scholarly journals Disruption of the Melanin-Concentrating Hormone Receptor 1 (MCH1R) Affects Thyroid Function

Endocrinology ◽  
2012 ◽  
Vol 153 (12) ◽  
pp. 6145-6154 ◽  
Author(s):  
Shinjae Chung ◽  
Xiao-Hui Liao ◽  
Caterina Di Cosmo ◽  
Jacqueline Van Sande ◽  
Zhiwei Wang ◽  
...  
Keyword(s):  
Thyroid Function ◽  
Hormone Secretion ◽  
Zona Incerta ◽  
Wild Type ◽  
Free T4 ◽  
Thyroid Follicular Cells ◽  
Pituitary Thyroid Axis ◽  
Melanin Concentrating Hormone ◽  
Thyroid Axis ◽  
Follicle Size

Abstract Melanin-concentrating hormone (MCH) is a peptide produced in the hypothalamus and the zona incerta that acts on one receptor, MCH receptor 1 (MCH1R), in rodents. The MCH system has been implicated in the regulation of several centrally directed physiological responses, including the hypothalamus-pituitary-thyroid axis. Yet a possible direct effect of the MCH system on thyroid function has not been explored in detail. We now show that MCH1R mRNA is expressed in thyroid follicular cells and that mice lacking MCH1R [MCH1R-knockout (KO)] exhibit reduced circulating iodothyronine (T4, free T4, T3, and rT3) levels and high TRH and TSH when compared with wild-type (WT) mice. Because the TSH of MCH1R-KO mice displays a normal bioactivity, we hypothesize that their hypothyroidism may be caused by defective thyroid function. Yet expression levels of the genes important for thyroid hormones synthesis or secretion are not different between the MCH1R-KO and WT mice. However, the average thyroid follicle size of the MCH1R-KO mice is larger than that of WT mice and contained more free and total T4 and T3 than the WT glands, suggesting that they are sequestered in the glands. Indeed, when challenged with TSH, the thyroids of MCH1R-KO mice secrete lower amounts of T4. Similarly, secretion of iodothyronines in the plasma upon 125I administration is significantly reduced in MCH1R-KO mice. Therefore, the absence of MCH1R affects thyroid function by disrupting thyroid hormone secretion. To our knowledge, this study is the first to link the activity of the MCH system to the thyroid function.

scholarly journals Chronothyroidology: Chronobiological Aspects in Thyroid Function and Diseases

Life ◽  
2021 ◽  
Vol 11 (5) ◽  
pp. 426
Author(s):  
Giuseppe Bellastella ◽  
Maria Ida Maiorino ◽  
Lorenzo Scappaticcio ◽  
Annamaria De Bellis ◽  
Silvia Mercadante ◽  
...  
Keyword(s):  
Thyroid Function ◽  
Biological Rhythms ◽  
Cellular Level ◽  
Scientific Discipline ◽  
Biological Phenomena ◽  
Pituitary Thyroid Axis ◽  
Circadian Organization ◽  
Thyroid Axis ◽  
Central Clock ◽  
Thyroid Dysfunctions

Chronobiology is the scientific discipline which considers biological phenomena in relation to time, which assumes itself biological identity. Many physiological processes are cyclically regulated by intrinsic clocks and many pathological events show a circadian time-related occurrence. Even the pituitary–thyroid axis is under the control of a central clock, and the hormones of the pituitary–thyroid axis exhibit circadian, ultradian and circannual rhythmicity. This review, after describing briefly the essential principles of chronobiology, will be focused on the results of personal experiences and of other studies on this issue, paying particular attention to those regarding the thyroid implications, appearing in the literature as reviews, metanalyses, original and observational studies until 28 February 2021 and acquired from two databases (Scopus and PubMed). The first input to biological rhythms is given by a central clock located in the suprachiasmatic nucleus (SCN), which dictates the timing from its hypothalamic site to satellite clocks that contribute in a hierarchical way to regulate the physiological rhythmicity. Disruption of the rhythmic organization can favor the onset of important disorders, including thyroid diseases. Several studies on the interrelationship between thyroid function and circadian rhythmicity demonstrated that thyroid dysfunctions may affect negatively circadian organization, disrupting TSH rhythm. Conversely, alterations of clock machinery may cause important perturbations at the cellular level, which may favor thyroid dysfunctions and also cancer.

