Caloric restriction induces energy-sparing alterations in skeletal muscle contraction, fiber composition and local thyroid hormone metabolism that persist during catch-up fat upon refeeding

Refeeding after caloric restriction induces weight regain and a disproportionate recovering of fat mass rather than lean mass (catch-up fat) that, in humans, associates with higher risks to develop chronic dysmetabolism. Studies in a well-established rat model of semistarvation-refeeding have reported that catch-up fat associates with hyperinsulinemia, glucose redistribution from skeletal muscle to white adipose tissue and suppressed adaptive thermogenesis sustaining a high efficiency for fat deposition. The skeletal muscle of catch-up fat animals exhibits reduced insulin-stimulated glucose utilization, mitochondrial dysfunction, delayed in vivo contraction-relaxation kinetics, increased proportion of slow fibers and altered local thyroid hormone metabolism, with suggestions of a role for iodothyronine deiodinases. To obtain novel insights into the skeletal muscle response during catch-up fat in this rat model, the functional proteomes of tibialis anterior and soleus muscles, harvested after 2 weeks of caloric restriction and 1 week of refeeding, were studied. Furthermore, to assess the implication of thyroid hormone metabolism in catch-up fat, circulatory thyroid hormones as well as liver type 1 (D1) and liver and skeletal muscle type 3 (D3) iodothyronine deiodinase activities were evaluated. The proteomic profiling of both skeletal muscles indicated catch-up fat-induced alterations, reflecting metabolic and contractile adjustments in soleus muscle and changes in glucose utilization and oxidative stress in tibialis anterior muscle. In response to caloric restriction, D3 activity increased in both liver and skeletal muscle, and persisted only in skeletal muscle upon refeeding. In parallel, liver D1 activity decreased during caloric restriction, and persisted during catch-up fat at a time-point when circulating levels of T4, T3 and rT3 were all restored to those of controls. Thus, during catch-up fat, a local hypothyroidism may occur in liver and skeletal muscle despite systemic euthyroidism. The resulting reduced tissue thyroid hormone bioavailability, likely D1- and D3-dependent in liver and skeletal muscle, respectively, may be part of the adaptive thermogenesis sustaining catch-up fat. These results open new perspectives in understanding the metabolic processes associated with the high efficiency of body fat recovery after caloric restriction, revealing new implications for iodothyronine deiodinases as putative biological brakes contributing in suppressed thermogenesis driving catch-up fat during weight regain.

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Selenium influences growth via thyroid hormone status in broiler chickens

British Journal Of Nutrition ◽

10.1017/s0007114500002087 ◽

2000 ◽

Vol 84 (5) ◽

pp. 727-732 ◽

Cited By ~ 47

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.

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Reduced Skeletal Muscle Protein Turnover and Thyroid Hormone Metabolism in Adaptive Thermogenesis That Facilitates Body Fat Recovery During Weight Regain

Frontiers in Endocrinology ◽

10.3389/fendo.2019.00119 ◽

2019 ◽

Vol 10 ◽

Cited By ~ 7

Author(s):

Julie Calonne ◽

Laurie Isacco ◽

Jennifer Miles-Chan ◽

Denis Arsenijevic ◽

Jean-Pierre Montani ◽

...

Keyword(s):

Skeletal Muscle ◽

Thyroid Hormone ◽

Body Fat ◽

Protein Turnover ◽

Weight Regain ◽

Muscle Protein ◽

Skeletal Muscle Protein ◽

Hormone Metabolism ◽

Thyroid Hormone Metabolism ◽

Adaptive Thermogenesis

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Differential effects of fasting vs food restriction on liver thyroid hormone metabolism in male rats

Journal of Endocrinology ◽

10.1530/joe-14-0533 ◽

2014 ◽

Vol 224 (1) ◽

pp. 25-35 ◽

Cited By ~ 14

Author(s):

E M de Vries ◽

H C van Beeren ◽

M T Ackermans ◽

A Kalsbeek ◽

E Fliers ◽

...

Keyword(s):

Thyroid Hormone ◽

Food Intake ◽

Caloric Restriction ◽

Food Restriction ◽

Male Rats ◽

Hormone Metabolism ◽

Thyroid Hormone Metabolism ◽

Limited Food ◽

Fasted Rats

A variety of illnesses that leads to profound changes in the hypothalamus–pituitary–thyroid (HPT) are axis collectively known as the nonthyroidal illness syndrome (NTIS). NTIS is characterized by decreased tri-iodothyronine (T3) and thyroxine (T4) and inappropriately low TSH serum concentrations, as well as altered hepatic thyroid hormone (TH) metabolism. Spontaneous caloric restriction often occurs during illness and may contribute to NTIS, but it is currently unknown to what extent. The role of diminished food intake is often studied using experimental fasting models, but partial food restriction might be a more physiologically relevant model. In this comparative study, we characterized hepatic TH metabolism in two models for caloric restriction: 36 h of complete fasting and 21 days of 50% food restriction. Both fasting and food restriction decreased serum T4concentration, while after 36-h fasting serum T3also decreased. Fasting decreased hepatic T3but not T4concentrations, while food restriction decreased both hepatic T3and T4concentrations. Fasting and food restriction both induced an upregulation of liver D3 expression and activity, D1 was not affected. A differential effect was seen inMct10mRNA expression, which was upregulated in the fasted rats but not in food-restricted rats. Other metabolic pathways of TH, such as sulfation and UDP-glucuronidation, were also differentially affected. The changes in hepatic TH concentrations were reflected by the expression of T3-responsive genesFasandSpot14only in the 36-h fasted rats. In conclusion, limited food intake induced marked changes in hepatic TH metabolism, which are likely to contribute to the changes observed during NTIS.

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Dysregulated Thyroid Hormone Metabolism Following Formoterol Stimulation In Thyroid Hormone Depleted Skeletal Muscle

Medicine & Science in Sports & Exercise ◽

10.1249/01.mss.0000685420.24493.06 ◽

2020 ◽

Vol 52 (7S) ◽

pp. 908-908

Author(s):

Gena D. Guerin ◽

Emily L. Zumbro ◽

Ryan A. Gordon ◽

Chase M. White ◽

Dreanna M. McAdams ◽

...

Keyword(s):

Skeletal Muscle ◽

Thyroid Hormone ◽

Hormone Metabolism ◽

Thyroid Hormone Metabolism

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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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