title: Effects of glucose infusion on neuroendocrine and cognitive parameters in Addison disease.
abstract: Sucrose intake has been shown to suppress increased adrenocorticotropic hormone (ACTH) levels in adrenalectomized rats, suggesting that increased cerebral energy supply can compensate for the loss of glucocorticoid feedback inhibition of the hypothalamo-pituitary-adrenal axis. We hypothesized that glucose infusion might acutely down-regulate increased ACTH secretion in patients with Addison disease. We studied 8 patients with primary adrenal insufficiency (Addison group) with short-term discontinuation of hydrocortisone substitution and 8 matched healthy controls in 2 randomized conditions. Subjects received either intravenous glucose infusion (0.75 g glucose per kilogram body weight for 2.5 hours) or placebo. Concentrations of ACTH, cortisol, catecholamines, growth hormone, glucagon, and insulin were measured; and cognitive functions as well as neuroglycopenic and autonomic symptoms were assessed. The ACTH concentrations were not affected by glucose infusion either in the Addison or in the control group. Likewise, concentrations of cortisol, epinephrine, norepinephrine, growth hormone, and glucagon remained unchanged in both groups. Neurocognitive performance and symptom scores were likewise not affected. Independent of glucose infusion, attention of the Addison patients was impaired in comparison with the control group. Our study in patients with Addison disease was not able to support the assumption of a compensatory effect of intravenous glucose infusion on hormonal parameters and neurocognitive symptoms in states of chronic cortisol deficiency. Further studies should examine whether different regimens of glucose administration are more effective.
authors.affiliation: Department of Internal Medicine I, University of Luebeck, 23538 Luebeck, Germany. Johanna.Klement@uk-sh.de
authors.forename: Johanna
authors.initials: J
authors.lastname: Klement
authors.forename: Christian
authors.initials: C
authors.lastname: Hubold
authors.forename: Manfred
authors.initials: M
authors.lastname: Hallschmid
authors.forename: Cecilia
authors.initials: C
authors.lastname: Loeck
authors.forename: Kerstin M
authors.initials: KM
authors.lastname: Oltmanns
authors.forename: Hendrik
authors.initials: H
authors.lastname: Lehnert
authors.forename: Jan
authors.initials: J
authors.lastname: Born
authors.forename: Achim
authors.initials: A
authors.lastname: Peters
mesh_terms: D000224:Addison Disease / Q000503:physiopathology* / Q000523:psychology*; D000324:Adrenocorticotropic Hormone / Q000097:blood; D000328:Adult; D000368:Aged; D001288:Attention / Q000187:drug effects / Q000502:physiology; D003071:Cognition / Q000187:drug effects*; D005260:Female; D005947:Glucose / Q000008:administration & dosage / Q000494:pharmacology*; D006728:Hormones / Q000097:blood; D006801:Humans; D007030:Hypothalamo-Hypophyseal System / Q000187:drug effects; D007262:Infusions, Intravenous; D007328:Insulin / Q000097:blood; D008297:Male; D008570:Memory, Short-Term; D008875:Middle Aged; D009483:Neuropsychological Tests; D009490:Neurosecretory Systems / Q000187:drug effects*; D010913:Pituitary-Adrenal System / Q000187:drug effects
chemical_list: D006728:Hormones; D007328:Insulin; D000324:Adrenocorticotropic Hormone; D005947:Glucose