Database : MEDLINE
Search on : Hyperphagia [Words]
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[PMID]: 29524451
[Au] Autor:Warren KR; Wehring HJ; Liu F; McMahon RP; Chen S; Chester C; Kelly DL
[Ad] Address:Maryland Psychiatric Research Center, University of Maryland, School of Medicine, PO Box 21247, Baltimore, MD 21228, United States; Morgan State University, Department of Psychology, 1700 East Cold Spring Lane, Baltimore, MD 21215, United States.
[Ti] Title:Effects of intranasal oxytocin on satiety signaling in people with schizophrenia.
[So] Source:Physiol Behav;, 2018 Mar 07.
[Is] ISSN:1873-507X
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Overweight and obesity in schizophrenia are prevalent, affecting half to three-quarters of people with schizophrenia. Hyperphagia and increased meal size have also been implicated as significant contributors to the weight gain problem. Oxytocin has shown to play a role in appetite control in humans and is considered an anorexigenic peptide. This two-day, within-subjects, challenge study involved the examination of satiety after administration of 24 IU oxytocin (intranasal) vs. placebo in participants with a DSM-IV diagnosis of schizophrenia (N = 16). Self reported satiety along with a preload-test meal paradigm were utilized as well as related laboratory measures (insulin, glucose, and leptin), and measures of taste and smell. There were no statistically significant differences between the groups on self-reported satiety or test meal consumption, insulin or glucose levels, or sensory measures. A significant treatment difference was found (F = 5.22, df = 1,97.6, p = 0.025), with a decrease in leptin in the oxytocin group post-administration, but no time effect (F = 1.67, df = 6,95.1, p = 0.180) or treatment by time interaction (F = 1.36. df = 3,4.16, p = 0.261). Despite the small sample and mostly negative findings, we encourage more work to use higher and repeated doses of oxytocin, and to further examine the effect of oxytocin on leptin in schizophrenia as this may be important for understanding both weight control and psychopathology.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  2 / 5314 MEDLINE  
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[PMID]: 29472710
[Au] Autor:Morris A
[Ti] Title:Genetics: Functional link to hyperphagia in PWS.
[So] Source:Nat Rev Endocrinol;14(4):192, 2018 Apr.
[Is] ISSN:1759-5037
[Cp] Country of publication:England
[La] Language:eng
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:In-Data-Review
[do] DOI:10.1038/nrendo.2018.19

  3 / 5314 MEDLINE  
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[PMID]: 29457782
[Au] Autor:Kim GH; Shi G; Somlo DR; Haataja L; Song S; Long Q; Nillni EA; Low MJ; Arvan P; Myers MG; Qi L
[Ad] Address:Department of Molecular & Integrative Physiology, University of Michigan Medical School, Ann Arbor, Michigan, USA.
[Ti] Title:Hypothalamic ER-associated degradation regulates POMC maturation, feeding, and age-associated obesity.
[So] Source:J Clin Invest;128(3):1125-1140, 2018 Mar 01.
[Is] ISSN:1558-8238
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Pro-opiomelanocortin (POMC) neurons function as key regulators of metabolism and physiology by releasing prohormone-derived neuropeptides with distinct biological activities. However, our understanding of early events in prohormone maturation in the ER remains incomplete. Highlighting the significance of this gap in knowledge, a single POMC cysteine-to-phenylalanine mutation at position 28 (POMC-C28F) is defective for ER processing and causes early onset obesity in a dominant-negative manner in humans through an unclear mechanism. Here, we report a pathologically important role of Sel1L-Hrd1, the protein complex of ER-associated degradation (ERAD), within POMC neurons. Mice with POMC neuron-specific Sel1L deficiency developed age-associated obesity due, at least in part, to the ER retention of POMC that led to hyperphagia. The Sel1L-Hrd1 complex targets a fraction of nascent POMC molecules for ubiquitination and proteasomal degradation, preventing accumulation of misfolded and aggregated POMC, thereby ensuring that another fraction of POMC can undergo normal posttranslational processing and trafficking for secretion. Moreover, we found that the disease-associated POMC-C28F mutant evades ERAD and becomes aggregated due to the presence of a highly reactive unpaired cysteine thiol at position 50. Thus, this study not only identifies ERAD as an important mechanism regulating POMC maturation within the ER, but also provides insights into the pathogenesis of monogenic obesity associated with defective prohormone folding.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:In-Data-Review