scholarly journals The Hypothalamic-Pituitary-Thyroid Axis in Preterm Infants; Changes in the First 24 Hours of Postnatal Life

2004 ◽  
Vol 89 (6) ◽  
pp. 2824-2831 ◽  
Author(s):  
Nuala Murphy ◽  
Robert Hume ◽  
Hans van Toor ◽  
Tom G. Matthews ◽  
Simon A. Ogston ◽  
...  
Keyword(s):  
Preterm Infants ◽  
Age Groups ◽  
Postnatal Life ◽  
Free T4 ◽  
Thyroxine Binding Globulin ◽  
Time Points ◽  
Pituitary Thyroid Axis ◽  
Serum T4 ◽  
Thyroid Axis ◽  
Immature Group

Abstract The purpose of this study was to measure serum T4, free T4, TSH, T3, rT3, T4 sulfate, and thyroxine binding globulin at four time points within the first 24 h of life (cord and 1, 7, and 24 h) in infants between 24 and 34 wk gestation. The infants were subdivided into gestational age groups: 24–27 wk (n = 22); 28–30 wk (n = 26); and 31–34 wk (n = 24). The TSH surge in the first hour of postnatal life was markedly attenuated in infants of 24–27 wk gestation [8 compared with 20 (28–30 wk) and 23 mU/liter (31–34 wk)]. T4 levels in the most immature group declined over the first 24 h, whereas levels increased in the more mature groups [mean cord and 24-h levels: 65 and 59 (NS) vs. 70 and 84 (P < 0.002) vs. 98 and 125 (NS) nmol/liter]. Free T4 and T3 showed only small, transient increases in the most immature group and progressively larger and sustained increases in the other gestational groups. rT3 and T4 sulfate levels in cord serum were higher in the most immature infants, and in all groups levels decreased initially and then variably increased. The features of a severely attenuated or failed hypothalamic-pituitary-thyroid response to delivery critically define this 24- to 27-wk group as distinct from more mature preterm infants.

scholarly journals The Hypothalamic-Pituitary-Thyroid Axis in Cushing Syndrome before and after Curative Surgery

2020 ◽  
Author(s):  
Skand Shekhar ◽  
Raven McGlotten ◽  
Sunyoung Auh ◽  
Kristina I Rother ◽  
Lynnette K Nieman
Keyword(s):  
Thyroid Function ◽  
Cushing’S Syndrome ◽  
Cushing Syndrome ◽  
Cushing's Syndrome ◽  
Curative Surgery ◽  
Central Hypothyroidism ◽  
Duration Of Symptoms ◽  
Before And After ◽  
Pituitary Thyroid Axis ◽  
Thyroid Axis

Abstract Background We do not fully understand how hypercortisolism causes central hypothyroidism or what factors influence recovery of the hypothalamic-pituitary-thyroid axis. We evaluated thyroid function during and after cure of Cushing’s syndrome (CS). Methods We performed a retrospective cohort study of adult patients with CS seen from 2005 – 2018 (cohort 1, c1, n=68) or 1985 – 1994 (cohort 2, c2, n=55) at a clinical research center. Urine (UFC) and diurnal serum cortisol (F: ~8AM and ~midnight (PM)), morning triiodothyronine (T3), free thyroxine (FT4) and thyroid stimulating hormone (TSH) (c1) or hourly TSH from 1500-1900h (day) and 2400-04000h (night) (c2), were measured before and after curative surgery. Results While hypercortisolemic, 53% of c1 had central hypothyroidism (low/low normal fT4 + unelevated TSH). Of those followed long-term, 31% and 44% had initially subnormal FT4 and T3, respectively, which normalized 6—12 months after cure. Hypogonadism was more frequent in hypothyroid (69%) compared to euthyroid (13%) patients. Duration of symptoms, AM and PM F, ACTH, and UFC were inversely related to TSH, FT4 and/or T3 levels (r -0.24 to -0.52, P <0.0001 to 0.02). In c2, the nocturnal surge of TSH (mIU/L) was subnormal before (day 1.00±0.04 vs night 1.08±0.05, p=0.3) and normal at a mean of 8 months after cure (day 1.30±0.14 vs night 2.17±0.27, p=0.01). UFC >1000 μg /day was an independent adverse prognostic marker of time to thyroid hormone recovery. Conclusions Abnormal thyroid function, likely mediated by subnormal nocturnal TSH, is prevalent in Cushing’s syndrome and is reversible after cure.

