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.

Thyroid function and thyroid hormone metabolism in elderly people low T3-syndrome in old age?

1981 ◽  
Vol 59 (7) ◽  
pp. 315-323 ◽  
Author(s):  
J. Herrmann ◽  
E. Heinen ◽  
H. J. Kr�ll ◽  
K. H. Rudorff ◽  
H. L. Kr�skemper
Keyword(s):  
Thyroid Hormone ◽  
Elderly People ◽  
Old Age ◽  
Thyroid Function ◽  
Hormone Metabolism ◽  
Low T3 Syndrome ◽  
Thyroid Hormone Metabolism ◽  
Low T3

scholarly journals Antiepileptic Drugs and Thyroid Hormone Homeostasis: Literature Review and Practical Guideline

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A824-A824
Author(s):  
Anne Maria Rochtus ◽  
Dorien Herijgers ◽  
Katrien Jansen ◽  
Brigitte Decallonne
Keyword(s):  
Thyroid Hormone ◽  
Thyroid Function ◽  
Cortical Excitability ◽  
System Development ◽  
Intractable Epilepsy ◽  
Nervous System Development ◽  
Hormone Metabolism ◽  
Cross Sectional ◽  
Thyroid Hormone Metabolism ◽  
Practical Guideline

Abstract Thyroid hormones play an essential role in central nervous system development, normal physiological brain function and repairing mechanisms. On one hand, thyroid hormone alterations influence cortical excitability and on the other hand anti-epileptic drugs (AEDs) are associated with alterations in thyroid hormone metabolism. Although this interaction has long been described, and epilepsy is a common and chronic neurological disease, studies describing the interplay are often small and retrospective. We performed a systematic review of the current literature on epilepsy, AED therapy and thyroid hormone metabolism. Forty-seven studies were included. Most studies were retrospective cross-sectional studies (n=25) and investigated thyroid function alterations in patients on older AEDs such as phenobarbital, phenytoin, carbamazepine and valproic acid. Overall, almost one third of patients with epilepsy had subclinical hypothyroidism, especially patients on valproate and carbamazepine. Studies with patients receiving polytherapy are scarce, but reported a higher risk for hypothyroidism in patients with older age, female sex, longer duration of epilepsy, intractable epilepsy and polytherapy. Studies on newer AEDs are also scarce and further studies essential to improve the care for epilepsy patients. AEDs are associated with alterations in thyroid hormone metabolism. Thyroid function monitoring is indicated in patients on AEDs, especially those with refractory chronic epilepsy and those on polytherapy. We provide a practical guideline for thyroid function monitoring for the clinician taking care of patients on AEDs.

Euthyroid sick syndrome in older people

2001 ◽  
Vol 11 (1) ◽  
pp. 1-4
Author(s):  
Nadya Kagansky ◽  
Sari Tal ◽  
Shmuel Levy
Keyword(s):  
Thyroid Hormone ◽  
Older People ◽  
Thyroid Function ◽  
Clinical Evidence ◽  
Thyroid Function Tests ◽  
Hormone Metabolism ◽  
Euthyroid Sick Syndrome ◽  
Thyroid Hormone Metabolism ◽  
Function Tests ◽  
Altered Thyroid

The term euthyroid sick syndrome (ESS) is used to describe abnormalities in thyroid function tests that are observed in patients with systemic non-thyroid illness. Despite these abnormalities, there is usually little clinical evidence of hypothyroidism. Patients with ESS are generally considered to have altered thyroid hormone metabolism and to be euthyroid.

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

2014 ◽  
Vol 224 (1) ◽  
pp. 25-35 ◽  
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.

Selenium substitution has no direct effect on thyroid hormone metabolism in critically ill patients

2004 ◽  
pp. 47-54 ◽  
Author(s):  
MW Angstwurm ◽  
J Schopohl ◽  
R Gaertner
Keyword(s):  
Severe Sepsis ◽  
Thyroid Hormone ◽  
Direct Effect ◽  
Apache Ii ◽  
Apache Ii Score ◽  
Hormone Metabolism ◽  
Plasma Selenium ◽  
Thyroid Hormone Metabolism ◽  
Selenium Substitution ◽  
Thyroid Hormone Levels

BACKGROUND: In severe illness, plasma selenium levels are decreased; a decreased activity of the selenoenzyme 5'-deiodinase has been hypothesized to contribute to low tri-iodothyronine (T3) levels in non-thyroidal illness (NTI) syndrome in these patients. OBJECTIVE: To analyse the influence of selenium substitution on thyroid hormone metabolism in patients with severe sepsis. DESIGN: A prospective, randomized, controlled study at the medical internal intensive care unit of the University of Munich. Results are for 41 consecutive patients with severe sepsis with an APACHE II score >15. Patients received either sodium selenite (500 microg/day for the first 3 days, reducing to 250 and then 125 microg/day every 3 days) or a placebo. RESULTS: At study entry, APACHE II score and demographics were identical in both groups. The mean levels of TSH, free tri-iodithyronine and total T3, as well as plasma selenium and selenium-dependent peroxidase (GSH-Px) activity, were decreased. Plasma selenium and GSH-Px activity were normalized on days 3, 7 and 14 in patients receiving selenium (n=21), but remained below normal in the control patients. Patients receiving selenium had a better clinical outcome and thyroid hormone levels normalized earlier. Thyroid hormone levels increased in patients who showed clinical improvement, independent of selenium levels or selenium substitution. CONCLUSIONS: Selenium substitution in patients with NTI improves morbidity, but has no direct effect on the free and total thyroid hormones. In severely ill patients, decreased deiodinase activity due to low plasma selenium levels seems unlikely. After clinical revival, TSH and then the thyroidal hormones normalize independently of selenium substitution.

