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Regulation of the Pituitary Gland by Dopamine
Published in Nira Ben-Jonathan, Dopamine, 2020
The regulation of TSH by thyroid hormones is fine tuned by their circulating levels. Thus, TSH synthesis and release are inhibited by high serum levels of T3 and T4 (hyperthyroidism) and are stimulated by low levels (hypothyroidism). Thyroid hormone action is mediated by thyroid hormone receptors (THR), encoded by two separate genes: Thrα and Thrβ, which generate several isoforms that are differentially expressed in a tissue-specific manner [81]. Thrα1 and Thrα2 are widely expressed. In contrast, Thrβ1 is primarily expressed in the liver, whereas expression of Thrβ2 is present mostly in the pituitary and hypothalamic TRH neurons.
Familial Inherited TSH Deficiency
Published in Geraldo Medeiros-Neto, John Bruton Stanbury, Inherited Disorders of the Thyroid System, 2019
Geraldo Medeiros-Neto, John Bruton Stanbury
Thyroid hormone is the major negative regulator of TSH-ß subunit gene expression. Dopamine and somatostatin are less important negative regulatory hormones. Thyroid hormone inhibits gene expression by binding to DNA ds-acting elements through a nuclear thyroid hormone receptor. Presumably it interacts with the transcription initiation complex.4
The laboratory and imaging approaches to thyroid disorders
Published in David S. Cooper, Jennifer A. Sipos, Medical Management of Thyroid Disease, 2018
Jacqueline Jonklaas, David S. Cooper
Patients with resistance to thyroid hormones have an inherited partial defect in tissue responsiveness to thyroid hormones. Serum concentrations of total and free thyroid hormones are both increased as compensation for partial resistance. Most kindreds that have been evaluated have been found to have a dominant negative mutation in a single allele of the thyroid hormone receptor beta gene. Although affected individuals are generally described as being clinically euthyroid, considerable variation exists in the measurable degrees of hormone resistance among specific target organs for thyroid hormone (31).
Icosabutate: targeting metabolic and inflammatory pathways for the treatment of NASH
Published in Expert Opinion on Investigational Drugs, 2022
David A Fraser, Stephen A Harrison, Detlef Schuppan
The ideal NASH therapeutic is one that is oral, once daily, safe, well tolerated with positive impact not only on histopathology, but also lipotoxic fat, glycemic control, atherogenic lipids, and weight loss. Currently, there is no single oral therapy that can achieve these laudatory goals, so combination therapy is felt to be the future of NASH management. Given the positive preclinical and clinical findings shown to date with icosabutate, it would make sense to consider combining icosabutate with another therapeutic agent that could not only accentuate the effects of icosabutate but provide additional benefits to include enhanced glycemic control, weight loss, and reduction in liver fat content. Preferably, this would be another oral medication that could ideally be dosed as a fixed dose combination regimen. Some mechanisms that could make sense to consider include the fatty acid synthase (FASN) inhibitor class [70], thyroid hormone receptor (THR)-β class, and pan-PPARs [19]. Alternatively, combining with GLP-1 receptor agonists [71] or the fibroblast growth factor (FGF)-21 agonists [72], albeit injectables, would potentially be impactful as well. Both classes of injectables could provide for improved glycemic control, further atherogenic lipid improvement, weight loss (modest with some FGF-21s), reduction in liver fat content, and potentially further anti-fibrotic efficacy.
Triiodothyronine stimulates VEGF expression and secretion via steroids and HIF-1α in murine Leydig cells
Published in Systems Biology in Reproductive Medicine, 2018
Bodhana Dhole, Surabhi Gupta, Senthil Kumar Venugopal, Anand Kumar
Since Leydig cells comprise <1% of total cells of the testis, it is difficult to obtain large quantities of highly viable Leydig cells and even a multi-step procedure cannot yield 100% purified Leydig cells (Salva et al. 2001). The present study required a large number of cells; hence, we chose MLTC-1 cells which behave physiologically in many ways and are a good model for studying Leydig cell biology. They express specific cell surface receptors for hCG which are coupled to adenylate cyclase; they express StAR and CYP17A1; they produce both progesterone and testosterone. Previous studies (Manna et al. 1999, 2001; Maran et al. 2000) have shown functional thyroid hormone receptor (TR) in MLTC-1 cells. They also showed that T3 stimulates StAR gene expression and steroid production in MLTC-1 cells similar to primary Leydig cells. However, future studies should be done on primary Leydig cells to show that similar effects are observed in those cells and the effects are not due to the MLTC-1 cell line being immortalized.
Action of Reverse T3 on Cancer Cells
Published in Endocrine Research, 2019
Hung-Yun Lin, Heng-Yuan Tang, Matthew Leinung, Shaker A. Mousa, Aleck Hercbergs, Paul J. Davis
It has recently been shown that rT3 is a ligand of the thyroid hormone receptor site on plasma membrane integrin αvβ3 in nerve cells.6 Heterodimeric integrin αvβ3 is overexpressed by cancer cells, and we7 and others8–11 have shown that T4 acts at the thyroid hormone receptor site on this integrin to promote tumor cell proliferation, tumor-relevant angiogenesis and to activate cancer cell defense pathways, such as anti-apoptosis.7,10,12–16 In the present studies, we have examined the possibility that rT3 is a tumor-support hormone. In the nonthyroidal illness syndrome (NTIS) that may be associated with advanced cancers,17 circulating T3 concentrations are reduced, but rT3 levels may be increased.18,19