Effects of Thyroid Hormones on Amino Acid and Protein Metabolism. II. Glutamate Concentration in Rat Tissues After Thyroidectomy and Thyroid Hormone Treatment

Endocrinology ◽  
1970 ◽  
Vol 87 (4) ◽  
pp. 816-818 ◽  
Author(s):  
AKIRA MOCHIZUKI ◽  
YA-PIN LEE
Keyword(s):  
Amino Acid ◽  
Thyroid Hormone ◽  
Thyroid Hormones ◽  
Protein Metabolism ◽  
Hormone Treatment ◽  
Rat Tissues ◽  
Glutamate Concentration

scholarly journals ATP synthase subunit c expression: physiological regulation of the P1 and P2 genes

1997 ◽  
Vol 323 (2) ◽  
pp. 379-385 ◽  
Author(s):  
Ulf ANDERSSON ◽  
Josef HOUŠTĚK ◽  
Barbara CANNON
Keyword(s):  
Thyroid Hormone ◽  
Cold Acclimation ◽  
Atp Synthase ◽  
Hormone Treatment ◽  
Rat Tissues ◽  
Mrna Levels ◽  
Subunit C ◽  
Brown Adipose ◽  
Mitochondrial Atp Synthase

Pre-translational regulation of subunit c has been suggested to control the biosynthesis of mitochondrial ATP synthase (ATPase) in brown adipose tissue (BAT). Subunit c is encoded by the genes P1 and P2, which encode identical mature proteins. We have determined here the levels of P1 and P2 mRNAs in different tissues, in response to cold acclimation in rats, during ontogenic development of BAT in hamsters, and following thyroid hormone treatment in rat BAT and liver. Quantitative ribonuclease protection analysis showed that both the P1 and P2 mRNAs were present in all rat tissues measured. Their total amount in each tissue corresponded well with the ATPase content of that tissue. While the P1/P2 mRNA ratio is high in ATPase-rich tissues, the P2 mRNA dominates in tissues with less ATPase. Cold acclimation affects P1 but not P2 gene expression in rat BAT. A rapid and transient increase in P1 mRNA is followed by sustained depression, which is accompanied by a decrease in ATPase content. Similarly, ontogenic suppression of ATPase content in hamster BAT was accompanied by suppression of the P1 mRNA levels, while P2 expression was virtually unchanged. Furthermore, when hypothyroid rats were treated with thyroid hormone, the steady-state level of P1 but not of P2 mRNA was significantly increased in liver. BAT was unaffected. We conclude that the P1 and P2 genes for subunit c are differentially regulated in vivo. While the P2 gene is expressed constitutively, the P1 gene responds to different physiological stimuli as a means of modulating the relative content of ATP synthase.

scholarly journals Involvement of the L-Type Amino Acid Transporter Lat2 in the Transport of 3,3′-Diiodothyronine across the Plasma Membrane

2015 ◽  
Vol 4 (Suppl. 1) ◽  
pp. 42-50 ◽  
Author(s):  
Anita Kinne ◽  
Melanie Wittner ◽  
Eva K. Wirth ◽  
Katrin M. Hinz ◽  
Ralf Schülein ◽  
...  
Keyword(s):  
Amino Acid ◽  
Thyroid Hormone ◽  
Thyroid Hormones ◽  
Surface Expression ◽  
Amino Acid Transporter ◽  
Cell System ◽  
Monocarboxylate Transporter ◽  
Cell Surface Expression ◽  
Xenopus Laevis Oocytes ◽  
Acid Transporter

Thyroid hormones are transported across cell membranes by transmembrane transporter proteins, for example by members of the monocarboxylate transporter (MCT) and the L-type amino acid transporter (LAT) families. LATs consist of a light chain (e.g. LAT2) and a heavy chain (CD98), which is essential for their cell surface expression and functionality. The specificity of Lat2 for thyroid hormones and their metabolites and its role in their transport was not fully clear. This fact motivated us to establish a cell system to elucidate the uptake of thyroid hormones and their metabolites by mouse Lat2. The coinjection of cRNA coding for Lat2 and CD98 into Xenopus laevis oocytes resulted in a markedly increased level of 3,3′-diiodo-L-thyronine (3,3′-T2) and to some extent also enhanced T3 transport. To gain insight into properties of thyroid hormones and their metabolites transported by Lat2, we inhibited 3,3′-T2 uptake by various iodothyronine derivatives. T1 and T2 derivatives as well as 2-aminobicyclo-[2,2,1]-heptane-2-carboxylic acid strongly competed with 3,3′-T2 uptake. In addition, we performed T2 uptake measurements with the thyroid hormone-specific transporter MCT8. For both Lat2 and MCT8, Km values in a low micromolar range were calculated. We demonstrated that oocytes are a suitable system for thyroid hormone transport studies mediated by Lat2. Our data indicates that Lat2 compared to other thyroid hormone transporters prefers 3,3′-T2 as the substrate. Thus, Lat2 might contribute to the availability of thyroid hormone by importing and/or exporting 3,3′-T2, which is generated either by T3 inactivation or by rapid deiodinase 1-mediated rT3 degradation.

scholarly journals Aminoaciduria, but normal thyroid hormone levels and signalling, in mice lacking the amino acid and thyroid hormone transporter Slc7a8

