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Regulation of the Pituitary Gland by Dopamine
Published in Nira Ben-Jonathan, Dopamine, 2020
As discussed in Chapter 4 and depicted in Figure 4.5, ACTH plays a pivotal role in the overall homeostasis, as well as the stress response and is a major component of the hypothalamo-pituitary-adrenal axis (HPA). ACTH is released from corticotrophs and its main target is the ACTH receptor, primarily found in the zona fasciculata of the adrenal cortex. Binding of ACTH to its receptor increases the production and release of glucocorticoids (cortisol in humans and corticosterone in rodents), which affect many central and peripheral sites as part of the stress response and fulfill important cardiovascular, metabolic, immunologic and homeostatic functions.
Melanotropin Receptors and Signal Transduction
Published in Mac E. Hadley, The Melanotropic Peptides, 2018
Tomi K. Sawyer, Mac E. Hadley, Victor J. Hruby
The isolation and characterization of purified MSH receptors has not yet been documented, but such research is in progress. (Schwyzer and co-workers, personal communication). This may provide insight to understanding the molecular basis of MSH specificity at melanocytes vs. other potential MSH target systems (i.e., adrenal gland, adipose tissue, and the brain) which are also adrenocorticotropin (ACTH) sensitive. Recently, the adrenal cell ACTH receptor has been purified, and the molecular structure and binding characteristics determined.26 A relevant question remaining to be answered is whether or not the structural homology between MSH and ACTH may also exist between MSH receptors and ACTH receptors. It is known that certain functional similarities exist between these two receptor types (vide infra) although the structure-activity relationships for α-MSH are quite different from those described for ACTH.27
Alopecia areata: Pathogenesis, clinical features, diagnosis, and management
Published in Jerry Shapiro, Nina Otberg, Hair Loss and Restoration, 2015
Along with IL-1α and IL-1β, TNF-a plays a major role in the pathogenesis of AA [105,106]. IL-1α, IL-1β, and TNF-α cause a decrease in the size of the matrix, disorganization of follicular melanocytes, and abnormal differentiation and keratinization of the precortical cells and the inner root sheath [46]. TNF-a levels in the skin correlate positively with plasma adrenocorticotropic hormone (ACTH) levels and cutaneous ACTH receptor expression levels under repeated stress in humans [107]. Elevated serum levels of B cell activating factor (BAFF), which belongs to the TNF family, were found in patients with AA [108,109]. BAFF may activate T cells and promote Th1 response, leading to the production of IFNγ and perpetuation of disease activity [97,110].
Adrenal function following acute discontinuation of glucocorticoids in children with acute lymphocytic leukemia: A prospective study
Published in Pediatric Hematology and Oncology, 2019
Noman Ahmad, Ibraheem Faisal Abosoudah, Mrouge Mohamed Sobaihi, Ali Hassan Algiraigri, Farh Roujouleh, Fatima Ghurab, Jean-Pierre Chanoine
The chronic use of GCs followed by abrupt cessation was shown to cause adrenal suppression for up to nine months when used for 1–10 years.13 This is due to suppression of the endogenous secretion of ACTH from the anterior pituitary, which leads to down regulation of the ACTH receptor mRNA, adrenal gland atrophy and transient hypo-responsiveness to ACTH.14 High dose GCs, even for short or intermediate duration, can lead to adrenal atrophy and suppression of HPA axis.15,16 The duration and severity of adrenal suppression cannot be reliably predicted by dose, duration or type of GC therapy.17 Adrenal function should eventually recover after different doses and duration of GCs but there exist great variability and uncertainty with regards to the time required for the HPA axis to recover.18. For this reason, we recommend a comprehensive education and provision of written information about symptoms of adrenal insufficiency for patients and parents.19
Increased symptoms of anxiety and depression in prepubertal girls, but not boys, with premature adrenarche: associations with serum DHEAS and daily salivary cortisol concentrations
Published in Stress, 2018
Chrisanthi Marakaki, Panagiota Pervanidou, Ioannis Papassotiriou, George Mastorakos, Ze’ev Hochberg, George Chrousos, Anastasios Papadimitriou
Premature adrenarche (PA) is defined as the early appearance (before the age of 8 years in girls and 9 years in boys) of clinical signs of androgen activity (pubic and/or axillary hair, adult-type body odor, oily hair, and acne) and it may be accompanied by an increase in serum adrenal androgen levels, mainly DHEAS. The etiology of PA is multifactoral. Environmental factors (such as intrauterine growth restriction and obesity) and genetic factors (genes encoding steroidogenic enzymes, insulin-IGF signaling, and androgen receptor sensitivity) have been associated with PA. Pituitary ACTH is essential for adrenal androgen production, as evidenced by the absence of adrenarche in children with hypopituitarism and in patients with ACTH receptor defect (Voutilainen & Jaaskelainen, 2015). Exaggerated reactivity of HPA axis has been proposed to account in part for the development of adrenal hyperandrogenism in PA girls (Cizza et al., 2001). However, ACTH is not considered to be the trigger for adrenarche and its initiating mechanisms remains at least partly obscure.
New and emerging drug therapies for Cushing’s disease
Published in Expert Opinion on Pharmacotherapy, 2018
Sylvère Störmann, Jochen Schopohl
The ACTH receptor of the adrenal gland is a melanocortin 2 receptor, one of five melanocortin receptors that are activated by POMC-derived polypeptides. ACTH is highly specific for its receptor, but designing a selective antagonist has proven challenging, as most POMC-derived ligands and their MCR share a common and evolutionary highly conserved amino-sequence [140]. Additionally, certain fragments of ACTH exert different effects across species so that preclinical positive effects may exert unwanted effects in humans. The idea of developing competitive antagonists of ACTH has been around for quite some time with early results being published in the 1970s, but ultimately unsuccessful [141]. In 2014, two new candidates for ACTH antagonism were proposed (GPS1573 and GPS1574) and showed promising antagonistic properties in cell cultures [142]. Recently, a study reported modest efficacy in reducing corticosterone response in neonatal rats that were injected with ACTH and up to 8000-fold higher GPS1574 doses [143]. Conversely, GPS1573 augmented corticosterone response in vivo.