THE EFFECT OF STREPTOZOTOCIN-INDUCED DIABETES ON THE PITUITARY-THYROID AXIS IN GOITROGEN-TREATED RATS

1977 ◽  
Vol 86 (1) ◽  
pp. 128-139 ◽  
Author(s):  
Isabel Pericás ◽  
Trinidad Jolín
Keyword(s):  
Body Weight ◽  
Thyroid Function ◽  
Growth Response ◽  
Thyroid Tissue ◽  
Diabetic Rats ◽  
Poor Growth ◽  
Pituitary Thyroid Axis ◽  
Tsh Secretion ◽  
Thyroid Axis ◽  
Intact Rats

ABSTRACT Studies of pituitary and thyroid function have been carried out in normal (intact) and diabetic Wistar rats. Diabetes was induced by a single streptozotocin injection (7 mg/100 g body weight). The animals were fed a low iodine diet (LID), and received a daily sc injection of either KClO4 (20 mg/100 g body weight) or propylthiouracil (PTU) (1.5 mg/100 g body weight) to induce hypothyroidism. Control groups received the same LID but supplemented with 0.8 μg I/g dry weight. In intact rats goitrogen-treatment induces an increase in thyroid weight and in plasma TSH concentration. However, the plasma TSH response to goitrogen-treatment in diabetics indicates that pituitary TSH secretion increases following a reduction in plasma PBI, but the response is less marked than in controls. The difference in plasma TSH between control and diabetic rats provides an explanation for the findings that diabetes diminishes the thyroid growth response to goitrogen-treatment. Moreover, in intact rats the low pituitary TSH content is a consequence of the increase in pituitary TSH secretion, while in the diabetics the low pituitary TSH content cannot be explained by an increase in TSH secretion. The effect of diabetes on the pituitary-thyroid axis cannot be attributed specifically to poor growth, because the changes in pituitary-thyroid function which are observed in the diabetic groups are not seen in intact rats with a growth rate similar to that of insulin deficient rats. Insulin administration to goitrogen-treated diabetic rats results in 1) an increase in the ability of the thyroid tissue to respond to its trophic hormone, 2) an increase in pituitary TSH secretion in response to the lowering of plasma PBI and, 3) an increase in thyroid growth response to goitrogen-treatment. Results are discussed in relation to the assumption that the lack of adequate insulin levels, or its metabolic defects, diminishes the full response of the thyroid to TSH, and affects the pituitary TSH secretion probably as a consequence of altered hypothalamic control of the pituitary function.

Systemic effects of 1,25-dihydroxyvitamin D3 on the pituitary-hypothalamic axis in rats

1987 ◽  
Vol 115 (2) ◽  
pp. 225-228 ◽  
Author(s):  
K. Törnquist ◽  
C. Lamberg-Allardt
Keyword(s):  
Hormone Secretion ◽  
Dihydroxyvitamin D3 ◽  
Hydroxyvitamin D ◽  
Dihydroxyvitamin D ◽  
1,25 Dihydroxyvitamin D ◽  
Pituitary Thyroid Axis ◽  
Thyroid Axis ◽  
25 Hydroxyvitamin D ◽  
Wet Weight ◽  
Indirect Action

Abstract. Treatment of rats with 1,25-dihydroxyvitamin D3 (1,25(OH)2D3) 0.05 μg/kg per day for three days was without any effect on serum T3, T4 or TSH concentrations, whereas serum PRL increased (20.6 ± 3.8 to 76.2 ± 19.1 μg/l, mean ± sem, N = 7–8; P < 0.01). Increased hypothalamic TRH levels (24.3 ± 3.9 to 45.7 ± 7.8 pmol/g wet weight; P < 0.01) may indicate an effect of 1,25(OH)2D3 on hypothalamic TRH homeostasis. This effect could probably be due to an indirect action of 1,25(OH)2D3, mediated by the increased serum calcium (2.77 ± 0.02 to 3.16 ± 0.08 mmol/l, mean ± sem, N = 7–8; P < 0.001). This assumption was, however, not tested. Neither the pituitary TSH nor PRL was affected. The treatment decreased the serum concentration of 25-hydroxyvitamin D3 (23.0 ± 1.3 to 16.8 ± 2.0 nmol/l, mean ± sem, N = 5–7; P < 0.01) and of 24,25-dihydroxyvitamin D3 (3.2 ± 0.3 to 2.1 ± 0.1 nmol/l, mean ± sem, N = 3–5; P < 0.05). The results show that in this experimental design, 1,25(OH)2D3 has no effect on basal hormone secretion from the pituitary-thyroid axis, and that 1,25(OH)2D3 decreases the synthesis of the vitamin D3 metabolites studied.