Interference of dimethyl α-(dimethoxyphosphinyl) p-chlorobenzyl phosphate (SR-202) in thyroid hormone. metabolism: evidence of inhibition of monodeiodination

1987 ◽  
Vol 112 (1) ◽  
pp. 171-175 ◽  
Author(s):  
C. Liniger ◽  
D. Pometta ◽  
A. G. Burger
Keyword(s):  
Thyroid Hormone ◽  
Thyroid Hormones ◽  
Thyroid Function ◽  
Clinical Investigation ◽  
Compelling Evidence ◽  
Hormone Metabolism ◽  
Thyroid Hormone Metabolism ◽  
Peripheral Conversion

ABSTRACT SR-202 is a non-iodinated potential lipid-altering agent. When administered (100 mg) three times per day for 3 days to six euthyroid subjects it was associated with a 30 ± 3% (mean ± s.e.m.) fall in 3,3′,5-tri-iodothyronine(T3)(P < 0·001), a reciprocal 104 ± 14% rise in 3,3′,5′-tri-iodothyronine (reverse T3, rT3) (P < 0·01), and a 37 ± 7% rise in thyroxine (T4) (P < 0·001). Basal and TRH-stimulated TSH did not change. These results suggested that SR-202 was acting as an inhibitor of the peripheral monodeiodination of T4 to T3. During a second study the same subjects received the same dose of SR-202 for a further 3 days following 15 days of progressive substitutive treatment with l-T4, which they continued to take at 200 μg/day until the end of the study. Despite higher levels of thyroid hormones in the substituted subjects, similar results were observed, serum T3 falling by 40 ± 2% (P < 0·001), serum rT3 and T4 rising by 168 ± 24% (P < 0·01) and 37 ± 9% (P < 0·01) respectively. These changes provide compelling evidence that SR-202 is an inhibitor of the peripheral conversion of T4 to T3 that acts on thyroid hormone metabolism without provoking a counter-regulatory pituitary response. It might prove to be a useful tool for the clinical investigation of thyroid function. J. Endocr. (1987) 112, 171–175

scholarly journals Developmentally defined regulation of thyroid hormone metabolism by glucocorticoids in the rat

2005 ◽  
Vol 185 (2) ◽  
pp. 327-336 ◽  
Author(s):  
S Van der Geyten ◽  
V M Darras
Keyword(s):  
Thyroid Hormone ◽  
Direct Consequence ◽  
Type I ◽  
Hormone Metabolism ◽  
Hormone Levels ◽  
Thyroid Hormone Metabolism ◽  
Rat Pups ◽  
Short Period ◽  
Thyroid Hormone Levels

Glucocorticoids are known regulators of thyroid function in vertebrates. In birds they have clear tissue-specific and age-dependent effects on thyroid hormone metabolism. In mammals, however, few studies exist addressing these aspects using an in vivo model system. We therefore set out to examine the acute effects of a single dose of dexamethasone (DEX) on plasma 3,5,3′-tri-iodothyronine (T3) and thyroxine (T4) levels, as well as on the activity of the different deiodinases in liver, kidney and brain in the developing rat. In 20-day-old fetuses (E20), glucocorticoids had no effects on circulating thyroid hormone levels despite their clear effects on hepatic and renal deiodinases, thereby indicating that under these conditions circulating thyroid hormone levels are more dependent on thyroidal secretion than on peripheral deiodination. In contrast, in 5-day-old rat pups, DEX did not seem to have any effects on hepatic and renal T3 production (via the type I deiodinase), whereas type III deiodinase (D3) activity in both these tissues increased significantly. These observations therefore suggested that the DEX-induced increase in circulating T3 levels is a direct consequence of the increase in plasma T4 levels. In 12-day-old pups (P12), however, the main effect of glucocorticoids on circulating levels was by increasing inner ring deiodination T3 through induction of D3 in both liver and kidney. Finally, in the brain, glucocorticoids stimulated thyroid hormone activity only during a short period of time (between E20 and P12) that largely overlaps with the transient window in time during which brain development is thyroid hormone sensitive. This was in contrast to the E20 and P12 brain, where the glucocorticoid-induced changes in type II deiodinase and D3 seemed to favor a status quo in local T3 availability.

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