View clinical trials related to Syndromic Obesity.
Filter by:Syndromic obesity are rare forms of obesity (1% of cases), involving severe obesity and early to multi organ involvement (mental retardation, dysmorphic, sensorineural damage and / or endocrine). To date, the genetic defects are identified in only 5% of cases (Prader-Willi syndrome, Bardet-Biedl syndrome, mutation of leptin or its receptor, the proconvertase-1, proopiomelanocortin or SIM-1 and TRKB genes, high resolution karyotype or abnormal DNA chips, ...). Precocity and severity of obesity are those for a little dependent genetic environment. The investigators aim is to identify new gene variants in subjects with syndromic obesity sharing common phenotypic features.
The overall objective is to explore the mechanisms by which macronutrients regulate food intake and weight gain in Prader Willi Syndrome (PWS). Previous studies from the investigators' labs suggest that the increased appetite of PWS may be triggered or maintained by an increase in the levels of ghrelin, an appetite-stimulating hormone produced primarily by the stomach. This study will compare the effects of low carbohydrate diet versus low fat diet on levels of ghrelin, appetite suppressing hormones and markers of insulin sensitivity in patients with PWS. The investigators hypothesize that the low carbohydrate diet will suppress plasma active ghrelin and increase appetite-suppressing hormones to a greater degree and for longer duration than the low fat diet and will thereby reduce hyperphagia and increase satiety. The investigators also hypothesize that the low carb diet will improve hormonal and metabolic markers (fatty acids, amino acids and organic acids) of insulin sensitivity and inflammatory cytokine profiles of children with PWS.
Comparative genomic hybridization (CGH) array technology has been used in numerous studies on mental retardation, and few chromosomal abnormalities have been identified in patients. Because chromosomal abnormalities have still been associated with obesity, we can expect that syndromic obesity is also associated with small deletions/duplications. Characterization of deleted or duplicated loci in these obese patients would mean that these loci include genes implicated in obesity. This will permit to propose new gene(s) involved in obesity. (In french: Caractérisation phénotypique et recherche de REManiements chromosomiques chez des patients présentant une OBésité syndromique de cause non identifiée : REMOB)