  4 / 5314 MEDLINE  
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[PMID]: 29376891
[Au] Autor:Rodriguez JA; Zigman JM
[Ad] Address:Division of Hypothalamic Research, Department of Internal Medicine.
[Ti] Title:Hypothalamic loss of Snord116 and Prader-Willi syndrome hyperphagia: the buck stops here?
[So] Source:J Clin Invest;128(3):900-902, 2018 Mar 01.
[Is] ISSN:1558-8238
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Hyperphagia and obesity are the best-known manifestations of Prader-Willi syndrome (PWS) and are responsible for most of the overall morbidity and mortality associated with the disease. Yet these PWS symptoms remain poorly understood and without effective pharmacologic therapies. Mouse models attempting to recapitulate both the genetic alterations and marked hyperphagia plus obesity of PWS have been enigmatic, leading to skepticism about the use of mouse models to investigate PWS. In this issue of the JCI, Polex-Wolf and colleagues challenge the skeptics by successfully inducing hyperphagia following bilateral mediobasal hypothalamic deletion of the Snord116 gene from adult mice. Obesity also resulted, although only in a subset of mice. While this approach represents an exciting advance, highlighting a pathologic effect of loss of mediobasal hypothalamic Snord116 expression on the development of PWS's hallmark symptoms, the variability in the body-weight and body composition responses to this site-selective gene deletion raises several questions.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1801
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:In-Data-Review

  5 / 5314 MEDLINE  
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[PMID]: 29376887
[Au] Autor:Polex-Wolf J; Lam BY; Larder R; Tadross J; Rimmington D; Bosch F; Cenzano VJ; Ayuso E; Ma MK; Rainbow K; Coll AP; O'Rahilly S; Yeo GS
[Ad] Address:Medical Research Council (MRC) Metabolic Diseases Unit, University of Cambridge Metabolic Research Laboratories, Wellcome Trust-MRC Institute of Metabolic Science, Addenbrooke's Hospital, Cambridge, United Kingdom.
[Ti] Title:Hypothalamic loss of Snord116 recapitulates the hyperphagia of Prader-Willi syndrome.
[So] Source:J Clin Invest;128(3):960-969, 2018 Mar 01.
[Is] ISSN:1558-8238
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Profound hyperphagia is a major disabling feature of Prader-Willi syndrome (PWS). Characterization of the mechanisms that underlie PWS-associated hyperphagia has been slowed by the paucity of animal models with increased food intake or obesity. Mice with a microdeletion encompassing the Snord116 cluster of noncoding RNAs encoded within the Prader-Willi minimal deletion critical region have previously been reported to show growth retardation and hyperphagia. Here, consistent with previous reports, we observed growth retardation in Snord116+/-P mice with a congenital paternal Snord116 deletion. However, these mice neither displayed increased food intake nor had reduced hypothalamic expression of the proprotein convertase 1 gene PCSK1 or its upstream regulator NHLH2, which have recently been suggested to be key mediators of PWS pathogenesis. Specifically, we disrupted Snord116 expression in the mediobasal hypothalamus in Snord116fl mice via bilateral stereotaxic injections of a Cre-expressing adeno-associated virus (AAV). While the Cre-injected mice had no change in measured energy expenditure, they became hyperphagic between 9 and 10 weeks after injection, with a subset of animals developing marked obesity. In conclusion, we show that selective disruption of Snord116 expression in the mediobasal hypothalamus models the hyperphagia of PWS.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1801
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:In-Data-Review

