Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020505 (hyperphagia)
 6,116 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We tested if there were any differences about nocturnal and diurnal anxiety between patients either affected by Binge Eating Disorder (BED) or Night eating Syndrome (NES). Fifty four patients affected by BED, 13 by NES and 16 by both BED and NES were tested using the Self Rating Anxiety Scale (SAS) and the Sleep Disturbance Questionnaire (SDQ). Their nocturnal eating behavior was ascertained through the Night Eating Questionnaire (NEQ). Patients affected by both BED and NES scored significantly higher on SAS than other patients. Among NES patients we found a correlation between a SDQ subscale and two subscales of the NEQ. Among BED patients we found a correlation between SAS scores and the nocturnal ingestion subscale of the NEQ. Nocturnal eating is related to nocturnal anxiety among NES patients while it is related to diurnal anxiety among patients affected by BED. These findings support the hypothesis that BED and NES are distinct syndromes sharing overeating but with different pathways to excessive food intake.
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PMID:Daily and nightly anxiety among patients affected by night eating syndrome and binge eating disorder. 1924 43

Smith-Magenis syndrome (SMS) is a genetic disorder caused by haploinsufficiency of the retinoic acid induced 1 (RAI1) gene. In addition to intellectual disabilities, behavioral abnormalities and sleep disturbances, a majority of children with SMS also have significant early-onset obesity. To study the role of RAI1 in obesity, we investigated the growth and obesity phenotype in a mouse model haploinsufficient for Rai1. Data show that Rai1(+/-) mice are hyperphagic, have an impaired satiety response and have altered abdominal and subcutaneous fat distribution, with Rai1(+/-) female mice having a higher proportion of abdominal fat when compared with wild-type female mice. Expression analyses revealed that Bdnf (brain-derived neurotrophic factor), a gene previously associated with hyperphagia and obesity, is downregulated in the Rai1(+/-) mouse hypothalamus, and reporter studies show that RAI1 directly regulates the expression of BDNF. Even though the Rai1(+/-) mice are significantly obese, serum analyses do not reveal any evidence of metabolic syndrome. Supporting these findings, a caregiver survey revealed that even though a high incidence of abdominal obesity is observed in females with SMS, they did not exhibit a higher incidence of indicators of metabolic syndrome above the general population. We conclude that Rai1 haploinsufficiency represents a single-gene model of obesity with hyperphagia, abnormal fat distribution and altered hypothalamic gene expression associated with satiety, food intake, behavior and obesity. Linking RAI1 and BDNF provides a more thorough understanding of the role of Rai1 in growth and obesity and insight into the complex pathogenicity of obesity, behavior and sex-specific differences in adiposity.
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PMID:Rai1 haploinsufficiency causes reduced Bdnf expression resulting in hyperphagia, obesity and altered fat distribution in mice and humans with no evidence of metabolic syndrome. 2066 24

Sleep and feeding rhythms are highly coordinated across the circadian cycle, but the brain sites responsible for this coordination are unknown. We examined the role of neuropeptide Y (NPY) receptor-expressing neurons in the mediobasal hypothalamus (MBH) in this process by injecting the targeted toxin, NPY-saporin (NPY-SAP), into the arcuate nucleus (Arc). NPY-SAP-lesioned rats were initially hyperphagic, became obese, exhibited sustained disruption of circadian feeding patterns, and had abnormal circadian distribution of sleep-wake patterns. Total amounts of rapid eye movement sleep (REMS) and non-REMS (NREMS) were not altered by NPY-SAP lesions, but a peak amount of REMS was permanently displaced to the dark period, and circadian variation in NREMS was eliminated. The phase reversal of REMS to the dark period by the lesion suggests that REMS timing is independently linked to the function of MBH NPY receptor-expressing neurons and is not dependent on NREMS pattern, which was altered but not phase reversed by the lesion. Sleep-wake patterns were altered in controls by restricting feeding to the light period, but were not altered in NPY-SAP rats by restricting feeding to either the light or dark period, indicating that disturbed sleep-wake patterns in lesioned rats were not secondary to changes in food intake. Sleep abnormalities persisted even after hyperphagia abated during the static phase of the lesion. Results suggest that the MBH is required for the essential task of integrating sleep-wake and feeding rhythms, a function that allows animals to accommodate changeable patterns of food availability. NPY receptor-expressing neurons are key components of this integrative function.
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PMID:Circadian integration of sleep-wake and feeding requires NPY receptor-expressing neurons in the mediobasal hypothalamus. 2188 Aug 63

