| Prader-Willi syndrome is associated with activation of the innate immune system independently of central adiposity and insulin resistance. | |
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MedLine Citation:
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PMID: 20444923 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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BACKGROUND: Subjects with Prader-Willi syndrome (PWS) have a reduced life expectancy due to cardiovascular disease. Increased systemic low-grade inflammation is postulated as a contributor, despite reported lower visceral fat mass and increased insulin sensitivity. OBJECTIVES: Our aim was to compare inflammatory markers and arterial stiffness in PWS and adiposity-matched obese control subjects. DESIGN: We conducted a cross-sectional cohort study comparing 12 PWS subjects, 12 obese subjects matched for percentage body fat and central abdominal fat mass, and 10 healthy normal-weight subjects. MAIN OUTCOME MEASURES: Dual-energy x-ray absorptiometry was used to assess body composition, flow cytometry to quantify activation markers on immun e cells, and ELISA for measurement of C-reactive protein, adiponectin, and IL-6. Insulin resistance was estimated by homeostasis model assessment and arterial stiffness by applanation tonometry. RESULTS: PWS and obese subjects had similarly increased homeostasis model assessment and arterial stiffness. Nevertheless, PWS subjects showed significantly higher IL-6 (4.9 + or - 1.0 vs. 2.5 + or - 0.4 pg/ml; P = 0.02) and nonsignificantly higher C-reactive protein (10.5 + or - 3.2 vs. 4.0 + or - 1.0 ng/ml; P = 0.08). Neutrophil activation markers CD66b and CD11b were higher in PWS compared to obese subjects (P < 0.01), reflecting an activated innate immune system. These markers were positively related to central adiposity in lean and obese subjects (r = 0.49; P < 0.05), but not in PWS subjects. CONCLUSIONS: PWS subjects compared to adiposity-matched obese subjects demonstrate similar insulin resistance but increased low-grade inflammation. The dissociation of inflammation and central adiposity suggests that activation of innate immunity may be either a specific genetic feature of PWS or linked to the commonly associated obstructive sleep apnea syndrome, and might offer a treatment target to reduce cardiovascular disease. |
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Authors:
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Alexander Viardot; Lisa Sze; Louise Purtell; Amanda Sainsbury; Georgina Loughnan; Ellie Smith; Herbert Herzog; Katharine Steinbeck; Lesley V Campbell |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't Date: 2010-05-05 |
Journal Detail:
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Title: The Journal of clinical endocrinology and metabolism Volume: 95 ISSN: 1945-7197 ISO Abbreviation: J. Clin. Endocrinol. Metab. Publication Date: 2010 Jul |
Date Detail:
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Created Date: 2010-07-08 Completed Date: 2010-07-26 Revised Date: - |
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: 3392-9 Citation Subset: AIM; IM |
Affiliation:
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Diabetes and Obesity Research Program, Garvan Institute of Medical Research, 384 Victoria Street, Sydney-Darlinghurst NSW 2010, Australia. a.viardot@garvan.org.au |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Absorptiometry, Photon Adiponectin / blood Adiposity / physiology* Antigens, CD / immunology, metabolism C-Reactive Protein / metabolism Cohort Studies Cross-Sectional Studies Enzyme-Linked Immunosorbent Assay Flow Cytometry Humans Immunity, Innate / physiology* Insulin Resistance / physiology* Interleukin-6 / blood Obesity / complications, immunology*, metabolism Prader-Willi Syndrome / complications, immunology*, metabolism |
| Chemical | |
Reg. No./Substance:
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0/Adiponectin; 0/Antigens, CD; 0/Interleukin-6; 9007-41-4/C-Reactive Protein |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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