ObesityGhrelinNCT00830141
Study of the Molecular Basis in the Pathophysiology of Food Intake and Growth in Children
An observational study of Obesity and Short Stature, run by HaEmek Medical Center, Israel.
Trial summary
Obesity, now a global epidemic, is a leading cause of illness and mortality in the developed world. To better understand the pathophysiological mechanisms that underlie weight disorders, increasing attention is being paid to central regulatory elements in energy homeostasis, including food intake and energy… Read more about this study
- Who is it for?
- Ages Up to 18 years
- Conditions the study is for
- Obesity, Short Stature
- How many people
- 259 participants
- Where
- No sites listed yet
- Study dates
- Jan 2009to Jan 2012
- Phase
- Observational
- Are there results?
- None posted in the registry
Key requirements
Who can take part, as listed by the sponsor. Only the study team can confirm whether you are eligible, so take this list to your doctor.
- Ages Up to 18 years
- All sexes
- No healthy volunteers
- Child, Adult
Study population: A total of 250 children followed in the pediatric endocrine department at Ha'Emek Medical Center will be divided into 5 groups: 50 children with GH deficiency,50 obese children, 50 children with failure to thrive (FTT)and 50 children with idiopathic short stature (ISS). 50 children without growth and weight disorders will be included as a control group.
Who may be able to join
- Group1: Children with GH deficiency diagnosed by 2 provocative tests with peak GH less than 10 ng/ml.
- Group 2:Children with height less than the 3rd centile without any etiology
- Group 3:children with failure to thrive until the age of 3 years.
- Group 4: children with obesity defined by BMI above the 90th centile for age and sex.
- Group 5: children with no endocrine diseases and without obesity or short stature.
Who cannot join
- Children with known pediatric or endocrine diseases.
About this study
Obesity, now a global epidemic, is a leading cause of illness and mortality in the developed world. To better understand the pathophysiological mechanisms that underlie weight disorders, increasing attention is being paid to central regulatory elements in energy homeostasis, including food intake and energy expenditure. The human hormone ghrelin is secreted as a preprohormone (preproghrelin), from which two hormones with antagonistic effects are derived: ghrelin, which has orexigenic effects and obestatin, which has anorexigenic effects. Ghrelin's actions are mediated by GH secretagogue receptor (GHSR). Ghrelin synthesis occurs predominantly in epithelial cells of the fundus of the stomach. . As the ligand for GHSR, ghrelin stimulates secretion of GH. In both rodents and humans, ghrelin regulates hunger though its action on hypothalamic feeding centers. Other effects of ghrelin include stimulating gastric emptying, positive effects on cardiovascular function, increasing intestinal peristalsis, and positive exocrine and paracrine pancreatic secretion. Despite its important physiological role, its precise regulatory mechanisms remain ambiguous. Thus, it has been suggested that mutations in ghrelin and its receptor will present clinically with obesity, eating disorders or growth disturbances. To date, only four different mutations have been reported in GHSR and no mutations have been found in the ghrelin gene.
Working hypothesis and aims: We hypothesize that mutations in ghrelin or in its receptor, GHSR, affect appetite regulation and cause growth and eating disorders.
Read the detailed description
Background: Obesity, now a global epidemic, is a leading cause of illness and mortality in the developed world. To better understand the pathophysiological mechanisms that underlie weight disorders, increasing attention is being paid to central regulatory elements in energy homeostasis, including food intake and energy expenditure. The human hormone ghrelin is secreted as a preprohormone (preproghrelin), from which two hormones with antagonistic effects are derived: ghrelin, which has orexigenic effects and obestatin, which has anorexigenic effects. Ghrelin's actions are mediated by GH secretagogue receptor (GHSR). Ghrelin synthesis occurs predominantly in epithelial cells of the fundus of the stomach. . As the ligand for GHSR, ghrelin stimulates secretion of GH. In both rodents and humans, ghrelin regulates hunger though its action on hypothalamic feeding centers. Other effects of ghrelin include stimulating gastric emptying, positive effects on cardiovascular function, increasing intestinal peristalsis, and positive exocrine and paracrine pancreatic secretion. Despite its important physiological role, its precise regulatory mechanisms remain ambiguous. Thus, it has been suggested that mutations in ghrelin and its receptor will present clinically with obesity, eating disorders or growth disturbances. To date, only four different mutations have been reported in GHSR and no mutations have been found in the ghrelin gene.
Working hypothesis and aims: We hypothesize that mutations in ghrelin or in its receptor, GHSR, affect appetite regulation and cause growth and eating disorders.
Methods: A total of 250 children followed in the pediatric endocrine department at Ha'Emek Medical Center will be divided into four groups: 50 children with GH deficiency, 50 obese children, 50 children with failure to thrive (FTT),and 50 children with idiopathic short stature (ISS). In addition, 50 children without growth or weight disorders will be included as a control group.
Genomic DNA will be isolated from the peripheral blood by standard methods. The corresponding intron-exon boundaries of the ghrelin and GHSR genes will be analyzed by direct sequencing using an ABI Prism 3100 DNA Analyzer.
