Characterization of Transcriptional Regulators of Ghrelin Hormone Which Causes Genetic Obesity

NCT01404624 | Completed DMC

• 1 other identifier: 2007-01-016
• Study Type: observational
• Target: 58
• Locations: 0 countries
• Sites: N/A

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.

Conditions

Prader Willi Syndrome; Obesity

Eligibility Criteria

• Age: 5 Years - 11 Years
• Sex: all
• Healthy Volunteers: Yes
• Age Groups: Child (0-17)
• 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.

You may qualify if:

• 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.

You may not qualify if:

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

Sponsors & Collaborators

• Samsung Medical Center: lead

MeSH Terms

Conditions

Prader-Willi Syndrome; Obesity

Condition Hierarchy (Ancestors)

Intellectual Disability; Neurobehavioral Manifestations; Neurologic Manifestations; Nervous System Diseases; Abnormalities, Multiple; Congenital Abnormalities; Congenital, Hereditary, and Neonatal Diseases and Abnormalities; Chromosome Disorders; Genetic Diseases, Inborn; Imprinting Disorders; Overweight; Overnutrition; Nutrition Disorders; Nutritional and Metabolic Diseases; Body Weight; Signs and Symptoms; Pathological Conditions, Signs and Symptoms

Study Officials

• Dong-Kyu Jin, M.D

  Samsung Medical Center, Sungkyunkwan University School of Medicine

  PRINCIPAL INVESTIGATOR

Study Design

• Study Type: observational
• Observational Model: CASE CONTROL
• Sponsor Type: OTHER

Study Record Dates

• First Submitted: July 26, 2011
• First Posted: July 28, 2011
• Study Start: January 1, 2005
• Study Completion: December 1, 2006
• Last Updated: July 28, 2011

Record last verified: 2011-07