scholarly journals Selenium influences growth via thyroid hormone status in broiler chickens

2000 ◽  
Vol 84 (5) ◽  
pp. 727-732 ◽  
Author(s):  
He Jianhua ◽  
Akira Ohtsuka ◽  
Kunioki Hayashi

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.

2015 ◽  
Vol 153 (5) ◽  
pp. 920-928 ◽  
Author(s):  
T. KAMIZONO ◽  
D. SAPUTRA ◽  
I. MIURA ◽  
M. KIKUSATO ◽  
K. HAYASHI ◽  
...  

SUMMARYButoxybutyl alcohol (BBA) is a possible growth promoter contained in the fermentation and distillation by-products of a traditional Japanese spirit, shochu. In the present study, BBA was synthesized and its chemical structure was confirmed by gas chromatography mass spectrometry and nuclear magnetic resonance. Then, two studies were conducted to investigate the effects of feeding the synthesized BBA on the growth and skeletal muscle proteolysis of broiler chickens. Ross male broiler chickens were divided into two groups, control (basal diet: 219 g crude protein/kg and 12·66 MJ metabolizable energy/kg) and BBA diet (30 mg BBA/kg basal diet), with the experimental diets being provided from 15 to 27 days and 0 to 27 days of age, for Studies 1 and 2, respectively. Butoxybutyl alcohol supplementation increased final body weight in both studies, whereas feed intake was unchanged, thereby indicating significantly increased feed efficiency. Furthermore, the synthesized BBA increased the weights of the pectoralis superficialis and profundus muscles, and the leg. The BBA decreased the Nτ-methylhistidine concentration in the excrement and plasma, which are indices of the rate of skeletal muscle protein degradation. It also decreased the mRNA levels of μ-calpain large subunit, atrogin-1/muscle atrophy F-box (MAFbx), ubiquitin and 20S proteasome C2 subunit. These suggest that growth promotion due to the feeding of synthesized BBA is caused by the suppression of skeletal muscle protein degradation, which is related to a decrease in gene expression in the calpain and ubiquitin–proteasome systems.


2020 ◽  
Vol 52 (7S) ◽  
pp. 908-908
Author(s):  
Gena D. Guerin ◽  
Emily L. Zumbro ◽  
Ryan A. Gordon ◽  
Chase M. White ◽  
Dreanna M. McAdams ◽  
...  

1990 ◽  
Vol 52 (2) ◽  
pp. 263-266 ◽  
Author(s):  
H L Katzeff ◽  
M U Yang ◽  
E Presta ◽  
R L Leibel ◽  
J Hirsch ◽  
...  

FEBS Letters ◽  
1985 ◽  
Vol 180 (2) ◽  
pp. 335-340 ◽  
Author(s):  
Jacques Gagnon ◽  
My Anh Ho-Kim ◽  
Chantal Champagne ◽  
Roland R. Tremblay ◽  
Peter A. Rogers

2000 ◽  
Vol 166 (3) ◽  
pp. 609-620 ◽  
Author(s):  
R Vasilatos-Younken ◽  
Y Zhou ◽  
X Wang ◽  
JP McMurtry ◽  
RW Rosebrough ◽  
...  

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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