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The Hypothalamic-Pituitary-Adrenal Axis in Fibromyalgia: Where Are We in 2001?
Published in Robert M. Bennett, The Clinical Neurobiology of Fibromyalgia and Myofascial Pain, 2020
Corticotropin-releasing hormone [CRH] is a principal neuropeptide regulator of the ΗΡΑ axis activity by virtue of its localization to the paraventricular nucleus of the hypothalamus. Corticotropin-releasing hormone receptors are, however, localized to many other brain regions and in those locations mediates other biological effects (4). In the prefrontal, cingulate, and insular cortices CRH plays a role in the affective response to stress. The behavioral and autonomic responses to stress are associated with CRH in the central nucleus of the amygdala. The interplay between the ΗΡΑ axis and the sympathetic nervous sys-tern is localized to the locus coeruleus, dorsal raphe nucleus, and ventral tegmental areas. Corticotropin-releasing hormone may also play a role in the descending modulation of pain perception as coordinated in the periaqueductal gray (5). Corticotropin-releasing hormone actions are mediated by two receptors, CRHR1 and CRHR2. They share approximately 71 percent amino acid homology, and are differentially localized to different central and peripheral sites (6).
Genetic and environmental determinants of adolescent alcohol use
Published in Ilana B. Crome, Richard Williams, Roger Bloor, Xenofon Sgouros, Substance Misuse and Young People, 2019
Toni-Kim Clarke, Richard C. Crist
Similar results were found for the CRHR1 gene. CRHR1 encodes the corticotrophin response hormone receptor, an important mediator of the endogenous cortisol stress response. Fifteen-year-olds who reported a higher than average number of negative life events showed significant increases in the lifetime rate of heavy drinking only if they had the C/C genotype at the rs1876831 locus (Blomeyer et al., 2008). Carriers of the T allele showed no effect of negative life events on alcohol consumption. Findings in other genes provide evidence that family environment can also negate genetic susceptibility to early alcohol use. A missense SNP (SNP that changes the protein sequence of a gene) in the ANKK1 gene, rs1800497, is associated with alcohol consumption in adolescents from households with permissive parents. Individuals carrying the minor allele of the polymorphism consumed significantly more alcohol than those homozygous for the major allele (van der Zwaluw et al., 2010a). This effect was completely abolished in the presence of parents who set strict rules regarding alcohol. An additional study confirmed this interaction and a similar protective effect in teenagers carrying the G allele of the A118G variant in OPRM1 has been identified (Pieters et al., 2012; Miranda et al., 2013).
Genetics and Asthma
Published in Jonathan A. Bernstein, Mark L. Levy, Clinical Asthma, 2014
Rebecca E. Slager, Xingnan Li, Deborah A. Meyers, Eugene R. Bleecker
A recent GWAS by Tantisira and colleagues evaluated four asthma treatment trials (n = 935) to identify pharmacogenetic associations related to the response to inhaled glucocorticoids. A significant, replicated association was found in two correlated SNPs in the glucocorticoid-induced transcript 1 (GLCCI1) gene, which confer a lung function response to inhaled glucocorticoids and reduced GLCCI1 expression. The overall mean (± standard error) increase in FEV1 for ICS-treated subjects homozygous for the risk allele was significantly less than for subjects homozygous for the common allele (3.2 ± 1.6% vs. 9.4 ± 1.1%, respectively). This is an example of a replicated pharmacogenetic analysis with functional verification.30 In addition, Tantisira et al. have also shown that a variation in the corticotrophin-releasing hormone receptor 1 gene (CRHR1) is associated with an improved lung function response to corticosteroids in three asthma clinical trial populations.31 Tantisira et al. found genetic variants in the T gene and correlated regions associated with a FEV1 response to ICS in an additional GWAS in the NHLBI Single-Nucleotide Polymorphism Health Association-Asthma Resource Project.32
Genetic susceptibility to nicotine and/or alcohol addiction: a systematic review
Published in Toxin Reviews, 2021
Isabel Legaz, M. D. Pérez-Cárceles, Irene de la Calle, Fuensanta Arjona, Miriam Roca, Pablo Cejudo, Aurelio Luna, Eduardo Osuna
CRHR1 gene encodes a G-protein-coupled receptor that binds neuropeptides of the corticotropin-releasing hormone family, major regulators of the hypothalamic-pituitary adrenal axis. Tang et al. (2015), observed that SNP rs171440 in the CRHR1 gene was significantly associated with smoking quantity (p = .032), the Fagerström test for nicotine dependence (p = .047). Further, haplotype-based association analysis revealed that haplotypes CCG (7.6%) and TCG (42.3%), formed by SNPs rs171440, rs1396862 and rs878886 were significantly associated with nicotine dependence.
The urocortin peptides: biological relevance and laboratory aspects of UCN3 and its receptor
Published in Critical Reviews in Clinical Laboratory Sciences, 2022
Norah J. Alghamdi, Christopher T. Burns, Roland Valdes
The HPA axis provides a basis to focus on a family of peptides comprised of corticotropin-releasing hormone (CRH), urocortin peptides (UCN 1, 2, and 3), and the two G protein-coupled receptors, CRH receptors (CHRH) CRHR1 and CRHR2. CRH is responsible for activating the hypothalamic-pituitary-adrenal axis during stress [3], whereas the urocortins contribute to the stress-recovery mechanism [4]. Understanding the regulatory physiology of the urocortins and the UCN3/CRHR2 axis, in particular, is necessary for establishing a viable clinical laboratory diagnostic targeting stress homeostasis.
Treatment response heterogeneity in asthma: the role of genetic variation
Published in Expert Review of Respiratory Medicine, 2018
Susanne J. H. Vijverberg, Niloufar Farzan, Elise M. A. Slob, Anne H. Neerincx, Anke H. Maitland-van der Zee
The release of endogenous glucocorticoids is regulated by corticotrophin releasing hormone regulated by the hypothalamic pituitary adrenal (HPA axis). CRHR1 encodes for corticotrophin-releasing hormone receptor 1. It has been hypothesized that variation in this gene influences the level of endogenous corticosteroid secretion and thereby alters the response to ICS. Several SNPs in this gene have been studied and two variants have been replicated at least once [30,46,47] in independent populations of children and adults with asthma; however, results have been inconsistent [48].