The diagnostic criteria for the Night Eating Syndrome (NES) published in 2010 require the presence of two core criteria: evening hyperphagia and/or nocturnal awakenings for ingestion of food and three of five diagnostic descriptors. One of the descriptors is as follows: "The belief that one must eat in order to fall asleep". In this study we evaluated whether this conviction is significantly more prominent in obese individuals suffering from insomnia and nocturnal eating, than among obese patients with insomnia who do not eat at night. Ninety-eight obese subjects afflicted by insomnia were included in this study. Eight were affected by NES, 33 by Binge Eating Disorder (BED), and 13 by both BED and NES. Subjects' insomnia and sleep disturbances were assessed using the Insomnia Severity Index and the Sleep Disturbance Questionnaire. The presence of the belief that one must eat at night in order to sleep was evaluated with the question: "Do you need to eat in order to get back to sleep when you wake up at night?" Patients affected by NES and by both BED and NES were convinced that nocturnal food intake was necessary in order to fall back asleep after a night time awakening. The presence of this belief seemed to be a critical factor in identifying the presence of the Night Eating Syndrome among obese subjects suffering from insomnia.
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PMID:Clinical validity of the descriptor. "presence of a belief that one must eat in order to get to sleep" in diagnosing the Night Eating Syndrome. 2436 11

Obesity has become a major health risk in industrialized countries, with disturbed sleep identified as a correlate. This study used data drawn from Taiwan's 2005 Social Development Trend Survey on Health and Safety and the propensity-score-matching method to shed light on gender-specific associations between sleep problems and obesity among 24,113 adults aged 20-64 years. The average increase in obesity prevalence among respondents with disrupted sleep was 1.85%, as compared to those who did not report disrupted sleep, with similar psycho-social attributes. Similarly, the prevalence of obesity among those who reported restless sleep was increased by an average of 1.40% compared to those who did not report restless sleep with similar psycho-social attributes. We also found gender-specific vulnerability to different types of sleep problems. Among men who reported disrupted sleep, we found a 3.12% increase in the prevalence of obesity. Among women exposed to restless sleep, the increase in obesity prevalence was 1.84%. The observed gender difference in the prevalence of increases in obesity may be attributed to gender-specific behavioral responses to poor sleep. With poor sleep, men may respond to hunger by overeating; women may respond by physical inactivity. Both can contribute to an elevated risk of obesity.
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PMID:Gender, sleep problems, and obesity in Taiwan: a propensity-score-matching approach. 2566 54

The development of hypothalamic obesity (HO) following craniopharyngioma (CP) and other suprasellar tumors leads to reduced patient quality of life. No treatment algorithms are currently available for management of HO. Depending on which hypothalamic nuclei are destroyed, the pathophysiologic mechanisms and clinical symptoms that contribute to HO differ among patients. Herein, we review the contribution of the hypothalamus to the pathophysiologic mechanisms and symptoms underlying CP-associated HO. Additionally, we performed a systematic search of MEDLINE and Embase to identify all intervention studies for weight management in patients with CP or other suprasellar tumors published until September 2017. The search yielded 1866 publications, of which 40 were included. Of these 40 studies, we identified four modalities for intervention (i.e., lifestyle, dietary, pharmacotherapeutic, or surgical) within six clinical domains (i.e., psychosocial disorders, hyperphagia, sleep disturbances, decreased energy expenditure, hyperinsulinemia, and hypopituitarism). We used the findings from our systematic review, in addition to current knowledge on the pathophysiology of HO, to develop an evidence-based treatment algorithm for patients with HO caused by CP or other suprasellar tumors. Although the individual effects of the HO interventions were modest, beneficial individual effects may be achieved when the pathophysiologic background and correct clinical domain are considered. These two aspects can be combined in an individualized treatment algorithm with a stepwise approach for each clinical domain. Recently elucidated targets for HO intervention were also explored to improve future management of HO for patients with CP and other suprasellar tumors.
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PMID:Pathophysiology and Individualized Treatment of Hypothalamic Obesity Following Craniopharyngioma and Other Suprasellar Tumors: A Systematic Review. 3024 42

Advances in technologies offer new opportunities to collect and integrate data from a broad range of sources to advance the understanding of rare diseases and support the development of new treatments. Prader-Willi syndrome (PWS) is a rare, complex neurodevelopmental disorder, which has a variable and incompletely understood natural history. PWS is characterized by early failure to thrive, followed by the onset of excessive appetite (hyperphagia). Additional characteristics include multiple endocrine abnormalities, hypotonia, hypogonadism, sleep disturbances, a challenging neurobehavioral phenotype, and cognitive disability. The Foundation for Prader-Willi Research's Global PWS Registry is one of more than twenty-five registries developed to date through the National Organization of Rare Disorders (NORD) IAMRARE Registry Program. The Registry consists of surveys covering general medical history, system-specific clinical complications, diet, medication and supplement use, as well as behavior, mental health, and social information. Information is primarily parent/caregiver entered. The platform is flexible and allows addition of new surveys, including updatable and longitudinal surveys. Launched in 2015, the PWS Registry has enrolled 1696 participants from 37 countries, with 23,550 surveys completed. This resource can improve the understanding of PWS natural history and support medical product development for PWS.
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PMID:The Global Prader-Willi Syndrome Registry: Development, Launch, and Early Demographics. 3154 Jan 8