scholarly journals Differential modulation of expression of the two acylphosphatase isoenzymes by thyroid hormone

1995 ◽  
Vol 311 (2) ◽  
pp. 567-573 ◽  
Author(s):  
P Chiarugi ◽  
G Raugei ◽  
R Marzocchini ◽  
T Fiaschi ◽  
C Ciccarelli ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Thyroid Hormone ◽  
State Level ◽  
K562 Cells ◽  
Hormone Treatment ◽  
Differential Regulation ◽  
Rapid Decrease ◽  
Differential Modulation ◽  
Hormone Administration ◽  
Specific Mrna

The modulation of expression of the skeletal muscle and erythrocyte acylphosphatase isoenzymes by thyroid hormone has been investigated. Our results indicate a differential regulation of the two enzymic isoforms by tri-iodothyronine (T3) in K562 cells in culture: an increase in the specific mRNA during T3-stimulation is shown only for the skeletal muscle isoenzyme. A fast and transient T3 induction of the accumulation of the specific mRNA can be observed, reaching a maximum 8 h after hormone treatment and then rapidly decreasing almost to the steady-state level after 24 h. A nuclear run-on assay was performed to explore the mechanisms of this regulation. These studies indicate that T3 induction of skeletal muscle acylphosphatase mRNA is due, at least in part, to a fast and transient increase in the rate of gene transcription, within 4 h after hormone administration. A very rapid decrease is then observed within a further 2 h. T3-dependent accumulation of the mRNA for the skeletal muscle acylphosphatase requires ongoing protein synthesis, as confirmed by inhibition with cycloheximide or puromycin. These findings indicate that the transcriptional regulation of the gene may be indirect.

Thyroid hormone specifically regulates skeletal muscle Na(+)-K(+)-ATPase alpha 2- and beta 2-isoforms

1993 ◽  
Vol 265 (3) ◽  
pp. C680-C687 ◽  
Author(s):  
K. K. Azuma ◽  
C. B. Hensley ◽  
M. J. Tang ◽  
A. A. McDonough
Keyword(s):  
Skeletal Muscle ◽  
Thyroid Hormone ◽  
State Level ◽  
Mrna Abundance ◽  
Northern Analysis ◽  
Protein Abundance ◽  
Constant Amount ◽  
Protein Levels ◽  
Subunit Expression ◽  
Beta 2

The purpose of this study was to determine the pattern of thyroid hormone (triiodothyronine, T3) regulation of the Na(+)-K(+)-adenosinetriphosphatase (Na(+)-K(+)-ATPase) alpha- and beta-subunit expression in skeletal muscle, which expresses alpha 1-, alpha 2-, beta 1-, and beta 2-subunits, and compare it with that seen in kidney, which expresses only alpha 1 and beta 1. Three steady states were studied: hypothyroid, euthyroid, and hyperthyroid (hypothyroids injected daily with 1 microgram T3/g body wt for 2-16 days). Protein and mRNA abundance, determined by Western and Northern analysis, were normalized to a constant amount of homogenate protein and total RNA, respectively. In skeletal muscle, there was no change in alpha 1- or beta 1-mRNA or protein levels in the transition from hypothyroid to hyperthyroid. However, alpha 2 was highly regulated; mRNA reached a new steady-state level of fivefold over hypothyroid by 8 days of T3 treatment and protein abundance increased threefold. In addition, beta 2-mRNA and protein were detected in skeletal muscle and were also highly regulated by T3; beta 2-mRNA increased nearly fourfold over hypothyroid level, and beta 2-protein abundance increased over twofold. In kidney in the transition from hypothyroid to hyperthyroid, there were coordinate 1.6-fold increases in both alpha 1- and beta 1-mRNA abundance that predicted the observed changes in alpha 1- and beta 1-protein levels and Na(+)-K(+)-ATPase activity.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of thyroid hormone on UTP content and uridine kinase activity of rat heart and skeletal muscle

1980 ◽  
Vol 238 (5) ◽  
pp. E443-E449 ◽  
Author(s):  
B. J. Gertz ◽  
E. S. Haugaard ◽  
N. Haugaard
Keyword(s):  
Skeletal Muscle ◽  
Thyroid Hormone ◽  
Kinase Activity ◽  
Actinomycin D ◽  
Hormone Treatment ◽  
Subcutaneous Injections ◽  
Uridine Kinase ◽  
Single Intraperitoneal Injection ◽  
Uracil Nucleotide ◽  
Prior Administration

In rats made hyperthyroid by daily intramuscular injections of 250 microgram thyroxine (T4)/100 g body wt for 5 days, uridine kinase activity of extracts of psoas and cardiac muscle was markedly increased Vmax of the enzyme was elevated with no change in the apparent Km for uridine. In animals treated as above, significant increases in UTP and total uracil nucleotide contents were observed in heart and skeletal muscle. Twelve hours after a single intraperitoneal injection of 30 microgram/100 g body wt of 3,5,3'-triiodothyronine (T3), cardiac uridine kinase was significantly increased. Brain uridine kinase was unaffected by thyroid hormone treatment. In thyroidectomized rats, uridine kinase activity was lower than normal. The effect of thyroidectomy on uridine kinase activity was overcome by daily subcutaneous injections of 3 microgram T4/100 g body wt for 7 days. The rise in cardiac uridine kinase activity produced by T3 could be prevented by prior administration of actinomycin D.

