scholarly journals Regulation of thyroid and pituitary function by bacterial lipopolysaccharide

2010 ◽  
Vol 56 (2) ◽  
pp. 179-186 ◽  
Author(s):  
N.V. Yaglova ◽  
T.T. Berezov
Keyword(s):  
Thyroid Hormone ◽  
Thyroid Gland ◽  
Binding Capacity ◽  
Hormone Secretion ◽  
Thyroid Stimulating Hormone ◽  
Bacterial Lipopolysaccharide ◽  
Hormone Production ◽  
Thyroid Cells ◽  
Stimulation Of ◽  
Stimulating Hormone

Activation of toll-like receptors-4 by bacterial lipopolysaccharide downregulates pituitary and thyroid function. Besides decrease of thyroid-stimulating hormone secretion lipopolysaccharide affects secretion in follicular thyroid cells directly. The endotoxin partialy activates and inhibits different phases of follicular thyrocytes' secretion. Lipopolysaccharide enhances thyroglobulin synthesis and exocytosis into follicular lumen and supresses its resorbtion.It results in sharp drop of blood thyroxine concentration without decrease of deiodinases-mediated thiroxine to triiodothyronine conversion. Stimulation of the lipopolysaccharide-pretreated thyroid gland with thyroid-stimulating hormone increases resorbtion of thyroglobulin and thyroid hormone production. Combined stimulation of the thyroid gland increases protein bound thyroxine and triiodothyronine serum concentration unlike only TSH stimulation resulting in increase of free thyroid hormone levels. It also prooves that binding capacity of thyroid hormone serum transport proteins during nonthyroidal illness syndrome remains normal.

Thyroid-stimulating hormone activates phospholipase D in FRTL-5 thyroid cells via stimulation of protein kinase C.

Endocrinology ◽  
1995 ◽  
Vol 136 (9) ◽  
pp. 3794-3799 ◽  
Author(s):  
S Gupta ◽  
A Gomez-Muñoz ◽  
W C Matowe ◽  
D N Brindley ◽  
J Ginsberg
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Phospholipase D ◽  
Thyroid Stimulating Hormone ◽  
Thyroid Cells ◽  
Kinase C ◽  
Stimulation Of ◽  
Stimulating Hormone

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

Endocrinology ◽  
2010 ◽  
Vol 151 (10) ◽  
pp. 5053-5062 ◽  
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.

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

1963 ◽  
Vol 42 (1) ◽  
pp. 1-11 ◽  
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.

STEROID HORMONE PRODUCTION FOLLOWING ADRENAL STIMULATION IN THE RHESUS MONKEY

1968 ◽  
Vol 58 (4) ◽  
pp. 637-642
Author(s):  
M. T. Scurry ◽  
J. Bruton
Keyword(s):  
Growth Hormone ◽  
Rhesus Monkey ◽  
Steroid Hormone ◽  
Thyroid Stimulating Hormone ◽  
Adrenal Androgen ◽  
Hormone Production ◽  
Melanocyte Stimulating Hormone ◽  
Adrenal Response ◽  
Stimulation Of ◽  
Stimulating Hormone

ABSTRACT The adrenal response to the infusion of various corticotrophin (ACTH) preparations and other hormones in the orchiectomized rhesus monkey has been measured by the excretion of 17-hydroxycorticosteroids, 17-ketosteroids, and 11-deoxy-17-ketosteroids. No difference was found in the response to genuine or synthetic ACTH. A response was demonstrated with 0.8 U or more of ACTH per 24 hours. No adrenal response was observed to infusions of various gonadotrophins, growth hormone, prolactin, α-melanocyte stimulating hormone, and thyroid stimulating hormone. Angiotensin selectively stimulated aldosterone excretion. No evidence was found for any selective stimulation of adrenal androgen production.

Auto-Regulation of the Thyroid Gland Beyond Classical Pathways

2020 ◽  
Vol 128 (06/07) ◽  
pp. 437-445 ◽  
Author(s):  
Klaudia Brix ◽  
Joanna Szumska ◽  
Jonas Weber ◽  
Maria Qatato ◽  
Vaishnavi Venugopalan ◽  
...  
Keyword(s):  
Thyroid Hormone ◽  
Thyroid Gland ◽  
Hormone Receptors ◽  
Self Regulation ◽  
Thyroid Stimulating Hormone ◽  
Apical Plasma Membrane ◽  
Deficient Mice ◽  
Stimulating Hormone

