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

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.

Meal-induced brown fat thermogenesis and thyroid hormone metabolism in rats

1985 ◽  
Vol 249 (5) ◽  
pp. E519-E524 ◽  
Author(s):  
Z. Glick ◽  
S. Y. Wu ◽  
J. Lupien ◽  
R. Reggio ◽  
G. A. Bray ◽  
...  
Keyword(s):  
Thyroid Hormone ◽  
Thyroid Hormones ◽  
Serum Concentrations ◽  
Hormone Metabolism ◽  
Thyroid Hormone Metabolism ◽  
Low Protein ◽  
Bat Mitochondria ◽  
Brown Adipose ◽  
Serum T3 ◽  
The Relationship

The relationship between the meal-induced increase in brown adipose tissue (BAT) thermogenesis, determined by the level of GDP binding to BAT mitochondria, and thyroid hormone metabolism have been examined. A single low-protein, high-carbohydrate meal resulted in a significant increase in the thermogenic activity of BAT. This effect on BAT thermogenesis was accompanied by significant increases in activity of thyroxine 5'-monodeiodinase in the BAT (P less than 0.05) and liver (P less than 0.02) but not with any significant changes in serum concentrations of the thyroid hormones. The stimulatory effects of the meal on BAT thermogenesis and hepatic thyroxine (T4) to triiodothyronine (T3) conversion persisted at least as late as 24 h after meal onset. Food deprivation for 40 h was associated with large reductions in serum concentrations of T3 (P less than 0.01) and T4 (P less than 0.001), but deprivation for 18 h had no significant effect on serum T3 and T4 concentrations. Our data indicate that the meal-induced increase in BAT thermogenesis can be independent from changes in serum concentrations of thyroid hormones and suggest that T3 produced in BAT in response to feeding may play a role in the thermic response of this tissue to meals.

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 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.

Interrelationships between energy metabolism and thyroid hormone metabolism during starvation in the rat

1980 ◽  
Vol 93 (3) ◽  
pp. 322-331 ◽  
Author(s):  
A. G. Burger ◽  
M. Berger ◽  
K. Wimpfheimer ◽  
E. Danforth
Keyword(s):  
Thyroid Hormone ◽  
Redox State ◽  
Plasma Concentrations ◽  
Intraperitoneal Administration ◽  
Metabolic Clearance ◽  
Hormone Metabolism ◽  
Short Term ◽  
Thyroid Hormone Metabolism ◽  
Peripheral Conversion ◽  
Pyruvate Ratio

Abstract. Thyroid hormone metabolism and plasma concentrations of TSH were studied after short-term hypocaloric refeeding of rats starved for 2–6 days. Carbohydrate and protein (10 kcal) refeeding after 4 days of starvation resulted in a rapid increase in serum T3 (P<0.01) and, less consistently of T4. Plasma TSH did not change. These findings were not due to changes in the metabolic clearance rates or in thyroid hormone binding proteins, as the disappearance of injected labelled T3 and T4, and the free fractions of T3 and T4, were unchanged. Increased thyroidal secretion, and for T3, increased peripheral conversion from T4 were therefore responsible for these changes. Fat refeeding had no immediate effect on plasma T4, T3 or TSH. After 6 days of starvation, refeeding of any nutrient was ineffective in altering the plasma concentrations of T3 and T4. The intraperitoneal administration of nicotinamide (100 mg/100 g body weight) to starving animals caused an increase in blood glucose and a decrease in blood betahydroxybutyrate similar to that which followed carbohydrate refeeding; T3, however, did not increase. In spite of producing a profile of substrates in the serum similar to that found following carbohydrate refeeding, nicotinamide administration had no effect on the blood lactate/ pyruvate ratio which was increased following carbohydrate refeeding. Therefore, the cytoplasmic redox state, as reflected by the lactate/pyruvate ratio, may be closely related to the control of peripheral thyroid hormone metabolism.

scholarly journals Plasma Membrane Transport of Thyroid Hormones and Its Role in Thyroid Hormone Metabolism and Bioavailability

2001 ◽  
Vol 22 (4) ◽  
pp. 451-476 ◽  
Author(s):  
Georg Hennemann ◽  
Roelof Docter ◽  
Edith C. H. Friesema ◽  
Marion de Jong ◽  
Eric P. Krenning ◽  
...  
Keyword(s):  
Plasma Membrane ◽  
Thyroid Hormone ◽  
Thyroid Hormones ◽  
Membrane Transport ◽  
Hormone Metabolism ◽  
Thyroid Hormone Metabolism

scholarly journals Transthyretin is not necessary for thyroid hormone metabolism in conditions of increased hormone demand

2005 ◽  
Vol 187 (2) ◽  
pp. 257-266 ◽  
Author(s):  
J C Sousa ◽  
G Morreale de Escobar ◽  
P Oliveira ◽  
M J Saraiva ◽  
J A Palha
Keyword(s):  
Thyroid Hormone ◽  
Thyroid Hormones ◽  
Stressful Events ◽  
Mrna Levels ◽  
Wild Type ◽  
Hormone Metabolism ◽  
Normal Thyroid ◽  
Hormone Synthesis ◽  
Thyroid Hormone Metabolism ◽  
Hormone Homeostasis

Thyroid hormones circulate in blood mainly bound to plasma proteins. Transthyretin is the major thyroxine plasma carrier in mice. Studies in transthyretin-null mice revealed that the absence of transthyretin results in euthyroid hypothyroxinemia and normal thyroid hormone tissue distribution, with the exception of the choroid plexus in the brain. Therefore, transthyretin does not influence normal thyroid hormone homeostasis under standard laboratory conditions. To investigate if transthyretin has a buffer/storage role we challenged transthyretin-null and wild-type mice with conditions of increased hormone demand: (i) exposure to cold, which elicits thermogenesis, a process that requires thyroid hormones; and (ii) thyroidectomy, which abolishes thyroid hormone synthesis and secretion and induces severe hypothyroidism. Transthyretin-null mice responded as the wild-type both to changes induced by stressful events, namely in body weight, food intake and thyroid hormone tissue content, and in the mRNA levels of genes whose expression is altered in such conditions. These results clearly exclude a role for transthyretin in thyroid hormone homeostasis even under conditions of increased hormone demand.

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