  6 / 5314 MEDLINE  
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[PMID]: 29220529
[Au] Autor:Hsu EA; Miller JL; Perez FA; Roth CL
[Ad] Address:Department of Psychiatry, Kaiser Permanente Medical Center, Oakland, California.
[Ti] Title:Oxytocin and Naltrexone Successfully Treat Hypothalamic Obesity in a Boy Post-Craniopharyngioma Resection.
[So] Source:J Clin Endocrinol Metab;103(2):370-375, 2018 Feb 01.
[Is] ISSN:1945-7197
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Context: Hypothalamic obesity, a treatment-resistant condition common to survivors of craniopharyngioma (CP), is strongly associated with a poor quality of life in this population. Oxytocin (OT), a hypothalamic neuropeptide, has been shown to play a role in the regulation of energy balance and to have anorexigenic effects in animal studies. Naltrexone (NAL), an opiate antagonist, has been shown to deter hedonic eating and to potentiate OT's effects. Design: In this parent-observed study, we tested the administration of intranasal OT for 10 weeks (phase 1), followed by a combination of intranasal OT and NAL for 38 weeks (phase 2) in a 13-year-old male with confirmed hypothalamic obesity and hyperphagia post-CP resection. Treatment resulted in 1) reduction in body mass index (BMI) z score from 1.77 to 1.49 over 10 weeks during phase 1; 2) reduction in BMI z score from 1.49 to 0.82 over 38 weeks during phase 2; 3) reduced hyperphagia during phases 1 and 2; 4) continued hedonic high-carbohydrate food-seeking in the absence of hunger during phases 1 and 2; and 5) sustained weight reduction during decreased parental monitoring and free access to unlocked food in the home during the last 10 weeks of phase 2. Conclusion: This successful intervention of CP-related hypothalamic obesity and hyperphagia by OT alone and in combination with NAL is promising for conducting future studies of this treatment-recalcitrant form of obesity.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1712
[Cu] Class update date: 180308
[Lr] Last revision date:180308
[St] Status:In-Data-Review
[do] DOI:10.1210/jc.2017-02080

  7 / 5314 MEDLINE  
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[PMID]: 29507217
[Au] Autor:Lanaspa MA; Kuwabara M; Andres-Hernando A; Li N; Cicerchi C; Jensen T; Orlicky DJ; Roncal-Jimenez CA; Ishimoto T; Nakagawa T; Rodriguez-Iturbe B; MacLean PS; Johnson RJ
[Ad] Address:Division of Renal Diseases and Hypertension, University of Colorado Anschutz Medical Campus, Aurora, CO 80045; miguel.lanaspagarcia@ucdenver.edu.
[Ti] Title:High salt intake causes leptin resistance and obesity in mice by stimulating endogenous fructose production and metabolism.
[So] Source:Proc Natl Acad Sci U S A;, 2018 Mar 05.
[Is] ISSN:1091-6490
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Dietary guidelines for obesity typically focus on three food groups (carbohydrates, fat, and protein) and caloric restriction. Intake of noncaloric nutrients, such as salt, are rarely discussed. However, recently high salt intake has been reported to predict the development of obesity and insulin resistance. The mechanism for this effect is unknown. Here we show that high intake of salt activates the aldose reductase-fructokinase pathway in the liver and hypothalamus, leading to endogenous fructose production with the development of leptin resistance and hyperphagia that cause obesity, insulin resistance, and fatty liver. A high-salt diet was also found to predict the development of diabetes and nonalcoholic fatty liver disease in a healthy population. These studies provide insights into the pathogenesis of obesity and diabetes and raise the potential for reduction in salt intake as an additional interventional approach for reducing the risk for developing obesity and metabolic syndrome.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180306
[Lr] Last revision date:180306
[St] Status:Publisher

  8 / 5314 MEDLINE  
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[PMID]: 29435959
[Au] Autor:Leigh SJ; Lee F; Morris MJ
[Ad] Address:Department of Pharmacology, School of Medical Sciences, UNSW Sydney, Sydney, NSW, 2052, Australia.
[Ti] Title:Hyperpalatability and the Generation of Obesity: Roles of Environment, Stress Exposure and Individual Difference.
[So] Source:Curr Obes Rep;7(1):6-18, 2018 Mar.
[Is] ISSN:2162-4968
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:PURPOSE OF REVIEW: This review investigates how exposure to palatable food and its associated cues alters appetite regulation and feeding behaviour to drive overeating and weight gain. RECENT FINDINGS: Both supraphysiological and physiological feeding systems are affected by exposure to palatable foods and its associated cues. Preclinical research, largely using rodents, has demonstrated that palatable food modulates feeding-related neural systems and food-seeking behaviour by recruiting the mesolimbic reward pathway. This is supported by studies in adolescents which have shown that mesolimbic activity in response to palatable food cues and consumption predicts future weight gain. Additionally, stress exposure, environmental factors and individual susceptibility have been shown to modulate the effects of highly palatable foods on behaviour. Further preclinical research using free-choice diets modelling the modern obesogenic environment is needed to identify how palatable foods drive overeating. Moreover, future clinical research would benefit from more appropriate quantification of palatability, making use of rating systems and surveys.
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Em] Entry month:1802
[Cu] Class update date: 180305
[Lr] Last revision date:180305
[St] Status:In-Process
[do] DOI:10.1007/s13679-018-0292-0

