The hypothalamic paraventricular nucleus is the center of the hypothalamo-pituitary-thyroid axis for regulating thyroid hormone levels

Thyroid ◽  
2021 ◽  
Author(s):  
Yuri Kondo ◽  
Atsushi Ozawa ◽  
Daisuke Kohno ◽  
Kazuma Saito ◽  
Battsetseg Buyandalai ◽  
...  
Keyword(s):  
Thyroid Hormone ◽  
Paraventricular Nucleus ◽  
Hypothalamic Paraventricular Nucleus ◽  
Hormone Levels ◽  
Pituitary Thyroid Axis ◽  
Thyroid Axis ◽  
Thyroid Hormone Levels

scholarly journals Neuropeptide Y1 and Y5 Receptors Mediate the Effects of Neuropeptide Y on the Hypothalamic-Pituitary-Thyroid Axis

Endocrinology ◽  
2002 ◽  
Vol 143 (12) ◽  
pp. 4513-4519 ◽  
Author(s):  
Csaba Fekete ◽  
Sumit Sarkar ◽  
William M. Rand ◽  
John W. Harney ◽  
Charles H. Emerson ◽  
...  
Keyword(s):  
Thyroid Hormone ◽  
Food Intake ◽  
Neuropeptide Y ◽  
Paraventricular Nucleus ◽  
Receptor Agonist ◽  
Pituitary Thyroid Axis ◽  
Thyroid Axis ◽  
Ad Libitum ◽  
Thyroid Hormone Levels ◽  
Hpt Axis

Abstract Neuropeptide Y (NPY) is one of the most important hypothalamic-derived neuropeptides mediating the effects of leptin on energy homeostasis. Central administration of NPY not only markedly stimulates food intake, but simultaneously inhibits the hypothalamic-pituitary-thyroid axis (HPT axis), replicating the central hypothyroid state associated with fasting. To identify the specific NPY receptor subtypes involved in the action of NPY on the HPT axis, we studied the effects of the highly selective Y1 ([Phe7,Pro34]pNPY) and Y5 ([chicken pancreatic polypeptide1–7, NPY19–23, Ala31, Aib32 (aminoisobutyric acid), Q34]human pancreatic polypeptide) receptor agonists on circulating thyroid hormone levels and proTRH mRNA in hypophysiotropic neurons of the hypothalamic paraventricular nucleus. The peptides were administered continuously by osmotic minipump into the cerebrospinal fluid (CSF) over 3 d in ad libitum-fed animals and animals pair-fed to artificial CSF (aCSF)-infused controls. Both Y1 and Y5 receptor agonists nearly doubled food intake compared with that of control animals receiving aCSF, similar to the effect observed for NPY. NPY, Y1, and Y5 receptor agonist administration suppressed circulating levels of thyroid hormones (T3 and T4) and resulted in inappropriately normal or low TSH levels. These alterations were also associated with significant suppression of proTRH mRNA in the paraventricular nucleus, particularly in the Y1 receptor agonist-infused group [aCSF, NPY, Y1, and Y5 (density units ± sem), 97.2 ± 8.6, 39.6 ± 8.4, 19.9 ± 1.9, and 44.6 ± 8.4]. No significant differences in thyroid hormone levels, TSH, or proTRH mRNA were observed between the agonist-infused FSanimals eating ad libitum and the agonist-infused animals pair-fed with vehicle-treated controls. These data confirm the importance of both Y1 and Y5 receptors in the NPY-mediated increase in food consumption and demonstrate that both Y1 and Y5 receptors can mediate the inhibitory effects of NPY on the HPT axis.

The effect of benziodarone on the thyroid hormone levels and the pituitary-thyroid axis

1986 ◽  
Vol 9 (4) ◽  
pp. 337-339 ◽  
Author(s):  
B. Xanthopoulos ◽  
D. A. Koutras ◽  
M. A. Boukis ◽  
G. D. Piperingos ◽  
J. Kitsopanides ◽  
...  
Keyword(s):  
Thyroid Hormone ◽  
Hormone Levels ◽  
Pituitary Thyroid Axis ◽  
Thyroid Axis ◽  
Thyroid Hormone Levels

scholarly journals Differential Effects of Central Leptin, Insulin, or Glucose Administration during Fasting on the Hypothalamic-Pituitary-Thyroid Axis and Feeding-Related Neurons in the Arcuate Nucleus

