title: Adiponectin regulate growth hormone secretion via adiponectin receptor mediated Ca(2+) signalling in rat somatotrophs in vitro.
abstract: Obesity is associated with reduced levels of growth hormone (GH) and the disruption of pulsatile GH secretion. This results in relative GH deficiency. It is likely that a regulatory relationship between GH secretion and adipose tissue exists as the secretion of GH recovers to normal levels after a reduction in body weight. This report characterise the expression and interaction of adiponectin receptors 1 and 2 (AdipoR1 and AdipoR2) and adiponectin, respectively, in regulating the activity of GH secreting cells. Polymerase chain reaction analysis of the GH3 cell line, rat anterior pituitary gland and isolated somatotroph cells from transgenic GFP expressing mice confirmed the expression of both AdipoR1 and AdipoR2 in GH secretory cells. Because GH cells expressed both receptors, it is likely that the measured increase in GH secretion, observed in primary cultured rat pituitary cells after 30 min of incubation with full-length murine adiponectin, was mediated by a direct receptor regulated process. Adiponectin induced an increase in intracellular Ca(2+) through both the influx of extracellular Ca(2+) and the release of intracellular Ca(2+) stores resulting in the secretion of GH. Furthermore, results confirm that this increase in GH secretion depended mainly on an increase in Ca(2+) influx through L-type Ca(2+) channels. It is concluded that adiponectin directly regulates GH secretion from somatotrophs by binding to either adiponectin receptor, and that this is mediated via a similar process observed after the stimulation of GH secretion by GH-releasing hormone.
authors.affiliation: School of Biomedical Science, University of Queensland, St Lucia, Brisbane, QLD, Australia.
authors.forename: F J
authors.initials: FJ
authors.lastname: Steyn
authors.forename: F
authors.initials: F
authors.lastname: Boehme
authors.forename: E
authors.initials: E
authors.lastname: Vargas
authors.forename: K
authors.initials: K
authors.lastname: Wang
authors.forename: H C
authors.initials: HC
authors.lastname: Parkington
authors.forename: J R
authors.initials: JR
authors.lastname: Rao
authors.forename: C
authors.initials: C
authors.lastname: Chen
mesh_terms: D052242:Adiponectin / Q000378:metabolism*; D000818:Animals; D030801:Animals, Genetically Modified; D002118:Calcium / Q000378:metabolism*; D002121:Calcium Channel Blockers / Q000378:metabolism; D020013:Calcium Signaling / Q000502:physiology*; D002478:Cells, Cultured; D013006:Growth Hormone / Q000378:metabolism*; D008297:Male; D051379:Mice; D009543:Nifedipine / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D054419:Receptors, Adiponectin / Q000235:genetics / Q000378:metabolism*; D052683:Somatotrophs / Q000378:metabolism*
chemical_list: D052242:Adiponectin; D002121:Calcium Channel Blockers; D054419:Receptors, Adiponectin; C475419:adiponectin receptor 1, mouse; C504339:adiponectin receptor 1, rat; C475421:adiponectin receptor 2, mouse; C506573:adiponectin receptor 2, rat; D013006:Growth Hormone; D009543:Nifedipine; D002118:Calcium