Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/10468
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dc.contributor.authorFedi, Marcoen
dc.contributor.authorBach, Leon Aen
dc.contributor.authorBerkovic, Samuel Fen
dc.contributor.authorWilloughby, John Oen
dc.contributor.authorScheffer, Ingrid Een
dc.contributor.authorReutens, David Cen
dc.date.accessioned2015-05-15T23:55:29Z
dc.date.available2015-05-15T23:55:29Z
dc.date.issued2007-11-27en
dc.identifier.citationThe Journal of Clinical Endocrinology and Metabolism 2007; 93(2): 634-7en
dc.identifier.govdoc18042647en
dc.identifier.otherPUBMEDen
dc.identifier.urihttp://ahro.austin.org.au/austinjspui/handle/1/10468en
dc.description.abstractPulsatile GH secretion from the anterior pituitary is a key mediator of human growth regulation and is affected by a number of genetic and environmental factors. Activation of neuronal nicotinic acetylcholine (nACh) receptors promotes GH release, but the role of these receptors in growth regulation is unknown.Our aim was to assess the effect of a mutation in the alpha4 subunit of the nACh receptor on cholinergic-mediated GH release.Forty-one healthy volunteers (24 male, age 36.2 +/- 12.2 yr, mean +/- sd) and 13 subjects with the alpha4-Ser248Phe mutation (four male, age 43.2 +/- 16.8 yr) were studied. Serum levels of GH, LH, FSH, prolactin, TSH, free T(4), and cortisol were measured at baseline and at regular intervals after infusion of physostigmine. Height and weight were recorded in all participants as well as from additional family members with (n = 11, four male) and without (n = 16, seven male) the mutation.Subjects with the mutation were shorter (1.62 +/- 0.08 vs. 1.72 +/- 0.09 m, P < 0.05) and had a greater body mass index (31 +/- 6 vs. 24 +/- 3 kg/m(2), P < 0.05) than healthy volunteers and unaffected members of the pedigree. In controls, physostigmine markedly increased the serum levels of GH (mean increase, +732%). In contrast, the response to physostigmine was markedly blunted in subjects with the mutation (+104%, P > 0.2 vs. control).These findings suggest a role of the nACh receptor in human growth regulation.en
dc.language.isoenen
dc.subject.otherAdolescenten
dc.subject.otherAdulten
dc.subject.otherAgeden
dc.subject.otherBody Height.geneticsen
dc.subject.otherBody Mass Indexen
dc.subject.otherCholinesterase Inhibitors.pharmacologyen
dc.subject.otherFemaleen
dc.subject.otherFollicle Stimulating Hormone.blooden
dc.subject.otherGrowth Disorders.blood.geneticsen
dc.subject.otherHuman Growth Hormone.blood.physiologyen
dc.subject.otherHumansen
dc.subject.otherHydrocortisone.blooden
dc.subject.otherLuteinizing Hormone.blooden
dc.subject.otherMaleen
dc.subject.otherMiddle Ageden
dc.subject.otherPhysostigmine.pharmacologyen
dc.subject.otherPoint Mutationen
dc.subject.otherProlactin.blooden
dc.subject.otherReceptors, Nicotinic.geneticsen
dc.subject.otherThyrotropin.blooden
dc.subject.otherThyroxine.blooden
dc.titleAssociation of a nicotinic receptor mutation with reduced height and blunted physostigmine-stimulated growth hormone release.en
dc.typeJournal Articleen
dc.identifier.journaltitleThe Journal of Clinical Endocrinology and Metabolismen
dc.identifier.affiliationDepartment of Medicine, Austin Hospital, The University of Melbourne, Heidelberg, Victoria 3084 Australiaen
dc.identifier.doi10.1210/jc.2007-1611en
dc.description.pages634-7en
dc.relation.urlhttps://pubmed.ncbi.nlm.nih.gov/18042647en
dc.type.austinJournal Articleen
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.fulltextNo Fulltext-
item.cerifentitytypePublications-
item.grantfulltextnone-
item.languageiso639-1en-
item.openairetypeJournal Article-
crisitem.author.deptEpilepsy Research Centre-
crisitem.author.deptNeurology-
crisitem.author.deptEpilepsy Research Centre-
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