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Study of the Molecular Basis in the Pathophysiology of Food Intake and Growth in Children

NCT00830141 · Status: COMPLETED · Type: OBSERVATIONAL · Enrollment: 259

Last updated 2015-07-03

No results posted yet for this study

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 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.

Conditions

Sponsors & Collaborators

  • HaEmek Medical Center, Israel

    lead OTHER

Principal Investigators

  • Yardena Tenenbaum-Rakover, MD · Ha"Emek Medical Center, Afula, ISRAEL

Eligibility

Max Age
18 Years
Sex
ALL
Healthy Volunteers
No

Timeline & Regulatory

Start
2009-01-31
Primary Completion
2011-01-31
Completion
2012-01-31

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Entities

Diseases

Read the full study record

This page highlights key information. For complete eligibility criteria, study locations, investigator contacts, and the full protocol, visit the original record on ClinicalTrials.gov.

View NCT00830141 on ClinicalTrials.gov