Effect of thyrotrophic hormone on the membrane potential of thyroid gland cells and on thyroid hormone secretion during aging

Abstract. Recently we found small amounts of TRH immunoreactivity in the thyroid gland of dogs and pigs. In the present study we investigated if exogenous TRH influences the release of T4, T3 and cAMP from the follicular cells, and calcitonin and somatostatin from the C-cells of perfused dog thyroid lobes. 10−5 mol/l TRH inhibited the TSH induced iodothyronine and cAMP release from the thyroid while 10−8 mol/l TRH had no effect. The relative proportions of T4 and T3 in thyroid secretion were not altered by TRH infusion. TRH did not influence the basal or the Ca++ induced release of somatostatin and calcitonin. Hence TRH has a direct inhibitory effect on the hormone secretion from thyroidal follicular cells. This opens the possibility that TRH in the thyroid participate in the regulation of thyroid hormone secretion. Even though the concentration of TRH found to be effective is high our results may indicate that TRH in the thyroid participates in the regulation of thyroid hormone secretion as an antagonist to TSH.

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Causes and laboratory investigation of hypothyroidism

Oxford Textbook of Endocrinology and Diabetes ◽

10.1093/med/9780199235292.003.3243 ◽

2011 ◽

pp. 530-537 ◽

Cited By ~ 1

Author(s):

Ferruccio Santini ◽

Aldo Pinchera

Keyword(s):

Thyroid Hormone ◽

Thyroid Gland ◽

Thyroid Hormones ◽

Thyroid Hormone Receptor ◽

Hormone Secretion ◽

Thyroid Tissue ◽

Clinical Manifestations ◽

Primary Hypothyroidism ◽

Central Hypothyroidism ◽

Resistance To Thyroid Hormones

Hypothyroidism is the clinical state that develops as a result of the lack of action of thyroid hormones on target tissues (1). Hypothyroidism is usually due to impaired hormone secretion by the thyroid, resulting in reduced concentrations of serum thyroxine (T4) and triiodothyronine (T3). The term primary hypothyroidism is applied to define the thyroid failure deriving from inherited or acquired causes that act directly on the thyroid gland by reducing the amount of functioning thyroid tissue or by inhibiting thyroid hormone production. The term central hypothyroidism is used when pituitary or hypothalamic abnormalities result in an insufficient stimulation of an otherwise normal thyroid gland. Both primary and central hypothyroidism may be transient, depending on the nature and the extent of the causal agent. Hypothyroidism following a minor loss of thyroid tissue can be recovered by compensatory hyperplasia of the residual gland. Similarly, hypothyroidism subsides when an exogenous inhibitor of thyroid function is removed. Peripheral hypothyroidism may also arise as a consequence of tissue resistance to thyroid hormones due to a mutation in the thyroid hormone receptor. Resistance to thyroid hormones is a heterogeneous clinical entity with most patients appearing to be clinically euthyroid while some of them have symptoms of thyrotoxicosis and others display selected signs of hypothyroidism. The common feature is represented by pituitary resistance to thyroid hormones, leading to increased secretion of thyrotropin that in turn stimulates thyroid growth and function. The variability in clinical manifestations depends on the severity of the hormonal resistance, the relative degree of tissue hyposensitivity, and the coexistence of associated genetic defects (see Chapter 3.4.8).

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Thyroid Hormone Secretion by the Fetal Thyroid Gland

Endocrinology ◽

10.1210/endo-80-4-545 ◽

1967 ◽

Vol 80 (4) ◽

pp. 545-551 ◽

Cited By ~ 2

Author(s):

WILLIAM H. BEIERWALTES

Keyword(s):

Thyroid Hormone ◽

Thyroid Gland ◽

Hormone Secretion ◽

Fetal Thyroid

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Impact of Monocarboxylate Transporter-8 Deficiency on the Hypothalamus-Pituitary-Thyroid Axis in Mice

Endocrinology ◽

10.1210/en.2010-0593 ◽

2010 ◽

Vol 151 (10) ◽

pp. 5053-5062 ◽

Cited By ~ 59

Author(s):

Marija Trajkovic-Arsic ◽

Julia Müller ◽

Veerle M. Darras ◽

Claudia Groba ◽

Sooyeon Lee ◽

...

