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

2000 ◽  
Vol 166 (3) ◽  
pp. 609-620 ◽  
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.

Activation of insulin-like growth factor gene expression during work-induced skeletal muscle growth

1990 ◽  
Vol 259 (1) ◽  
pp. E89-E95 ◽  
Author(s):  
D. L. DeVol ◽  
P. Rotwein ◽  
J. L. Sadow ◽  
J. Novakofski ◽  
P. J. Bechtel
Keyword(s):  
Gene Expression ◽  
Skeletal Muscle ◽  
Growth Factor ◽  
Muscle Growth ◽  
Experimental Period ◽  
Mrna Levels ◽  
Insulin Like Growth Factor ◽  
Muscle Weight ◽  
Skeletal Muscle Growth ◽  
Igf I

We have investigated the hypothesis that there is local regulation of insulin-like growth factor (IGF) gene expression during skeletal muscle growth. Compensatory hypertrophy was induced in the soleus, a predominantly slow-twitch muscle, and plantaris, a fast-twitch muscle, in 11- to 12-wk-old female Wistar rats by unilateral cutting of the distal gastrocnemius tendon. Animals were killed 2, 4, or 8 days later, and muscles of the nonoperated leg served as controls. Muscle weight increased throughout the experimental period, reaching 127% (soleus) or 122% (plantaris) of control values by day 8. In both growing muscles, IGF-I mRNA, quantitated by a solution-hybridization nuclease-protection assay, rose by nearly threefold on day 2 and remained elevated throughout the experimental period. IGF-II mRNA levels also increased over controls. A more dramatic response was seen in hypophysectomized rats, where IGF-I mRNA levels rose by 8- to 13-fold, IGF-II values by 3- to 7-fold, and muscle mass increased on day 8 to 149% (soleus) or 133% (plantaris) of the control contralateral limb. These results indicate that signals propagated during muscle hypertrophy enhance the expression of both IGF genes, that modulation of IGF-I mRNA levels can occur in the absence of growth hormone, and that locally produced IGF-I and IGF-II may play a role in skeletal muscle growth.

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
Keyword(s):  
Skeletal Muscle ◽  
Thyroid Hormone ◽  
Broiler Chickens ◽  
Muscle Protein ◽  
Skeletal Muscle Protein ◽  
Hormone Metabolism ◽  
Deficient Diet ◽  
Thyroid Hormone Metabolism ◽  
Iopanoic Acid ◽  
Hormone Status

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.

scholarly journals Mitochondrial And Myogenic Gene Expression Pathways Are Influenced By The Exercise Mimetic Formoterol In Human Myotubes

2021 ◽  
Author(s):  
Anthony A. Duplanty ◽  
Emily L. Zumbro ◽  
Ryan A. Gordon ◽  
Gena D. Guerin ◽  
Matthew F. Brisebois ◽  
...  
Keyword(s):  
Gene Expression ◽  
Thyroid Hormone ◽  
Mitochondrial Biogenesis ◽  
Hormone Metabolism ◽  
Cellular Homeostasis ◽  
Thyroid Hormone Metabolism ◽  
Human Myotubes ◽  
Thyroid Metabolism ◽  
Expression Pathways

Abstract Background: Exercise is an effective treatment for establishing and maintaining skeletal muscle (SKM) health. The interconnected cascade of gene expression pathways related to myogenesis, mitochondrial homeostasis, and thyroid hormone metabolism are critical to SKM health. This in vitro study was conducted to investigate the effects of exercise mimetic (formoterol) stimulation on human SKM cell signaling during myogenesis, and to provide insight on potential targets for future studies exploring therapies for SKM atrophy.Methods: Human myoblasts were cultured and differentiated to evaluate the effects of exercise mimetic stimulation on gene expression during mid and late myogenesis. We characterized the expression of 24 genes related to myogenesis, mitochondrial biogenesis, thyroid hormone metabolism, and cellular homeostasis.Results: Formoterol stimulated the gene expression for SKM pathways related to mitochondrial biogenesis, thyroid metabolism, and cellular homeostasis. Additionally, formoterol resulted in a myogenic program that appears to favor prolonged myoblast proliferation and delayed myotube maturation.Conclusion: Robust, yet differential effects of exercise mimetic stimulation on gene expression during mid-myogenesis and at terminal differentiation were found. The results of our study support the groundwork for establishing further experiments utilizing exercise signaling as a therapeutic treatment in models targeting dysfunctional SKM cell growth.

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

1993 ◽  
Vol 70 (2) ◽  
pp. 585-592 ◽  
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.

Amiodarone and thyroid hormone metabolism in the rat heart

1991 ◽  
Vol 125 (6) ◽  
pp. 675-679
Author(s):  
Liv S. Bjørn-Hansen Gøtzsche ◽  
Niels Boye
Keyword(s):  
Thyroid Hormone ◽  
Heart Muscle ◽  
High Dose ◽  
Dependent Manner ◽  
Hormone Metabolism ◽  
Tissue Concentrations ◽  
Cardiac Sarcolemma ◽  
Thyroid Hormone Metabolism ◽  
Liver And Kidney ◽  
Dose Dependent

Abstract. The effect of amiodarone on thyroid hormone metabolism in heart, muscle, liver and kidney was investigated. Rats were treated ip with a high (100 mg · kg−1 · day−1) or a low (50 mg · kg−1 · day−1) dose of amiodarone for 10 days. Serum T3 was dose-dependently depressed (mean 30 and 54% of controls, respectively, p<0.01). rT3 was elevated (to 663 and 313% of controls, p<0.01 and 0.05, respectively). Serum T4 was depressed only in the high-dose group (to mean 80%, p<0.05). Tissue concentrations of T3 in the heart and muscle from treated animals did not differ from controls, whereas liver and kidney T3 contents were markedly reduced in both groups (p<0.05). Heart T4 and rT3 were elevated to about 200% of controls (p<0.01 and 0.05, respectively). The same pattern was observed in the other tissues. Iodothyronine-5'-monodeiodinase activity was significantly depressed in all tissues; heart: 32 and 28% of controls (p<0.05); muscle: 36 and 49% (p<0.01); liver: 11 and 13% (p<0.01); kidney: 22 and 28% (p<0.01), respectively. In conclusion, amiodarone depresses iodothyronine-5'-monodeiodinase activity in the heart, muscle, liver and kidney in a dose-dependent manner, resulting in lowered T3 concentrations in the liver and kidney, whereas no reduction of tissue T3 content is observed in the heart and muscle. This may indicate that T3 from plasma may cross the cardiac sarcolemma without hindrance.

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