Endocrinology ◽  
2006 ◽  
Vol 147 (1) ◽  
pp. 520-529 ◽  
Author(s):  
Csaba Fekete ◽  
Praful S. Singru ◽  
Edith Sanchez ◽  
Sumit Sarkar ◽  
Marcelo A. Christoffolete ◽  
...  
Keyword(s):  
Thyroid Hormone ◽  
Arcuate Nucleus ◽  
Mrna Levels ◽  
Central Administration ◽  
Hormone Levels ◽  
Intracerebroventricular Infusion ◽  
Essential Components ◽  
Pituitary Thyroid Axis ◽  
Thyroid Axis ◽  
Thyroid Hormone Levels

The reductions in circulating levels of leptin, insulin, and glucose with fasting serve as important homeostasis signals to neurons of the hypothalamic arcuate nucleus that synthesize neuropeptide Y (NPY)/agouti-related protein (AGRP) and α-MSH/cocaine and amphetamine-regulated transcript. Because the central administration of leptin is capable of preventing the inhibitory effects of fasting on TRH mRNA in hypophysiotropic neurons primarily through effects on the arcuate nucleus, we determined whether the continuous administration of 30 mU/d insulin or 648 μg/d glucose into the cerebrospinal fluid by osmotic minipump might also have similar effects on the hypothalamic-pituitary-thyroid axis. As anticipated, the intracerebroventricular infusion of leptin reduced fasting-induced elevations in NPY and AGRP mRNA and increased proopiomelanocortin and cocaine and amphetamine-regulated transcript mRNA in the arcuate nucleus. In addition, leptin prevented fasting-induced reduction in pro-TRH mRNA levels in the paraventricular nucleus and in circulating thyroid hormone levels. In contrast, whereas insulin increased proopiomelanocortin mRNA and both insulin and glucose reduced NPY mRNA in arcuate nucleus neurons, neither prevented the fasting-induced suppression in hypophysiotropic TRH mRNA or circulating thyroid hormone levels. We conclude that insulin and glucose only partially replicate the central effects of leptin and may not be essential components of the hypothalamic-pituitary-thyroid regulatory system during fasting.

N-acetyltransferase activity in the Harderian glands of the Syrian hamster, Mesocricetus auratus, is regulated by androgens and by hormones of the pituitary-thyroid axis

1990 ◽  
Vol 127 (1) ◽  
pp. 59-67 ◽  
Author(s):  
G. R. Buzzell ◽  
A. Menendez-Pelaez ◽  
R. A. Hoffman ◽  
M. K. Vaughan ◽  
R. J. Reiter
Keyword(s):  
Thyroid Hormone ◽  
Thyroid Hormones ◽  
Harderian Gland ◽  
Hormone Levels ◽  
Harderian Glands ◽  
Pituitary Thyroid Axis ◽  
Thyroid Axis ◽  
Serum Thyroid Hormone ◽  
Thyroid Hormone Levels ◽  
Tsh Levels

ABSTRACT This study tested the hypothesis that activity of the enzyme N-acetyltransferase (NAT) in the Harderian gland of the Syrian hamster is regulated both by androgens and by hormones of the pituitary-thyroid axis. To test the effects of castration and hypothyroidism, intact or castrated male hamsters were given either tap water or methimazole in their drinking water for 3 weeks. Methimazole suppresses iodination of thyroglobulin, thereby decreasing circulating levels of thyroid hormones and increasing TSH levels. Hypothyroidism or castration caused elevated or depressed Harderian gland NAT activities respectively, compared with euthyroid controls. When castration and hypothyroidism were combined, the animals exhibited high NAT activity compared with castrated euthyroid males. To test the effects of castration and hyperthyroidism, male hamsters were given daily injections of thyroxine (T4) or diluent and were either castrated or left intact for 4 weeks. Intact animals given T4 had depressed Harderian NAT activity; serum thyroid hormone levels were elevated and TSH levels were depressed compared with those of intact controls. Castrated animals had depressed NAT activity below that of intact controls; serum thyroid hormone levels were normal but TSH levels were depressed. Castrated animals given T4 injections had NAT activity similar to that of euthyroid castrated hamsters; thyroid hormone levels were elevated but TSH levels were similar to those seen in euthyroid castrated hamsters. In another experiment, both T4 and tri-iodothyronine (T3) were equally effective in decreasing NAT activity in intact males. To determine the effects of the removal of pituitary influences, male hamsters were hypophysectomized. NAT activity in the Harderian glands of these animals was reduced compared with intact controls. Injection of T4 in hypophysectomized male hamsters did not alter NAT activity from that of hypophysectomized hamsters. Female hamsters given methimazole for 3 weeks had elevated Harderian NAT activity compared with controls. Injection of T4 or T3 for 4 weeks led to significantly reduced Harderian gland NAT activity compared with untreated controls. This response to thyroid hormones was the same, whether T4 or T3 was used. These results can be explained by androgens stimulating Harderian NAT activity, as has been suggested by previous published reports, and by NAT activity being inhibited by thyroid hormones or stimulated by TSH. Journal of Endocrinology (1990) 127, 59–67