scholarly journals SAT-449 Factors Associated with Reduced Thyroid Hormones in Cushing Syndrome Patients Before and After Surgical Cure

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Skand Shekhar ◽  
Raven McGlotten ◽  
Lynnette K Nieman
Keyword(s):  
Thyroid Hormones ◽  
Thyroid Function ◽  
Cushing Syndrome ◽  
Hormone Secretion ◽  
Free T4 ◽  
Curative Surgery ◽  
Duration Of Symptoms ◽  
Free Cortisol ◽  
Hpt Axis ◽  
Pearson Correlations

Abstract Background: Hypercortisolemia adversely affects thyroid hormone secretion. We previously described the temporal pattern of thyroid function recovery in 23 patients (1). However, the factors leading to suppression and recovery of the hypothalamic-pituitary-thyroid (HPT) axis in Cushing’s syndrome (CS) are not fully understood. We performed two separate studies to investigate these factors. Methods: In study 1, we examined patients (pts, n=62) with CS who underwent curative surgery and recorded their serum morning and evening cortisol, ACTH, tumor volume and duration of symptoms and 24-hour urine free cortisol (UFC) at baseline and the morning serum free T4, TSH and T3 at six-month intervals after cure. Data were log-transformed and Pearson correlations were performed. Linear mixed models were used to study factors that predict recovery of thyroid function. In study 2, we examined the diurnal variation of TSH by performing hourly TSH measurement between 3—7 PM and 12—4 AM on a cohort of pts (n=45) before surgery. Wilcoxon Signed-Rank method was used for comparisons of mean TSH across time and Pearson correlations were performed on log-transformed data. P values &lt;.05 were considered significant. Results: Study 1: In this larger cohort, we confirmed previous findings of suppressed or low normal fT4 and TSH values with active hypercortisolism, with normalization after cure that reflected changes in the T3:TSH, fT4:TSH and T3:fT4 ratios. There were inverse linear correlations between log10 UFC, serum AM and PM cortisol; and log10 TT3, fT4 and TSH before surgery. Independent negative prognosticators of circulating fT4 recovery included UFC greater than 1000mcg/day (nl: 3.5—45mcg/day), duration of symptoms of less than one year, and ACTH levels greater than 60pg/mL(nl: 5—45pg/mL) Study 2: The nocturnal (12 - 4AM) TSH surge was reduced, so that the difference in day and night TSH values was not statistically significant; this contrasts with the 30—50% nocturnal TSH increase above daytime values seen in healthy subjects. There was an inverse relationship between UFC and nocturnal TSH, daytime TSH and TBG values, but there was no direct relationship between UFC and percent changes in nocturnal TSH values. Conclusions: Our findings suggest that a deficit in TSH stimulation of the thyroid gland may explain the reduction in T3 and T4 levels. There is a dose-response relationship between various measures of hypercortisolemia and both thyroid hormones and the pattern of TSH secretion. Finally, the severity of hypercortisolism correlates with a longer time to recovery of the HPT axis in pts with CS after curative surgery. 1. Shekhar S et al. HPG and HPT Axes in Cushing Syndrome. J Endocr Soc, 3 S1, April May 2019

Somatostatin immunoneutralization stimulates thyroid function in fowl

1986 ◽  
Vol 110 (1) ◽  
pp. 127-132 ◽  
Author(s):  
S.-K. Lam ◽  
S. Harvey ◽  
T. R. Hall ◽  
G. S. G. Spencer
Keyword(s):  
Thyroid Gland ◽  
Thyroid Function ◽  
Inhibitory Control ◽  
Domestic Fowl ◽  
Pituitary Thyroid Axis ◽  
Thyroid Axis