Expected results: We anticipate that mutations in ghrelin or its receptor will affect growth and appetite regulation.
Importance: The findings of this study will expand our understanding of ghrelin's role in growth and appetite regulation.
Probable implications for medicine: The development of more specific therapeutic modalities for the treatment of short stature and obesity in children may become possible.
- Conditions
- Obesity, Short Stature
- Keywords
- Ghrelin, obesity, idiopathic short stature (ISS)
- Medical subject headings
- Obesity, Dwarfism
What participants receive
What participants receive. In a randomised study each person is assigned to one group by chance.
| Study group | Role | What they receive |
|---|---|---|
| 1 | 50 children with GH deficiency | |
| 2 | 50 children with ISS | |
| 3 | 50 children with FTT | |
| 4 | 50 children with obesity | |
| 5 | 50 children without short stature or obesity will serve as controls |
Timeline
From the start of the study to its completion; the mark is today. Estimated dates are the sponsor’s plan.
- First posted27 Jan 2009 (estimated)
- Study startJan 2009
- Primary completionJan 2011
- Study completionJan 2012
Resources
- Official record on ClinicalTrials.govThe registry entry this page is built from, with its full change history.
- Other trials for ObesityStudies of the same condition, open and under way.
- What the trial phases meanHow a treatment moves from first tests in people to approval.
More details
For doctors and researchers: how the study is designed, who runs it, and its registry IDs.
Study design
- Study type
- Observational
- Observational model
- Case-control
- Time perspective
- Prospective
- Enrolment
- 259 participants (actual)
Sponsor and investigators
- Lead sponsor
- HaEmek Medical Center, Israel
- Sponsor type
- University, hospital or other
- Responsible party
- Principal investigator, Yardena Tenenbaum-Rakover, HaEmek Medical Center, Israel
- Investigators
- Yardena Tenenbaum-Rakover, MD, Principal investigator, Ha"Emek Medical Center, Afula, ISRAEL
IDs, dates and publications
- ClinicalTrials.gov ID
- NCT00830141
- Sponsor's protocol ID
- 0040-08-EMC
- Acronym
- Ghrelin
- Status last verified
- Jul 2015
- First submitted
- 25 Jan 2009
- Last updated
- 3 Jul 2015
- Results posted
- No
- Data monitoring committee
- No
Study at a glance
From the registry record, last updated by the sponsor on 3 Jul 2015. Recruitment status is as the sponsor reported it: confirm with the study team.
- Official title
- Study of the Molecular Basis in the Pathophysiology of Food Intake and Growth in Children
- ClinicalTrials.gov ID
- NCT00830141
- Acronym / sponsor ID
- Ghrelin / 0040-08-EMC
- Conditions
- Obesity, Short Stature
- Keywords
- Ghrelin, obesity, idiopathic short stature (ISS)
- Study type
- Observational
- Recruitment status
- Completed
- Enrolment
- 259 participants (actual)
- Lead sponsor
- HaEmek Medical Center, IsraelUniversity, hospital or other
- Study start
- Jan 2009
- Primary completion
- Jan 2011 (actual)
- Study completion
- Jan 2012 (actual)
- First posted
- 27 Jan 2009 (estimated)
- Results
- Not posted in the source record
Clinical summary
The research question as the sponsor registered it. This describes what the study plans to test, not what it found.
Obesity, now a global epidemic, is a leading cause of illness and mortality in the developed world. To better understand the pathophysiological mechanisms that underlie weight disorders, increasing attention is being paid to central regulatory elements in energy homeostasis, including food intake and energy expenditure. The human hormone ghrelin is secreted as a preprohormone (preproghrelin), from which two hormones with antagonistic effects are derived: ghrelin, which has orexigenic effects and obestatin, which has anorexigenic effects. Ghrelin's actions are mediated by GH secretagogue receptor (GHSR). Ghrelin synthesis occurs predominantly in epithelial cells of the fundus of the stomach. . As the ligand for GHSR, ghrelin stimulates secretion of GH. In both rodents and humans, ghrelin regulates hunger though its action on hypothalamic feeding centers. Other effects of ghrelin include stimulating gastric emptying, positive effects on cardiovascular function, increasing intestinal peristalsis, and positive exocrine and paracrine pancreatic secretion. Despite its important physiological role, its precise regulatory mechanisms remain ambiguous. Thus, it has been suggested that mutations in ghrelin and its receptor will present clinically with obesity, eating disorders or growth disturbances. To date, only four different mutations have been reported in GHSR and no mutations have been found in the ghrelin gene.
Working hypothesis and aims: We hypothesize that mutations in ghrelin or in its receptor, GHSR, affect appetite regulation and cause growth and eating disorders.