  9 / 5314 MEDLINE  
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[PMID]: 29496979
[Au] Autor:McCarthy JM; McCann-Crosby BM; Rech ME; Yin J; Chen CA; Ali MA; Nguyen HN; Miller JL; Schaaf CP
[Ad] Address:Jan and Dan Duncan Neurological Research Institute at Texas Children's Hospital, Houston, Texas, USA.
[Ti] Title:Hormonal, metabolic and skeletal phenotype of Schaaf-Yang syndrome: a comparison to Prader-Willi syndrome.
[So] Source:J Med Genet;, 2018 Mar 01.
[Is] ISSN:1468-6244
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:BACKGROUND: Nonsense and frameshift mutations in the maternally imprinted, paternally expressed gene located in the Prader-Willi critical region 15q11-15q13, have been reported to cause Schaaf-Yang syndrome (SYS), a genetic disorder that manifests as developmental delay/intellectual disability, hypotonia, feeding difficulties and autism spectrum disorder. Prader-Willi syndrome (PWS) is a genetic disorder characterised by severe infantile hypotonia, hypogonadotrophic hypogonadism, early childhood onset obesity/hyperphagia, developmental delay/intellectual disability and short stature. Scoliosis and growth hormone insufficiency are also prevalent in PWS.There is extensive documentation of the endocrine and metabolic phenotypes for PWS, but not for SYS. This study served to investigate the hormonal, metabolic and body composition phenotype of SYS and its potential overlap with PWS. METHODS: In nine individuals with SYS (5 female/4 male; aged 5-17 years), we measured serum ghrelin, glucose, insulin-like growth factor 1 (IGF-1), insulin-like growth factor binding protein 3, follicle-stimulating hormone, luteinising hormone, thyroid-stimulating hormone, free T4, uric acid and testosterone, and performed a comprehensive lipid panel. Patients also underwent X-ray and dual-energy X-ray absorptiometry analyses to assess for scoliosis and bone mineral density. RESULTS: Low IGF-1 levels despite normal weight/adequate nutrition were observed in six patients, suggesting growth hormone deficiency similar to PWS. Fasting ghrelin levels were elevated, as seen in individuals with PWS. X-rays revealed scoliosis >10 in three patients, and abnormal bone mineral density in six patients, indicated by Z-scores of below -2 SDs. CONCLUSION: This is the first analysis of the hormonal, metabolic and body composition phenotype of SYS. Our findings suggest that there is marked, but not complete overlap between PWS and SYS.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180302
[Lr] Last revision date:180302
[St] Status:Publisher

  10 / 5314 MEDLINE  
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[PMID]: 29425059
[Au] Autor:Ehrhart F; Janssen KJM; Coort SL; Evelo CT; Curfs LMG
[Ad] Address:a GCK , Maastricht University Medical Centre , Maastricht , The Netherlands.
[Ti] Title:Prader-Willi syndrome and Angelman syndrome: Visualisation of the molecular pathways for two chromosomal disorders.
[So] Source:World J Biol Psychiatry;:1-13, 2018 Mar 01.
[Is] ISSN:1814-1412
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:OBJECTIVES: Prader-Willi syndrome (PWS) and Angelman syndrome (AS) are two syndromes that are caused by the same chromosomal deletion on 15q11.2-q13. Due to methylation patterns, different genes are responsible for the two distinct phenotypes resulting in the disorders. Patients of both disorders exhibit hypotonia in neonatal stage, delay in development and hypopigmentation. Typical features for PWS include hyperphagia, which leads to obesity, the major cause of mortality, and hypogonadism. In AS, patients suffer from a more severe developmental delay, they have a distinctive behaviour that is often described as unnaturally happy, and a tendency for epileptic seizures. For both syndromes, we identified and visualised molecular downstream pathways of the deleted genes that could give insight on the development of the clinical features. METHODS: This was done by consulting literature, genome browsers and pathway databases to identify molecular interactions and to construct downstream pathways. RESULTS: A pathway visualisation was created and uploaded to the open pathway database WikiPathways covering all molecular pathways that were found. CONCLUSIONS: The visualisation of the downstream pathways of PWS- and AS-deleted genes shows that some of the typical symptoms are caused by multiple genes and reveals critical gaps in the current knowledge.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180301
[Lr] Last revision date:180301
[St] Status:Publisher
[do] DOI:10.1080/15622975.2018.1439594


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