Na+,K+-ATPase enzyme units in lean and obese (ob/ob) thyroxine-injected mice.

1979 ◽  
Vol 237 (3) ◽  
pp. E265
Author(s):  
M H Lin ◽  
J G Vander Tuig ◽  
D R Romsos ◽  
T Akera ◽  
G A Leveille
Keyword(s):  
Skeletal Muscle ◽  
Thyroid Hormone ◽  
Large Dose ◽  
Binding Sites ◽  
Hormone Treatment ◽  
Obese Mice ◽  
Ouabain Binding ◽  
Hindlimb Muscles

The possible involvement of Na+,K+-ATPase in the etiology of obesity in the obese (ob/ob) mouse was explored. The number of Na+,K+-ATPase enzyme units in skeletal muscle, liver, and kidneys from 4- and 8-wk-old obese and lean mice was estimated from saturable [3H]ouabain binding to particulate fractions. Neither phenotype nor age altered the Kd value for ouabain binding in these three tissue preparations. The total number of [3H]ouabain binding sites in hindlimb muscles was 35--55% lower in 4- and 8-wk-old obese mice than in their lean counterparts. However, the total number of [3H]ouabain binding sites in liver and kidneys of obese mice was similar to values observed in their lean counterparts. Because it has been suggested that ob/ob mice are hypothyroid, we investigated the response of Na+,K+-ATPase in these mice to thyroid hormone treatment (approximately 5 microgram thyroxine/day for 2 wk). The number of [3H]ouabain binding sites in the three tissues increased in both obese and lean mice injected with this relatively large dose of thyroxine, but the obese mice were 2--3 times more responsive than lean mice.

Effects of thyroid hormone administration on skeletal muscle mitochondria

1975 ◽  
Vol 228 (5) ◽  
pp. 1341-1345 ◽  
Author(s):  
WW Winder ◽  
KM Baldwin ◽  
RL Terjung ◽  
JO Holloszy
Keyword(s):  
Skeletal Muscle ◽  
Thyroid Hormone ◽  
Citrate Synthase ◽  
Marker Enzymes ◽  
Mitochondrial Marker ◽  
Respiratory Capacity ◽  
Mitochondrial Markers ◽  
Glycerophosphate Dehydrogenase ◽  
Skeletal Muscle Mitochondria ◽  
Hormone Administration

The effects of thyroid hormone administration on the levels of a number of mitochondrial markers were measured in skeletal muscle and liver of normal rats. Injection of 18 mug of L-thyroxine (T4) per 100 g body wt every 4th day for 3 wk had no effect on the concentrations of cytochrome c, on citrate synthase activity, or on respiratory capacity of skeletal muscle. Injection of 200 mug of L-triiodothyronine (T3) daily for 5 days, or feeding 23 mg T4 and 7 mg T3/kg of diet for 2 wk, resulted in thyrotoxicosis and large increases in the activity of hepatic alpha-glycerophosphate dehydrogenase and other mitochondrial markers; however, the levels of activity of mitochondrial marker enzymes in gastrocnemius and quadriceps muscles were not significantly changed. Only when rats were fed 3 mg T4 and 1 mg T3/kg diet for a 6-wk period did we observe an increase in skeletal muscle mitochondrial markers. Thus, thyroxine treatment must be sufficiently prolonged if it is to be used as a tool for studying skeletal muscle mitochondrial biogenesis.

scholarly journals A child with a deletion in the monocarboxylate transporter 8 gene: 7-year follow-up and effects of thyroid hormone treatment

2011 ◽  
Vol 165 (5) ◽  
pp. 823-830 ◽  
Author(s):  
Amnon Zung ◽  
Theo J Visser ◽  
André G Uitterlinden ◽  
Fernando Rivadeneira ◽  
Edith C H Friesema
Keyword(s):  
Thyroid Hormone ◽  
Snp Array ◽  
Hormone Treatment ◽  
Neurological Status ◽  
Psychomotor Retardation ◽  
Monocarboxylate Transporter ◽  
High Dose ◽  
Hormone Administration ◽  
Hormone Analogs

