Introduction Prader-Willi syndrome (PWS) is a complicated neurodevelopmental genetic disorder stemming from the loss of expression imprinted genes within 15q11-q13 region. It characterized by impaired hypothalamic development and function. Infants with PWS typically present hypotonia feeding difficulties, which in later stages childhood progress to hyperphagia, obesity, endocrine dysfunctions. ...

Leptin is vital for maintaining energy homeostasis, by controlling food intake and regulating expenditure (fatty acids). It also participates in glycemic thyroid activity, reproductive immune functions. resistance a phenomenon that appears gradually does not simultaneously affect all organs tissues equally. In models of obesity induced high-fat diet, leptin initially manifests the hypothalamus....

Brown adipose tissue-deficient [uncoupling protein (UCP)-promoter-driven diphtheria toxin A (DTA)] mice develop obesity as a result of both decreased energy expenditure and hyperphagia. The hyperphagia occurs despite high serum leptin levels. Hence, this is a model of leptin-resistant obesity in which the mechanism driving hyperphagia is unknown. Leptin is a regulator of a number of hypothalami...

BACKGROUND Prader-Willi syndrome (PWS) is a genetic, neurodevelopmental disorder characterized by intellectual disabilities, growth hormone dysregulation, hyperphagia, increased risks of morbid obesity, compulsive behaviors, and irritability. As aberrant serotonergic functioning is strongly implicated in PWS, we examined associations between the PWS phenotype and polymorphisms in tryptophan hyd...

Zucker obese (fa/fa) and lean (Fa/Fa) rats were fed a soy protein diet ad libitum under barrier conditions from 4 wk of age until death. Obese rats were also pair fed with lean controls to prevent hyperphagia. Time of death was determined and tissues collected at necropsy for histologic examination. Lean rats had longer 10th percentile survivorship (males 966 compared with 667 d, females 983 co...