| The metabolic phenotype of Prader-Willi syndrome (PWS) in childhood: heightened insulin sensitivity relative to body mass index. | |
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MedLine Citation:
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PMID: 20962018 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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CONTEXT: Insulin sensitivity is higher in patients with Prader-Willi syndrome (PWS) than in body mass index-matched obese controls (OCs). Factors contributing to the heightened insulin sensitivity of PWS remain obscure. We compared the fasting levels of various hormones, cytokines, lipids, and liver function tests in 14 PWS patients and 14 OCs with those in 14 age- and gender-matched lean children (LC). We hypothesized that metabolic profiles of children with PWS are comparable with those of LC, but different from those of OCs. RESULTS: Leptin levels were comparable in PWS patients and OCs, suggesting comparable degrees of adiposity. Glucose levels were comparable among groups. However, fasting insulin concentrations and homeostasis model assessment insulin resistance index were lower in PWS patients than in OCs (P < 0.05) and similar to LC. Moreover, high-density lipoprotein levels were lower and triglycerides higher in OCs (P < 0.05) but not PWS patients. Total adiponectin, high-molecular-weight (HMW) adiponectin and the HMW to total adiponectin ratio were higher in PWS patients (P < 0.05) than in OCs and similar to LC. High-sensitivity C-reactive protein and IL-6 levels were higher in OCs than in PWS patients or LC (P < 0.05). Nevertheless, PAI-1 levels were elevated in both OC and PWS patients. There were no group differences in glucagon-like peptide-1, macrophage chemoattractant protein-1, TNFα, IL-2, IL-8, IL-10, IL-12p40, IL-18, resistin, total or low-density lipoprotein cholesterol, aspartate aminotransferase, or alanine aminotransferase. CONCLUSIONS: The heightened insulin sensitivity of PWS patients relative to OCs is associated with higher levels of adiponectin and lower levels of high-sensitivity C-reactive protein and IL-6. Future studies will determine whether PWS children are protected from obesity comorbidities such as type 2 diabetes, hyperlipidemia, and nonalcoholic fatty liver disease. |
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Authors:
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Andrea M Haqq; Michael J Muehlbauer; Christopher B Newgard; Steven Grambow; Michael Freemark |
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Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't Date: 2010-10-20 |
Journal Detail:
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Title: The Journal of clinical endocrinology and metabolism Volume: 96 ISSN: 1945-7197 ISO Abbreviation: J. Clin. Endocrinol. Metab. Publication Date: 2011 Jan |
Date Detail:
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Created Date: 2011-01-06 Completed Date: 2011-02-04 Revised Date: 2012-01-02 |
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: E225-32 Citation Subset: AIM; IM |
Affiliation:
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Division of Pediatric Endocrinology, Department of Pediatrics, University of Alberta, Edmonton, Alberta, Canada. andrea.haqq@albertahealthservices.ca |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Blood Glucose
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metabolism Body Mass Index Child Cytokines / blood* Humans Insulin / metabolism* Insulin Resistance / physiology* Leptin / blood Prader-Willi Syndrome / metabolism* |
| Grant Support | |
ID/Acronym/Agency:
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1K23-RR-021979/RR/NCRR NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Blood Glucose; 0/Cytokines; 0/Insulin; 0/Leptin |
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