ObjectiveThe monocarboxylate transporter 8 (MCT8; SLC16A2) has a pivotal role in neuronal triiodothyronine (T3) uptake. Mutations of this transporter determine a distinct X-linked psychomotor retardation syndrome (Allan–Herndon–Dudley syndrome (AHDS)) that is attributed to disturbed thyroid hormone levels, especially elevated T3 levels. We describe the genetic analysis of the MCT8 gene in a patient suspected for AHDS and the clinical and endocrine effects of L-thyroxine (LT4) or liothyronine (LT3) treatment intending to overcome the T3 uptake resistance through alternative transporters.MethodsThe six exons of the MCT8 gene were amplified individually by PCR. As multiple exons were missing, the length of the X-chromosomal deletion was determined by a dense SNP array, followed by PCR-based fine mapping to define the exact borders of the deleted segment. The clinical and endocrine data of the patient during 6.5 years of LT4 treatment and two periods (3 months each) of low- and high-dose LT3 were evaluated.ResultsA partial deletion of the MCT8 gene (comprising five of six exons) was detected, confirming the suspected AHDS. MCT8 dysfunction was associated with partial resistance to T3 at the hypothalamus and pituitary level, with normal responsiveness at the peripheral organs (liver and cardiovascular system). Thyroid hormone administration had no beneficial effect on the neurological status of the patient.ConclusionWe identified a 70 kb deletion encompassing exons 2–6 of the MCT8 gene in our AHDS patient. Both LT4 and LT3 administration had no therapeutic effect. Alternatively, treatment of AHDS patients with thyroid hormone analogs should be considered.

Thyroid hormone effects on LKB1, MO25, phospho-AMPK, phospho-CREB, and PGC-1α in rat muscle

2008 ◽  
Vol 105 (4) ◽  
pp. 1218-1227 ◽  
Author(s):  
D. J. Branvold ◽  
D. R. Allred ◽  
D. J. Beckstead ◽  
H. J. Kim ◽  
N. Fillmore ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Thyroid Hormone ◽  
Thyroid Hormones ◽  
Uncoupling Protein ◽  
Mitochondrial Protein ◽  
Hormone Treatment ◽  
Peroxisome Proliferator ◽  
Hexokinase Ii ◽  
Hormone Synthesis ◽  
Ampk Activity

Expression of all of the isoforms of the subunits of AMP-activated protein kinase (AMPK) and AMPK activity is increased in skeletal muscle of hyperthyroid rats. Activity of AMPK in skeletal muscle is regulated principally by the upstream kinase, LKB1. This experiment was designed to determine whether the increase in AMPK activity is accompanied by increased expression of the LKB1, along with binding partner proteins. LKB1, MO25, and downstream targets were determined in muscle extracts in control rats, in rats given 3 mg of thyroxine and 1 mg of triiodothyronine per kilogram chow for 4 wk, and in rats given 0.01% propylthiouracil (PTU; an inhibitor of thyroid hormone synthesis) in drinking water for 4 wk (hypothyroid group). LKB1 and MO25 increased in the soleus of thyroid hormone-treated rats vs. the controls. In other muscle types, LKB1 responses were variable, but MO25 increased in all. In soleus, MO25 mRNA increased with thyroid hormone treatment, and STRAD mRNA increased with PTU treatment. Phospho-AMPK and phospho-ACC were elevated in soleus and gastrocnemius of hyperthyroid rats. Thyroid hormone treatment also increased the amount of phospho-cAMP response element binding protein (CREB) in the soleus, heart, and red quadriceps. Four proteins having CREB response elements (CRE) in promoter regions of their genes (peroxisome proliferator-activated receptor-γ coactivator-1α, uncoupling protein 3, cytochrome c, and hexokinase II) were all increased in soleus in response to thyroid hormones. These data provide evidence that thyroid hormones increase soleus muscle LKB1 and MO25 content with subsequent activation of AMPK, phosphorylation of CREB, and expression of mitochondrial protein genes having CRE in their promoters.

Linear modulation of serum thyrotrophin by thyroid hormone treatment in hypothyroidism

1980 ◽  
Vol 95 (4) ◽  
pp. 472-478 ◽  
Author(s):  
A. Eugene Pekary ◽  
Jerome M. Hershman ◽  
Clark T. Sawin
Keyword(s):  
Thyroid Hormone ◽  
Hormone Replacement ◽  
Hormone Treatment ◽  
Significant Negative Correlation ◽  
Thyroid Hormone Replacement ◽  
Basal Serum ◽  
Thyroid Hormone Levels ◽  
Peak Versus ◽  
Hypothyroid Patients ◽  
Serum Tsh

Abstract. Basal serum TSH and the peak TSH response to a 500 μg TRH bolus were measured in 57 euthyroid and in 29 hypothyroid subjects either receiving graded thyroid hormone replacement or acutely removed from full replacement therapy. Serum TSH, total T4 and T3 were determined by sensitive radioimmunoassay methods. The peak versus basal TSH data for hypothyroid patients were linear within individuals. The regression slope of the peak versus basal TSH data for all hypothyroid subjects did not differ significantly from the corresponding slope for all euthyroid subjects. Basal and peak TSH versus T3 and T4 data for hypothyroid patients were also linear within each individual. Moreover, the regression of the basal TSH values averaged over the non-replacement to full replacement state against the TSH versus T3 slope had a significant negative correlation. This trend leads to an array of regression lines which average to the familiar hyperbolic relationship between thyrotrophin and thyroid hormone levels in man.

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