title: Acute hyperglycemia and activation of the beta-adrenergic system do not exhibit synergistic inhibitory actions on thyrotropin-releasing hormone (TRH)-induced thyroid stimulating hormone (TSH) secretion.
abstract: Thyrotropin-releasing hormone (TRH)-stimulated thyroid stimulating hormone (TSH) response in normal subjects is suppressed by oral glucose administration. Pharmacologic studies indicate that this suppressive action of glucose is mediated by an increase in hypothalamic somatostatin (SRIH) tone. Since activation of the beta-adrenergic system also suppresses basal TSH secretion by enhancing SRIH release we sought to determine whether isoproterenol alters the suppression of TRH-induced TSH response induced by the stimulation of glucose. Four tests were performed in seven healthy young men: Test 1: 200 microg TRH (iv) at 0 min; Test 2: 100 g oral glucose at -30 min and TRH at 0 min; Test 3: TRH at 0 min with isoproterenol (0.012 microg/kg, iv) infused continuously; Test 4: oral glucose at -30 min, TRH at 0 min with isoproterenol infused continuously. Pretreatment with glucose significantly suppressed TRH-induced TSH secretion. Isoproterenol infusion also suppressed the TRH-induced TSH secretion, but it did not enhance the inhibitory action of glucose on TSH secretion. The degree of suppression induced by glucose was significantly higher than that achieved by isoproterenol. These data suggest that combined administration of glucose and isoproterenol does not exhibit synergistic inhibitory actions on TRH-stimulated TSH secretion, and that the glucose-TRH test could be used for the evaluation of the hypothalamic somatostatinergic activity.
authors.affiliation: Department of Internal Medicine, College of Medicine, Hallym University, Hallym Sacred Heart Hospital, Kyunggi, Korea.
authors.forename: Cheolyoung
authors.initials: C
authors.lastname: Park
authors.forename: Eunhee
authors.initials: E
authors.lastname: Kim
authors.forename: Sookjin
authors.initials: S
authors.lastname: Sohn
authors.forename: Inmyung
authors.initials: I
authors.lastname: Yang
authors.forename: Gwanpyo
authors.initials: G
authors.lastname: Koh
authors.forename: Seungjoon
authors.initials: S
authors.lastname: Oh
authors.forename: Jeongtaek
authors.initials: J
authors.lastname: Woo
authors.forename: Sungwoon
authors.initials: S
authors.lastname: Kim
authors.forename: Jinwoo
authors.initials: J
authors.lastname: Kim
authors.forename: Youngseol
authors.initials: Y
authors.lastname: Kim
authors.forename: Kiwon
authors.initials: K
authors.lastname: Oh
authors.forename: Sungwoo
authors.initials: S
authors.lastname: Park
authors.forename: Seungjoon
authors.initials: S
authors.lastname: Park
mesh_terms: D000208:Acute Disease; D000284:Administration, Oral; D000318:Adrenergic beta-Agonists / Q000008:administration & dosage / Q000494:pharmacology; D000328:Adult; D004357:Drug Synergism; D005947:Glucose / Q000008:administration & dosage / Q000494:pharmacology; D006801:Humans; D006943:Hyperglycemia / Q000378:metabolism*; D007262:Infusions, Intravenous; D007545:Isoproterenol / Q000008:administration & dosage / Q000494:pharmacology; D008297:Male; D011943:Receptors, Adrenergic, beta / Q000378:metabolism*; D013972:Thyrotropin / Q000037:antagonists & inhibitors / Q000378:metabolism*; D013973:Thyrotropin-Releasing Hormone / Q000378:metabolism*
chemical_list: D000318:Adrenergic beta-Agonists; D011943:Receptors, Adrenergic, beta; D013973:Thyrotropin-Releasing Hormone; D013972:Thyrotropin; D005947:Glucose; D007545:Isoproterenol