Detailed description
Background: Obesity, now a global epidemic, is a leading cause of illness and mortality in the developed world. To better understand the pathophysiological mechanisms that underlie weight disorders, increasing attention is being paid to central regulatory elements in energy homeostasis, including food intake and energy expenditure. The human hormone ghrelin is secreted as a preprohormone (preproghrelin), from which two hormones with antagonistic effects are derived: ghrelin, which has orexigenic effects and obestatin, which has anorexigenic effects. Ghrelin's actions are mediated by GH secretagogue receptor (GHSR). Ghrelin synthesis occurs predominantly in epithelial cells of the fundus of the stomach. . As the ligand for GHSR, ghrelin stimulates secretion of GH. In both rodents and humans, ghrelin regulates hunger though its action on hypothalamic feeding centers. Other effects of ghrelin include stimulating gastric emptying, positive effects on cardiovascular function, increasing intestinal peristalsis, and positive exocrine and paracrine pancreatic secretion. Despite its important physiological role, its precise regulatory mechanisms remain ambiguous. Thus, it has been suggested that mutations in ghrelin and its receptor will present clinically with obesity, eating disorders or growth disturbances. To date, only four different mutations have been reported in GHSR and no mutations have been found in the ghrelin gene.
Working hypothesis and aims: We hypothesize that mutations in ghrelin or in its receptor, GHSR, affect appetite regulation and cause growth and eating disorders.
Methods: A total of 250 children followed in the pediatric endocrine department at Ha'Emek Medical Center will be divided into four groups: 50 children with GH deficiency, 50 obese children, 50 children with failure to thrive (FTT),and 50 children with idiopathic short stature (ISS). In addition, 50 children without growth or weight disorders will be included as a control group.
Genomic DNA will be isolated from the peripheral blood by standard methods. The corresponding intron-exon boundaries of the ghrelin and GHSR genes will be analyzed by direct sequencing using an ABI Prism 3100 DNA Analyzer.
Expected results: We anticipate that mutations in ghrelin or its receptor will affect growth and appetite regulation.
Importance: The findings of this study will expand our understanding of ghrelin's role in growth and appetite regulation.
Probable implications for medicine: The development of more specific therapeutic modalities for the treatment of short stature and obesity in children may become possible.
Study design
- Observational model
- Case-control
- Time perspective
- Prospective
- Number of arms
- 5
| Arm | Type | Receives |
|---|---|---|
| 1 | – | –50 children with GH deficiency |
| 2 | – | –50 children with ISS |
| 3 | – | –50 children with FTT |
| 4 | – | –50 children with obesity |
| 5 | – | –50 children without short stature or obesity will serve as controls |
Who may qualify
- Ages
- Up to 18 years
- Sex
- All
- Healthy volunteers
- Not accepted
- Age groups
- Child, Adult
- Study population
- A total of 250 children followed in the pediatric endocrine department at Ha'Emek Medical Center will be divided into 5 groups: 50 children with GH deficiency,50 obese children, 50 children with failure to thrive (FTT)and 50 children with idiopathic short stature (ISS). 50 children without growth and weight disorders will be included as a control group.
Key inclusion criteria (5 listed)
- Group1: Children with GH deficiency diagnosed by 2 provocative tests with peak GH less than 10 ng/ml.
- Group 2:Children with height less than the 3rd centile without any etiology
- Group 3:children with failure to thrive until the age of 3 years.
- Group 4: children with obesity defined by BMI above the 90th centile for age and sex.
- Group 5: children with no endocrine diseases and without obesity or short stature.
Key exclusion criteria (1 listed)
- Children with known pediatric or endocrine diseases.
Eligibility is decided by the study team after screening; this overview does not establish that a patient qualifies. Full inclusion and exclusion criteria.
Primary outcome
Not reported in the source record.
Results and safety
The study is completed, but results are not available in the source record. That does not mean the treatment did or did not work.
Research links
- Official record on ClinicalTrials.govLast updated by the sponsor 3 Jul 2015.
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Referral and contact
AzTrials does not enrol participants or take referrals. Contact the study team or a site listed below; they decide who can take part. This study is not recruiting at the moment.
Yardena Tenenbaum-Rakover, MD principal investigator
Ha"Emek Medical Center, Afula, ISRAEL
Questions about this trial
What is this clinical trial studying?
An observational study of Obesity and Short Stature, run by HaEmek Medical Center, Israel.
The full registered description is in the About this study section and the official record.
Who may be eligible to take part?
The sponsor lists 5 inclusion and 1 exclusion criteria. Eligibility is decided by the study team after screening, so read the full criteria and contact a listed site.
Is this clinical trial currently recruiting?
The record says: finished, as of the sponsor's last update on 3 Jul 2015. Status can change between updates, so confirm with the study contact before making plans.
What are the possible benefits and risks?
They depend on the study and the treatment, and no study can promise a benefit. The study team explains the known risks during informed consent, before anyone joins; the record itself does not list them.
Are results available for this study?
The study is completed, but results are not available in the source record. That does not mean the treatment did or did not work.
How can a doctor refer a patient or contact the research team?
The record lists no contact. The official record names the sponsor, who can be asked directly. AzTrials does not enrol participants or take referrals.
Where can I read the original study information?
Does a listing mean the treatment is approved or proven to work?
No. A listing means the study is registered. It does not show that the treatment is safe, works, or is approved by a regulator.
How often is this information updated?
AzTrials copies changed records from ClinicalTrials.gov every night and reloads the whole registry every week. The sponsor last updated this record on 3 Jul 2015.