal Zinc Deficiency ◽

Thyroid Hormone Levels

The hypothesis tested was that Zn deficiency aggravates impaired thyroid function as induced by I deficiency. In two separate experiments male rats were fed on diets either deficient in Zn or in I, or deficient in both. An identical, restricted amount of food was given to each rat so that body-weight gain of the experimental groups was comparable. Zn deficiency was evidenced by reduced tibial Zn concentrations. I deficiency was evidenced by goitre, reduced urinary I excretion, reduced plasma thyroxine concentrations and reduced absolute amounts and concentrations of thyroxine in the thyroid. Zn deficiency had no effect on the raised thyroid weight as induced by I deficiency. Zn restriction from 184 μmol Zn/kg diet to 31 μmol Zn/kg diet, hut not to 92 μmol Zn/kg diet, significantly lowered plasma thyroxine concentration. There were no interrelated effects of Zn and I deficiencies on thyroid hormone levels. These results indicate that marginal Zn deficiency does not influence thyroid hormone metabolism in I deficiency.

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Altered chicken thyroid hormone metabolism with chronic GH enhancement in vivo: consequences for skeletal muscle growth

Journal of Endocrinology ◽

10.1677/joe.0.1660609 ◽

2000 ◽

Vol 166 (3) ◽

pp. 609-620 ◽

Cited By ~ 25

Author(s):

R Vasilatos-Younken ◽

Y Zhou ◽

X Wang ◽

JP McMurtry ◽

RW Rosebrough ◽

...

Keyword(s):

Gene Expression ◽

Skeletal Muscle ◽

Body Weight ◽

Thyroid Hormone ◽

Muscle Growth ◽

Somatic Growth ◽

Hormone Metabolism ◽

Thyroid Hormone Metabolism ◽

Igf I ◽

Dose Dependent

In contrast to most vertebrates, GH reportedly has no effect upon somatic growth of the chicken. However, previous studies employed only one to two dosages of the hormone, and limited evidence exists of a hyperthyroid response that may confound its anabolic potential. This study evaluated the effects of 0, 10, 50, 100 and 200 microgram/kg body weight per day chicken GH (cGH) (0-200 GH) infused i.v. for 7 days in a pulsatile pattern to immature, growing broiler chickens (9-10 birds/dosage). Comprehensive profiles of thyroid hormone metabolism and measures of somatic growth were obtained. Overall (average) body weight gain was reduced 25% by GH, with a curvilinear, dose-dependent decrease in skeletal (breast) muscle mass that was maximal (12%) at 100 GH. This profile mirrored GH dose-dependent decreases in hepatic type III deiodinase (DIII) activity and increases in plasma tri-iodothyronine (T(3)), with bot! h also maximal (74 and 108% respectively) at 100 GH. No effect on type I deiodinase was observed. At the maximally effective dosage, hepatic DIII gene expression was reduced 44% versus controls. Despite dose-dependent, fold-increases in hepatic IGF-I protein content, circulating IGF-I was not altered with GH infusion, suggesting impairment of hepatic IGF-I release. Significant, GH dose-dependent increases in plasma non-esterified fatty acid and glucose, and overall decreases in triacylglycerides were also observed. At 200 GH, feed intake was significantly reduced (19%; P<0.05) versus controls; however, additional control birds pair-fed to this level did not exhibit any responses observed for GH-treated birds. The results of this study support a pathway by which GH impacts on thyroid hormone metabolism beginning at a pretranslational level, with reduced hepatic DIII gene expression, translating to reduced protein (enzyme) ex! pression, and reflected in a reduced level of peripheral T(3)-degrading activity. This contributes to decreased conversion of T(3) to its inactive form, thereby elevating circulating T(3) levels. The hyper-T(3) state leads to reduced net skeletal muscle deposition, and may impair release of GH-enhanced, hepatic IGF-I. In conclusion, GH has significant biological effects in the chicken, but profound metabolic actions predominate that may confound positive, IGF-I-mediated skeletal muscle growth.

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Inhibition of type I and type II iodothyronine deiodinase activity in rat liver, kidney and brain produced by selenium deficiency

Biochemical Journal ◽

10.1042/bj2590887 ◽

1989 ◽

Vol 259 (3) ◽

pp. 887-892 ◽

Cited By ~ 75

Author(s):

G J Beckett ◽

D A MacDougall ◽

F Nicol ◽

J R Arthur

Keyword(s):

Body Weight ◽

Thyroid Hormone ◽

Feedback Inhibition ◽

Selenium Deficiency ◽

Stress Factors ◽

Type I ◽

Type Ii ◽

Hormone Metabolism ◽

Iodothyronine Deiodinase ◽

Thyroid Hormone Metabolism

Selenium deficiency for periods of 5 or 6 weeks in rats produced an inhibition of tri-iodothyronine (T3) production from added thyroxine (T4) in brain, liver and kidney homogenate. This inhibition was reflected in plasma T4 and T3 concentrations, which were respectively increased and decreased in selenium-deficient animals. Although plasma T4 levels increased in selenium-deficient animals, this did not produce the normal feedback inhibition on thyrotropin release from the pituitary. Selenium deficiency was confirmed in the animals by decreased selenium-dependent glutathione peroxidase (Se-GSH-Px) activity in all of these tissues. Administration of selenium, as a single intraperitoneal injection of 200 micrograms of selenium (as Na2SeO3)/kg body weight completely reversed the effects of selenium deficiency on thyroid-hormone metabolism and partly restored the activity of Se-GSH-Px. Selenium administration at 10 micrograms/kg body weight had no significant effect on thyroid-hormone metabolism or on Se-GSH-Px activity in any of the tissues studied. The characteristic changes in plasma thyroid-hormone levels that occurred in selenium deficiency appeared not to be due to non-specific stress factors, since food restriction to 75% of normal intake or vitamin E deficiency produced no significant changes in plasma T4 or T3 concentration. These data are consistent with the view that the Type I and Type II iodothyronine deiodinase enzymes are seleno-enzymes or require selenium-containing cofactors for activity.

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