2011 ◽  
Vol 439 (2) ◽  
pp. 249-255 ◽  
Author(s):  
Doreen Braun ◽  
Eva K. Wirth ◽  
Franziska Wohlgemuth ◽  
Nathalie Reix ◽  
Marc O. Klein ◽  
...  
Keyword(s):  
Amino Acids ◽  
Amino Acid ◽  
Thyroid Hormone ◽  
Thyroid Hormones ◽  
Cell Types ◽  
Monocarboxylate Transporter ◽  
Functional Compensation ◽  
Neutral Amino Acids ◽  
System L ◽  
Neurological Phenotype

LAT2 (system L amino acid transporter 2) is composed of the subunits Slc7a8/Lat2 and Slc3a2/4F2hc. This transporter is highly expressed along the basolateral membranes of absorptive epithelia in kidney and small intestine, but is also abundant in the brain. Lat2 is an energy-independent exchanger of neutral amino acids, and was shown to transport thyroid hormones. We report in the present paper that targeted inactivation of Slc7a8 leads to increased urinary loss of small neutral amino acids. Development and growth of Slc7a8−/− mice appears normal, suggesting functional compensation of neutral amino acid transport by alternative transporters in kidney, intestine and placenta. Movement co-ordination is slightly impaired in mutant mice, although cerebellar development and structure remained inconspicuous. Circulating thyroid hormones, thyrotropin and thyroid hormone-responsive genes remained unchanged in Slc7a8−/− mice, possibly because of functional compensation by the thyroid hormone transporter Mct8 (monocarboxylate transporter 8), which is co-expressed in many cell types. The reason for the mild neurological phenotype remains unresolved.

Response of glucose disposal to hyperinsulinaemia in human hypothyroidism and hyperthyroidism

2002 ◽  
Vol 104 (1) ◽  
pp. 7-15 ◽  
Author(s):  
C. ROCHON ◽  
I. TAUVERON ◽  
C. DEJAX ◽  
P. BENOIT ◽  
P. CAPITAN ◽  
...  
Keyword(s):  
Amino Acid ◽  
Thyroid Hormone ◽  
Healthy Volunteers ◽  
Plasma Insulin ◽  
Hormone Treatment ◽  
Glucose Disposal ◽  
Amino Acid Infusion ◽  
Before And After ◽  
Hypothyroid Patients ◽  
Incremental Increase

We have examined insulin action on glucose metabolism in six hypothyroid patients before and after regular thyroid hormone treatment, and in six healthy volunteers before and after transient induction of moderate hyperthyroidism. Insulin was infused under euglycaemic and eukalaemic clamps. An appropriate amino acid infusion was used to blunt insulin-induced decreases in amino acid levels. Glucose kinetics were assessed using a primed continuous infusion of [6,6-2H2]glucose. The results showed that basal plasma insulin and glucose levels (i.e. before infusion) were similar in each case. Despite similar insulin infusion rates, the plateau value of insulin was lower after thyroid treatment in both hypothyroid patients and healthy volunteers. The rate of exogenous glucose needed to maintain plasma glucose at a steady-state level was increased by thyroid hormone in hypothyroid patients (P<0.05), but not in healthy volunteers. Thyroid treatment resulted in a significant increase in basal glucose disposal in both groups (P<0.05). Insulin, in conjunction with glucose and amino acids, significantly stimulated glucose disposal (P<0.05) under all conditions. The incremental increase in glucose disposal after infusion tended to be higher following thyroid hormone treatment, but this was not statistically significant. However, the ratio of the incremental increase in glucose disposal to the increase in plasma insulin was significantly improved after thyroid hormone treatment in hypothyroid patients (P<0.05). It was also increased in healthy volunteers, but not significantly. We conclude that thyroid hormones improve the ability of insulin to stimulate glucose disposal related to insulinaemia. This phenomenon may be highly sensitive, because it was only apparent at low thyroid hormone levels.

scholarly journals Novel uses of thyroid hormones in cardiovascular conditions

Endocrine ◽  
2019 ◽  
Vol 66 (1) ◽  
pp. 115-123 ◽  
Author(s):  
Salman Razvi
Keyword(s):  
Cardiovascular Diseases ◽  
Thyroid Hormone ◽  
Thyroid Hormones ◽  
Hormone Therapy ◽  
Large Scale ◽  
Experimental Studies ◽  
Hormone Treatment ◽  
Limited Data ◽  
Hormone Levels ◽  
Thyroid Hormone Levels

Abstract Thyroid hormone levels are reduced in cardiovascular diseases and this phenomenon is associated with worse outcomes. It is unclear whether the changes in thyroid hormone bioavailability to the affected myocardium are beneficial or if this is a maladaptive response. Experimental studies from animal models of acute myocardial infarction (AMI) suggest that thyroid hormone treatment may be beneficial. There is limited data available on the use of thyroid hormones in patients with AMI and heart failure and this suggests that treatment to normalise thyroid hormone levels may be safe and potentially efficacious. Similarly, evidence of thyroid hormone therapy in patients undergoing cardiac surgery or during cardiac transplantation is limited. It is therefore difficult to draw any firm conclusions about benefits or risks of thyroid hormone treatment in these conditions. Large scale clinical trials of thyroid hormones in patients with cardiac conditions are required to confirm safety and evaluate efficacy. Furthermore, it needs to be elucidated which hormone to administer (thyroxine or triiodothyronine), when in the disease pathway to treat, dose of thyroid hormone to administer, and which parameters to utilise to assess safety and efficacy. Until these important questions are answered thyroid hormone therapy in cardiovascular diseases must remain within the research domain.

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.

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