Keyword(s):

Thyroid Hormone ◽

Thyroid Gland ◽

Hormone Replacement ◽

Hormone Secretion ◽

High Serum ◽

Monocarboxylate Transporter ◽

Neurological Deficits ◽

Serum Concentrations ◽

Hormone Production ◽

Serum T3

In patients, inactivating mutations in the gene encoding the thyroid hormone-transporting monocarboxylate transporter 8 (Mct8) are associated with severe mental and neurological deficits and disturbed thyroid hormone levels. The latter phenotype characterized by high T3 and low T4 serum concentrations is replicated in Mct8 knockout (ko) mice, indicating that MCT8 deficiency interferes with thyroid hormone production and/or metabolism. Our studies of Mct8 ko mice indeed revealed increased thyroidal T3 and T4 concentrations without overt signs of a hyperactive thyroid gland. However, upon TSH stimulation Mct8 ko mice showed decreased T4 and increased T3 secretion compared with wild-type littermates. Moreover, similar changes in the thyroid hormone secretion pattern were observed in Mct8/Trhr1 double-ko mice, which are characterized by normal serum T3 levels and normal hepatic and renal D1 expression in the presence of very low T4 serum concentrations. These data strongly indicate that absence of Mct8 in the thyroid gland affects thyroid hormone efflux by shifting the ratio of the secreted hormones toward T3. To test this hypothesis, we generated Mct8/Pax8 double-mutant mice, which in addition to Mct8 lack a functional thyroid gland and are therefore completely athyroid. Following the injection of these animals with either T4 or T3, serum analysis revealed T3 concentrations similar to those observed in Pax8 ko mice under thyroid hormone replacement, indicating that indeed increased thyroidal T3 secretion in Mct8 ko mice represents an important pathogenic mechanism leading to the high serum T3 levels.

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Neuropeptide Y in the Thyroid Gland: Neuronal Localization and Enhancement of Stimulated Thyroid Hormone Secretion*

Endocrinology ◽

10.1210/endo-115-4-1537 ◽

1984 ◽

Vol 115 (4) ◽

pp. 1537-1542 ◽

Cited By ~ 69

Author(s):

T. GRUNDITZ ◽

R. HÅKANSON, ◽

C. RERUP ◽

F. SUNDLER ◽

R. UDDMAN

Keyword(s):

Thyroid Hormone ◽

Thyroid Gland ◽

Neuropeptide Y ◽

Hormone Secretion

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THE EFFECT OF PREDNISONE ON THE THYROID FUNCTION WITH SPECIAL REFERENCE TO THE IN VITRO UPTAKE BY ERYTHROCYTES OF L-TRIIODOTHYRONINE LABELED WITH 131I

Acta Endocrinologica ◽

10.1530/acta.0.0420001 ◽

1963 ◽

Vol 42 (1) ◽

pp. 1-11 ◽

Cited By ~ 8

Author(s):

Thorkild Friis ◽

Vagn Reinicke

Keyword(s):