EFFECTS OF TRIMETHOPRIM AND SULPHONAMIDE PREPARATIONS ON THE PITUITARY–THYROID AXIS OF RODENTS

1981 ◽  
Vol 91 (2) ◽  
pp. 299-303 ◽  
Author(s):  
H. N. COHEN ◽  
J. A. FYFFE ◽  
W. A. RATCLIFFE ◽  
A. M. McNICOL ◽  
H. McINTYRE ◽  
...  
Keyword(s):  
Thyroid Hormone ◽  
Thyroid Stimulating Hormone ◽  
Histological Evidence ◽  
Hormone Levels ◽  
Gland Weight ◽  
Pituitary Thyroid Axis ◽  
Thyroid Axis ◽  
Thyroid Hormone Levels ◽  
Bacterial Preparations ◽  
Thyroid Gland Weight

The effects on pituitary–thyroid function of the commonly prescribed anti-bacterial preparations co-trimoxazole and co-trifamole, and their component drugs, have been studied in the rat and compared to the changes caused by propylthiouracil. Co-trimoxazole and co-trifamole, in doses 20-fold in excess of a pharmacological dose administered for 10 days, produced marked changes in hormone levels consistent with blocking of thyroidal activity. Significant increases in thyroid gland weight, with histological evidence of hyperplastic goitre formation, were also demonstrated. Propylthiouracil produced less marked changes of thyroid hormone levels but higher levels of thyroid-stimulating hormone. Pharmacological doses of co-trimoxazole and co-trifamole and sulphamoxole, the sulphonamide component of co-trifamole, caused significant changes in thyroid hormone levels consistent with anti-thyroidal activity. In contrast, there was no evidence that trimethoprim, which is common to both preparations, or sulphamethoxazole, the sulphonamide component of co-trimoxazole, had an anti-thyroidal action, indeed, serum thyroxine levels were significantly increased at pharmacological dosage. We have concluded that the new commonly prescribed combination preparations retain the goitrogenic properties of the earlier sulphonamides.

scholarly journals Synthetic gene network restoring endogenous pituitary–thyroid feedback control in experimental Graves’ disease

2016 ◽  
Vol 113 (5) ◽  
pp. 1244-1249 ◽  
Author(s):  
Pratik Saxena ◽  
Ghislaine Charpin-El Hamri ◽  
Marc Folcher ◽  
Henryk Zulewski ◽  
Martin Fussenegger
Keyword(s):  
Thyroid Hormone ◽  
Feedback Control ◽  
Thyroid Stimulating Hormone ◽  
Graves Disease ◽  
Hormone Levels ◽  
Pituitary Thyroid Axis ◽  
Thyroid Axis ◽  
Thyroid Hormone Levels ◽  
Hormone Homeostasis ◽  
Stimulating Hormone

Graves’ disease is an autoimmune disorder that causes hyperthyroidism because of autoantibodies that bind to the thyroid-stimulating hormone receptor (TSHR) on the thyroid gland, triggering thyroid hormone release. The physiological control of thyroid hormone homeostasis by the feedback loops involving the hypothalamus–pituitary–thyroid axis is disrupted by these stimulating autoantibodies. To reset the endogenous thyrotrophic feedback control, we designed a synthetic mammalian gene circuit that maintains thyroid hormone homeostasis by monitoring thyroid hormone levels and coordinating the expression of a thyroid-stimulating hormone receptor antagonist (TSHAntag), which competitively inhibits the binding of thyroid-stimulating hormone or the human autoantibody to TSHR. This synthetic control device consists of a synthetic thyroid-sensing receptor (TSR), a yeast Gal4 protein/human thyroid receptor-α fusion, which reversibly triggers expression of the TSHAntag gene from TSR-dependent promoters. In hyperthyroid mice, this synthetic circuit sensed pathological thyroid hormone levels and restored the thyrotrophic feedback control of the hypothalamus–pituitary–thyroid axis to euthyroid hormone levels. Therapeutic plug and play gene circuits that restore physiological feedback control in metabolic disorders foster advanced gene- and cell-based therapies.

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