| Hypothalamic-pituitary-adrenal axis dysregulation and memory impairments in type 2 diabetes. | |
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MedLine Citation:
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PMID: 17426095 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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CONTEXT: There is evidence of both hypothalamic-pituitary-adrenocortical (HPA) axis and cognitive dysfunction in type 2 diabetes mellitus (T2DM). However, the exact nature and the associations between these abnormalities remain unclear. OBJECTIVES: The aim of the study was to characterize the nature of the HPA dysregulation in T2DM and ascertain whether impaired cognition in T2DM could be attributed to these abnormalities. DESIGN: A cross-sectional study was performed, contrasting matched groups on HPA axis function and cognition by using the combined dexamethasone (DEX)/CRH test and a neuropsychological battery assessing declarative and working memory, attention, and executive function. SETTING: The study was conducted in a research clinic in an academic medical center. PARTICIPANTS: Participants were volunteers functioning in the cognitively normal range. We studied 30 middle-aged individuals with T2DM, on average 7.5 yr since diabetes diagnosis, and 30 age-, gender-, and education-matched controls. MAIN OUTCOME MEASURES: Basal cortisol levels, cortisol levels during the DEX/CRH test, and performance on neuropsychological tests were measured. RESULTS: Individuals with T2DM had elevated basal plasma cortisol levels, higher levels after DEX suppression, and a larger response to CRH (all P <or= 0.005). Among individuals with T2DM, cortisol levels during the DEX/CRH test were positively associated with glycosylated hemoglobin (P = 0.05), independent of age, body mass index, hypertension, and dyslipidemia. Diabetic subjects showed cognitive impairments restricted to declarative memory. Across all subjects, declarative memory was inversely associated with cortisol levels; however, these associations were subsumed by glycemic control (glycosylated hemoglobin). CONCLUSIONS: HPA hyperactivity and declarative memory deficits are present in T2DM. Both alterations may reflect the negative impact of poor glycemic control on the hippocampal formation. |
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Authors:
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Hannah Bruehl; Melanie Rueger; Isabel Dziobek; Victoria Sweat; Aziz Tirsi; Elizabeth Javier; Alyssa Arentoft; Oliver T Wolf; Antonio Convit |
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Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural Date: 2007-04-10 |
Journal Detail:
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Title: The Journal of clinical endocrinology and metabolism Volume: 92 ISSN: 0021-972X ISO Abbreviation: J. Clin. Endocrinol. Metab. Publication Date: 2007 Jul |
Date Detail:
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Created Date: 2007-07-09 Completed Date: 2007-08-28 Revised Date: 2007-12-03 |
Medline Journal Info:
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Nlm Unique ID: 0375362 Medline TA: J Clin Endocrinol Metab Country: United States |
Other Details:
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Languages: eng Pagination: 2439-45 Citation Subset: AIM; IM |
Affiliation:
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Department of Psychiatry, New York University School of Medicine, 550 First Avenue, New York, New York 10016, USA. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Aged Cognition Cognition Disorders / diagnosis, etiology, physiopathology Cross-Sectional Studies Dexamethasone / diagnostic use Diabetes Mellitus, Type 2 / complications, physiopathology* Female Glucocorticoids / diagnostic use Humans Hydrocortisone / blood Hypothalamo-Hypophyseal System / physiopathology* Male Memory Disorders / diagnosis, etiology, physiopathology* Middle Aged Neuropsychological Tests Pituitary-Adrenal System / physiopathology* |
| Grant Support | |
ID/Acronym/Agency:
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DK064087/DK/NIDDK NIH HHS; M01 RR00096/RR/NCRR NIH HHS; P30-AG-08051/AG/NIA NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Glucocorticoids; 50-02-2/Dexamethasone; 50-23-7/Hydrocortisone |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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