Thyroid Hormone ◽

Thyroid Gland ◽

Thyroid Function ◽

Serum Proteins ◽

Binding Capacity ◽

Hormone Secretion ◽

Steroid Treatment ◽

Secretion Rate ◽

In Vitro Uptake

ABSTRACT In order to study the effect of steroids on the function of the thyroid gland, the uptake by erythrocytes of l-triiodothyronine labeled with 131I was investigated in 29 euthyroid patients treated with prednisone. At the same time the thyroid function was studied by determinations of the serum PBI, the thyroid 131I-uptake and the thyroid hormone secretion rate. In addition some studies of the renal 131I-clearance were performed. Prednisone was found to increase the erythrocyte uptake of the thyroid hormone triiodothyronine in two-thirds of the patients investigated probably as a result of decreased binding capacity of the serum proteins. Simultaneously, the function of the thyroid gland was found to decrease, according to the thyroid 131I-uptake and the thyroid hormone secretion rate. A slightly increased renal 131I-clearance was found during the steroid treatment. This increase cannot completely explain the decreased thyroid 131I-uptake The relation between the decreased function of the thyroid gland and the increased uptake of triiodothyronine in erythrocytes during steroid treatment is discussed.

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Thyroid function as measured by 131iodine release rate, weight and RNA/DNA in growing lambs, and its relation to growth rate

Animal Science ◽

10.1017/s0003356100027045 ◽

1969 ◽

Vol 11 (3) ◽

pp. 399-407 ◽

Cited By ~ 6

Author(s):

S. A. Draper ◽

N. B. Haynes ◽

I. R. Falconer ◽

G. E. Lamming

Keyword(s):

Growth Rate ◽

Thyroid Hormone ◽

Thyroid Gland ◽

Thyroid Function ◽

Rate Constant ◽

Release Rate ◽

Hormone Secretion ◽

Thyroid Status ◽

Thyroid Activity ◽

Ad Libitum

SUMMARYThyroid activity was assessed in two groups of crossbred lambs and in Dorset Horn lambs fed ad libitum, by measuring the rate constant (K4) for the release of 131iodine from the gland. The results demonstrated a highly significant curvilinear correlation (P<0·001) between growth rate and the rate constant (K4) in experiments based on individual measurements in animals from three populations.Separate work carried out on the measurements of both thyroid size and RNA/DNA ratio suggests a need for caution when these are interpreted as parameters of thyroid activity. In the growing animal these may be more reflective of the growth of the thyroid gland itself, differences which may be governed by factors not directly related to variations in hormone secretion rate.The findings are discussed in terms of an explanation of the contradictory results obtained where attempts have been made to alter the thyroid status of growing animals by the use of thyroid hormone analogues and thyroid depressant drugs.

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CHARACTERIZATION OF T3 IMMUNOREACTIVITY RELEASE FROM THYROID GLAND IN VITRO: A REFLECTION OF COLLOID DROPLET FORMATION

Acta Endocrinologica ◽

10.1530/acta.0.0860119 ◽

1977 ◽

Vol 86 (1) ◽

pp. 119-127 ◽

Cited By ~ 1

Author(s):

Sadhana Chatterjee ◽

Masaru Takaishi ◽

Taeko Shimizu ◽

Yoshimasa Shishiba

Keyword(s):

Thyroid Hormone ◽

Thyroid Gland ◽

Hormone Secretion ◽

Droplet Formation ◽

Considerable Extent ◽

Sephadex Column ◽

Hormone Synthesis ◽

Thyroid Glands

ABSTRACT T3 immunoreactivity release from the thyroid gland in vitro was shown to be increased by TSH. In the present study, we sought to determine whether the T3 immunoreactivity release is an indicator of thyroid hormone secretion or due to hormone synthesis. When thyroid glands from mice were incubated with TSH, T3 immunoreactivity release was increased in parallel with intracellular colloid droplet formation in a dose related manner. When colchicine, a known inhibitor of colloid droplet formation, was added, both T3 immunoreactivity release and colloid droplet formation were inhibited, whereas MMI, an inhibitor of hormone synthesis, failed to influence both aspects. Thus, T3 immunoreactivity release as a reflection of colloid droplet formation was demonstrated. The analysis of the released immunoreactivity by Sephadex column and subsequent radioimmunoassay suggested that the T3 immunoreactivity was, to a considerable extent, due to macromolecule instead of T3 itself. The effect of I− or Li+ to inhibit thyroid hormone secretion was shown to be on the step prior to, but not subsequent to, colloid droplet formation.

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