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Characterization of Transcriptional Regulators of Ghrelin Hormone Which Causes Genetic Obesity

The safety and scientific validity of this study is the responsibility of the study sponsor and investigators. Listing a study does not mean it has been evaluated by the U.S. Federal Government. Read our disclaimer for details. Identifier: NCT01404624
Recruitment Status : Completed
First Posted : July 28, 2011
Last Update Posted : July 28, 2011
Information provided by:
Samsung Medical Center

Brief Summary:
The problem point of the Prader-Willi Syndrome (PWS) patient is the obesity which is intense and the plasma ghrelin level which increases unusual from the recently PWS patients was discovered. The Ghrelin is endogeneous ligand of growth hormone secretagogue receptor with peptide hormone and the location is 3p26-p25. Becomes the secretion even from nervous system but from dignity X/A cell it is secreted mainly and growth is important even in the vagal control against food and intake and a dignity function even on the action outside which promotes the secretion which drives it operates. It increases food intake specially and in order to accomplish the action which diminishes fat utilization the obesity with the week cause which it does the mortar it is thought. Active the ghrelin of the form is essential in hormonal activity of the ghrelin and appetite and growth hormone it participates to the secretion promotion which drives. Action of the Ghrelin measuring the quantitative change in middle acylated of the PWS patient ghrelin in order to happen after the acylation initially by one interest ghrelin which is attempted the appetite of the PWS patient is is controlled the method it will be able to prove the thing directly, it used the RIA kit and the ELISA it will be able to measure kit it will be able to measure the whole ghrelin to pick the PWS patient and the blood of the normal army and active ghrelin it measured a change.

Condition or disease
Prader Willi Syndrome Obesity

Detailed Description:
It will reach to respect, in 5 ' -flanking region of the ghrelin 2000 bp focus it let and it got luciferase assay it led and and it searched for the binding it sorted it put out and and to sleep the transcription factor which and and is the possibility of doing the essential region in the transcription and and it did an order deletion clone and and. is important in result and ghrelin activity the region role, -300~-200 region Basic helix-loop-helix (bHLH) are containing -USF (-236 to -231) binding site specially to be compressed in -500~-400 and -300~-200 two portions.

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Study Type : Observational
Actual Enrollment : 58 participants
Observational Model: Case-Control
Official Title: Increased Density of Ghrelin-Expressing Cells in the Gastric Fundus and Body in Prader-Willi Syndrome
Study Start Date : January 2005
Actual Study Completion Date : December 2006

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Information from the National Library of Medicine

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Ages Eligible for Study:   5 Years to 11 Years   (Child)
Sexes Eligible for Study:   All
Accepts Healthy Volunteers:   Yes
Sampling Method:   Probability Sample
Study Population
Sixteen PWS patients [age, 8.1 +- 2.6 yr; 12 males, 4 females; body mass index (BMI), 25+-1.5 kg/m2], 19 healthy normal lean subjects (age, 8.9 +- 1.4 yr; 14 males, 5 females; BMI, 16.5 +- 0.42 kg/m2), 13 GHD patients (age, 9.1 +- 1.8 yr; 9 males, 4 females; BMI, 27 +- 1.8 kg/m2), and 10 healthy normal obese subjects (age, 8.7 +- 2.3 yr; 7 males, 3 females; BMI, 26 +- 1.7 kg/m2) were enrolled in the study. The subjects had no history of GH treatment and were not being treated with GH at study commencement.

Inclusion Criteria:

  • PWS patients were genetically confirmed using the standard methylation test. GHD was diagnosed using a GH stimulation test. The lean and obese normal subjects (comparison group) enrolled were the children or siblings of hospital staff who understood the purpose of and the procedures used.

Exclusion Criteria:

  • GHD patients had no history of GH treatment, and were not being treated with GH at study commencement

Information from the National Library of Medicine

To learn more about this study, you or your doctor may contact the study research staff using the contact information provided by the sponsor.

Please refer to this study by its identifier (NCT number): NCT01404624

Sponsors and Collaborators
Samsung Medical Center
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Principal Investigator: Dong-Kyu Jin, M.D Samsung Medical Center, Sungkyunkwan University School of Medicine
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Responsible Party: Dong-Kyu Jin, Samsung Medical Center Identifier: NCT01404624    
Other Study ID Numbers: 2007-01-016
First Posted: July 28, 2011    Key Record Dates
Last Update Posted: July 28, 2011
Last Verified: July 2011
Additional relevant MeSH terms:
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Prader-Willi Syndrome
Pathologic Processes
Nutrition Disorders
Body Weight
Intellectual Disability
Neurobehavioral Manifestations
Neurologic Manifestations
Nervous System Diseases
Abnormalities, Multiple
Congenital Abnormalities
Chromosome Disorders
Genetic Diseases, Inborn