ABSTRACT The influence of somatostatin on thyroid function has been examined in immature domestic fowl passively immunized with somatostatin antiserum. Plasma thyroxine (T4) and tri-iodothyronine (T3) concentrations were markedly increased within 10 min of antisomatostatin administration and remained raised for at least 5 h. The increases in the T3 and T4 concentrations following somatostatin immunoneutralization were directly related to the volume of antisera administered. The increase in the T3 concentration exceeded the increase in the T4 concentration, resulting in a T3: T4 ratio greater than unity. While the raised T4 concentration began to decline 30 min after antisomatostatin administration, raised T3 concentrations were sustained for at least 2 h, and further increased the plasma T3: T4 ratio. These results demonstrate that somatostatin immunoneutralization stimulates thyroid function in fowl. The magnitude and rapidity of the thyroidal responses to somatostatin immunoneutralization suggests that they occur independently of the hypothalamic-pituitary-thyroid axis. Somatostatin appears to exert a tonic inhibitory control on avian thyroid function, possibly by effects mediated at the thyroid gland to inhibit T4 release and by peripheral effects to suppress the conversion of T4 and T3. J. Endocr. (1986) 110, 127–132

Interleukin 6 effects on the pituitary–thyroid axis in the rat

1994 ◽  
Vol 131 (3) ◽  
pp. 302-306 ◽  
Author(s):  
Luigi Bartalena ◽  
Lucia Grasso ◽  
Sandra Brogioni ◽  
Enio Martino
Keyword(s):  
Thyroid Hormone ◽  
Interleukin 6 ◽  
Saline Solution ◽  
Hormone Secretion ◽  
Neutralizing Antibody ◽  
Control Group ◽  
Apparent Lack ◽  
Tnf Α ◽  
Pituitary Thyroid Axis ◽  
Thyroid Axis

Bartalena L, Grasso L, Brogioni S, Martino E. Interleukin 6 effects on the pituitary–thyroid axis in the rat. Eur J Endocrinol 1994;131:302–6. ISSN 0804–4643 It has been postulated recently that cytokines, and in particular interleukin 1 (IL-1) and tumor necrosis factor-α TNF-α), may have a role in the pathogenesis of the changes of serum thyroid hormone concentrations that are encountered in patients with non-thyroidal illness (NTI). Many of the IL-1 and TNF-α effects are believed to be mediated by the induction of IL-6 synthesis, which might, therefore, represent an important mediator of thyroid hormone changes in NTI. To address this problem, male Wistar rats were injected subcutaneously with 2.5 μg of recombinant human IL-6 (rhIL-6, in 500 μl of saline solution), with 2.5 μg of rhIL-6 preincubated with 100 μl of anti-IL-6 neutralizing antibody or with saline solution alone (control group). Administration of rhIL-6 resulted in a significant decrease of thyroxine (T4) from 82 ± 4 nmol/l (mean± sem) to a nadir of 33 ± 3 nmol/l (p < 0.0001) after 48 h, and of triiodothyronine (T3) from 1.6 ± 0.1 to 0.8 ± 0.1 nmol/l after 48 h (p < 0.0001). A slight decrease in serum T4 and T3 concentrations also was observed in the control group, but the lowest values (T4, 66 ± 3 nmol/l; T3, 1.2 ± 0.1 nmol/l) were significantly higher (p < 0.0001) than in IL-6-treated rats. The IL-6-induced changes could be prevented by preincubation of rhIL-6 with its neutralizing antibody. Slight but not significant changes occurred in serum reverse T3 (rT3) concentration, so that the T4/rT3 ratio remained substantially unchanged after rhIL-6 injection, whereas the T4/T3 ratio decreased significantly from 53.6 to 39.9 (p < 0.02) in IL-6-treated rats. The effects of IL-6 on thyrotropin (TSH) were investigated after rendering the rats hypothyroid by methimazole administration for 3 weeks. Serum TSH decreased from 19.0 ± 6.8 to 13.3 ± 3.8 μg/l after 48 h (p < 0.01) in IL-6-treated rats, while it increased from 17.2 ± 2.8 to 25.8 ± 4.0 μg/l (p < 0.01) in the control group. These results show that a single injection of rhIL-6 causes a decrease in serum T4, T3 and TSH concentrations in the rat, without affecting serum rT3 levels. This is compatible with a predominantly central effect of the cytokine. The apparent lack of inhibition of 5′-deiodinating activity, a key feature of NTI, suggests that IL-6, if involved, is only one of the factors responsible for the changes of thyroid hormone secretion and metabolism observed in NTI. Luigi Bartalena, Istituto di Endocrinologia, University of Pisa, Viale del Tirreno 64, 56018 Tirrenia-Pisa, Italy

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