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The purpose of this study is to investigate the effects of a GLP-1 agonist on satiety hormones in patients with Prader-Willi Syndrome (genetic defect causing obesity).
Prader-Willi Syndrome (PWS) is the most frequent known genetic disorder of obesity. Hyperphagia is the main barrier to independent living in adults with PWS, and hitherto behavioural restraints and environmental modification are the only effective management measure. The emerging costs for professional care are immense. Thus, there is an urgent need for treatment which reduce appetite and food intake in this patient group. Agonists of the gut derived hormone GLP-1 which reduces food intake and causes weight loss due to slowed gastric emptying and through direct central effects. The aim of this pilot drug trial is to analyse the effect of a GLP-1 agonist on appetite regulating hormones, insulin secretion and energy expenditure before and after a meal.
Allocation: Randomized, Control: Placebo Control, Endpoint Classification: Efficacy Study, Intervention Model: Crossover Assignment, Masking: Double Blind (Subject, Investigator), Primary Purpose: Treatment
Garvan Institute of Medical Research
New South Wales
Garvan Institute of Medical Research
Published on BioPortfolio: 2014-08-27T03:35:23-0400
The purpose of the study is to find out if people with Prader-Willi syndrome have a difference in the protein which changes inactive cortisone to the active stress hormone cortisol.
The objective of this study is to collect data on tolerance and effects of early treatment with oxytocin in children with Prader Willi Syndrome aged from 3 to 4 years and to compare these ...
The purpose of this is study is to evaluate the long term safety of DCCR (diazoxide choline controlled release tablets) in children and adults with Prader-Willi syndrome.
The purpose of this study is to evaluate the effects of a once daily subcutaneous (SC) injectable formulation of RM-493 in obese subjects with Prader-Willi syndrome on tolerability, weight...
The aim of this study is to evaluate efficacy, safety, and pharmacokinetics of GLWL-01 in the treatment of patients with Prader-Willi Syndrome (PWS).
Prader Willi syndrome is characterized not only by hyperphagia frequently resulting in obesity, but also by endocrine dysfunction across a variety of axes. This article reviews the most recent literat...
This study aimed to measure quality of life (QOL) in primary caregivers of young childrenwith Prader-Willi syndrome (PWS).
Prader-Willi syndrome (PWS) is a complex genetic condition characterized by hyperphagia, hypotonia, low muscle mass, excess body fat, developmental delays, intellectual disability, behavioral problems...
Data sharing is not applicable to this article as no new data were created or analyzed in this study. We would like to thank the authors for their commentary as it gives us the opportunity to repeat o...
Prader-Willi syndrome (PWS) and recurrent 15q13.3 microdeletion syndrome can be caused by genomic rearrangements in the complex 15q11q13 chromosomal region. Here, we describe the first female child wi...
An autosomal dominant disorder caused by deletion of the proximal long arm of the paternal chromosome 15 (15q11-q13) or by inheritance of both of the pair of chromosomes 15 from the mother (UNIPARENTAL DISOMY) which are imprinted (GENETIC IMPRINTING) and hence silenced. Clinical manifestations include MENTAL RETARDATION; MUSCULAR HYPOTONIA; HYPERPHAGIA; OBESITY; short stature; HYPOGONADISM; STRABISMUS; and HYPERSOMNOLENCE. (Menkes, Textbook of Child Neurology, 5th ed, p229)
Condition with a variable constellation of phenotypes due to deletion polymorphisms at chromosome location 22q11. It encompasses several syndromes with overlapping abnormalities including the DIGEORGE SYNDROME, VELOCARDIOFACIAL SYNDROME, and CONOTRUNCAL AMOMALY FACE SYNDROME. In addition, variable developmental problems and schizoid features are also associated with this syndrome. (From BMC Med Genet. 2009 Feb 25;10:16) Not all deletions at 22q11 result in the 22q11deletion syndrome.
Rare congenital disorder with multiple anomalies including: characteristic dysmorphic craniofacial features, musculoskeletal abnormalities, neurocognitive delay, and high prevalence of cancer. Germline mutations in H-Ras protein can cause Costello syndrome. Costello syndrome shows early phenotypic overlap with other disorders that involve MAP KINASE SIGNALING SYSTEM (e.g., NOONAN SYNDROME and cardiofaciocutaneous syndrome).
An autosomal dominant aneurysm with multisystem abnormalities caused by increased TGF-BETA signaling due to mutations in type I or II of TGF-BETA RECEPTOR. Additional craniofacial features include CLEFT PALATE; CRANIOSYNOSTOSIS; HYPERTELORISM; or bifid uvula. Phenotypes closely resemble MARFAN SYNDROME; Marfanoid craniosynostosis syndrome (Shprintzen-Goldberg syndrome); and EHLERS-DANLOS SYNDROME.
Birth defect that results in a partial or complete absence of the CORPUS CALLOSUM. It may be isolated or a part of a syndrome (e.g., AICARDI'S SYNDROME; ACROCALLOSAL SYNDROME; ANDERMANN SYNDROME; and HOLOPROSENCEPHALY). Clinical manifestations include neuromotor skill impairment and INTELLECTUAL DISABILITY of variable severity.
Diabetes Diabetes Endocrine Disorders Obesity Oxycontin Renal Disease Thyroid Disorders Endocrinology is the study of the endocrine glands and the hormones that they secrete (Oxford Medical Dictionary). There are several g...
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Food is any substance consumed to provide nutritional support for the body. It is usually of plant or animal origin, and contains essential nutrients, such as carbohydrates, fats, proteins, vitamins, or minerals. The substance is ingested by an organism ...