- ICH GCP
- US Clinical Trials Registry
- Clinical Trial NCT00800852
Increased Expression of Adiponectin Receptor 2 in the Mononuclear Cells in Children With Prader-Willi Syndrome
The inflammatory process is involved in the pathogenesis of obesity. Prader-Willi syndrome (PWS) is a genetic model of syndromic obesity. Adiponectin is an adipokine with potent anti-inflammatory properties, and its effect is mediated through adiponectin receptors 1 (adipoR1) and 2 (adipoR2).
Objective of this study is to compare the expression of adipoR1, adipoR2, and adiponectin in peripheral blood mononuclear cells (PBMCs) in PWS children and obese control and to correlate receptor expression with insulin sensitivity and obesity-related parameters.
Study Overview
Status
Conditions
Study Type
Participation Criteria
Eligibility Criteria
Ages Eligible for Study
Accepts Healthy Volunteers
Genders Eligible for Study
Sampling Method
Study Population
Description
Inclusion Criteria:
- children with Prader-willi syndrome
- children with simple obesity
Exclusion Criteria:
- subjects with diabetes mellitus (fasting plasma glucose > 126 mg/dL with a 2-h oral glucose tolerance test value of >200 mg/dl)
Study Plan
How is the study designed?
Collaborators and Investigators
Sponsor
Investigators
- Principal Investigator: Don-Kyu Jin, M.D., Samsung Medical Center, Sungkyunkwan Uiversity School of Medicine
Study record dates
Study Registration Dates
First Submitted
First Submitted That Met QC Criteria
First Posted (Estimate)
Study Record Updates
Last Update Posted (Estimate)
Last Update Submitted That Met QC Criteria
Last Verified
More Information
Terms related to this study
Additional Relevant MeSH Terms
- Pathologic Processes
- Nervous System Diseases
- Neurologic Manifestations
- Neurobehavioral Manifestations
- Disease
- Congenital Abnormalities
- Overnutrition
- Nutrition Disorders
- Genetic Diseases, Inborn
- Intellectual Disability
- Abnormalities, Multiple
- Chromosome Disorders
- Obesity
- Syndrome
- Prader-Willi Syndrome
Other Study ID Numbers
- 2008-10-040
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