AbstractThis mini-review asks how self-regulation of the thyroid gland is realized at the cellular and molecular levels by canonical and non-canonical means. Canonical pathways of thyroid regulation comprise thyroid stimulating hormone-triggered receptor signaling. As part of non-canonical regulation, we hypothesized an interplay between protease-mediated thyroglobulin processing and thyroid hormone release into the circulation by means of thyroid hormone transporters like Mct8. We proposed a sensing mechanism by different thyroid hormone transporters, present in specific subcellular locations of thyroid epithelial cells, selectively monitoring individual steps of thyroglobulin processing, and thus, the cellular thyroid hormone status. Indeed, we found that proteases and thyroid hormone transporters are functionally inter-connected, however, in a counter-intuitive manner fostering self-thyrotoxicity in particular in Mct8- and/or Mct10-deficient mice. Furthermore, the possible role of the G protein-coupled receptor Taar1 is discussed, because we detected Taar1 at cilia of the apical plasma membrane of thyrocytes in vitro and in situ. Eventually, through pheno-typing Taar1-deficient mice, we identified a co-regulatory role of Taar1 and the thyroid stimulating hormone receptors. Recently, we showed that inhibition of thyroglobulin-processing enzymes results in disappearance of cilia from the apical pole of thyrocytes, while Taar1 is re-located to the endoplasmic reticulum. This pathway features a connection between thyrotropin-stimulated secretion of proteases into the thyroid follicle lumen and substrate-mediated self-assisted control of initially peri-cellular thyroglobulin processing, before its reinternalization by endocytosis, followed by extensive endo-lysosomal liberation of thyroid hormones, which are then released from thyroid follicles by means of thyroid hormone transporters.

Effects of trifluoperazine on rat prolactin, growth hormone, thyroid stimulating hormone and adrenocorticotrophin secretion in vitro

1983 ◽  
Vol 103 (4) ◽  
pp. 492-496 ◽  
Author(s):  
Ruth C. Powell ◽  
Mark Daniels ◽  
Graham K. Innes ◽  
Michael J. Ashby ◽  
Keith Mashiter
Keyword(s):  
Growth Hormone ◽  
Primary Cultures ◽  
Hormone Secretion ◽  
Thyroid Stimulating Hormone ◽  
Pituitary Hormone ◽  
Gh Secretion ◽  
Tsh Secretion ◽  
Stimulation Of ◽  
Stimulating Hormone

Abstract. We have studied the effects of trifluoperazine, a proposed inhibitor of calmodulin directed cellular function, on adrenocorticotrophic hormone (ACTH), thyroid stimulating hormone (TSH), prolactin (Prl) and growth hormone (GH) secretion from primary cultures of rat adenohypophyseal cells. 5 × 10−6 m and 10−5 m trifluoperazine caused a significant (P < 0.005) reversible dose-related decrease in basal Prl secretion but was less effective on basal GH secretion, significant reversible inhibition (P< 0.005) occurring only with 10−5 m. Trifluoperazine did not consistently alter basal ACTH or TSH secretion but did inhibit 10−2 m theophylline stimulation of ACTH, Prl and GH secretion and 1.5 × 10−7 m TRH stimulation of TSH and Prl secretion. Paradoxically 10−5 m trifluoperazine enhanced theophylline stimulation of TSH secretion. Our results show trifluoperazine to have differential effects on Prl, GH, ACTH and TSH secretion, which are consistent with the known calcium dependence of pituitary hormone secretion and may suggest a role for calmodulin in this process.

Variable biological activity of thyroid-stimulating hormone

1994 ◽  
Vol 131 (4) ◽  
pp. 331-340 ◽  
Author(s):  
Paolo Beck-Peccoz ◽  
Luca Persani
Keyword(s):  
Biological Activity ◽  
Thyroid Hormone ◽  
Hormone Secretion ◽  
Feedback System ◽  
Normal Subjects ◽  
Thyroid Stimulating Hormone ◽  
Primary Hypothyroidism ◽  
Oligosaccharide Structure ◽  
Pathological Conditions ◽  
Stimulating Hormone

Beck-Peccoz P, Persani L. Variable biological activity of thyroid-stimulating hormone. Eur J Endocrinol 1994;131:331–40. ISSN 0804–4643 Thyroid-stimulating hormone (TSH), like the other pituitary glycoprotein hormones, is produced and secreted as a mixture of isoforms, the majority of which represent differences in oligosaccharide structure and possess different bioactivity. When samples are quantified simultaneously by immunometric assay and bioassay, the ratio between bioactivity (B) and immunoreactivity (I) may serve as an index of the overall potency of TSH. Variations of the TSH B/I ratio have been documented in both physiological and pathological conditions associated with alteration of the two most important mechanisms controlling TSH synthesis and secretion, i.e. TRH release and the thyroid hormone feedback system. Major examples of this assumption are the low TSH bioactivity found in samples from patients lacking TRH and thus bearing a hypothalamic hypothyroidism, and the enhanced bioactivity that is invariably found in TSH from patients with thyroid hormone resistance. Moreover, variations of TSH bioactivity have been recorded in normal subjects during the nocturnal TSH surge, in normal fetuses during the last trimester of pregnancy, in patients with primary hypothyroidism and in patients with TSH-secreting pituitary adenoma and non-thyroidal illness. In conclusion, the secretion of TSH molecules with altered bioactivity plays an important pathogenetic role in various thyroid disorders, while in some particular physiological conditions the bioactivity of TSH may vary in order to adjust thyroid hormone secretion to temporary needs. Paolo Beck-Peccoz, Istituto di Scienze Endocrine, Ospedale Maggiore IRCCS, Via F. Sforza 35, 1-20122 Milano, Italy

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