WordNet

a disorder of eating seen among young women who go on eating binges and then feel guilt and depression and self-condemnation (同)binge-eating syndrome
pathologically insatiable hunger (especially when caused by brain lesions)
suffering from bulimia
a person suffering from bulimia

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出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2017/10/30 17:29:16」(JST)

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Polyphagia or hyperphagia is excessive hunger or increased appetite.^[1]

In medicine

In medicine, polyphagia (sometimes known as hyperphagia) is a medical sign meaning excessive hunger and abnormally large intake of solids by mouth. It can be caused by disorders such as diabetes, Kleine–Levin syndrome (a malfunction in the hypothalamus),^{[citation needed]} and the genetic disorders Prader–Willi syndrome and Bardet–Biedl syndrome.^[2] Knocking out vagal nerve receptors has been shown to cause hyperphagia.^[3]

Causes

Causes of increased appetite include:^[4]

Anxiety
Depression
Certain drugs
Diabetes mellitus
Hyperthyroidism
Hypoglycemia
Premenstrual syndrome
Prader–Willi syndrome
Bulimia
Graves' disease
Kleine–Levin syndrome

Diabetic ketoacidosis

Polyphagia usually occurs early in the course of diabetic ketoacidosis.^[5] However, once insulin deficiency becomes more severe and ketoacidosis develops, appetite is suppressed.^[6]

Etymology and pronunciation

The word polyphagia (/ˌpɒliˈfeɪdʒiə/) uses combining forms of poly- + -phagia, from the Greek words πολύς (polys), "very much" or "many", and φαγῶ (phago), "eating" or "devouring".

References

^ Berthoud HR, Lenard NR, Shin AC (2011). "Food reward, hyperphagia, and obesity.". Am J Physiol Regul Integr Comp Physiol. 300 (6): R1266–77. PMC 3119156 . PMID 21411768. doi:10.1152/ajpregu.00028.2011.
^ OMIM::Prader-WilliOMIM::Bardet-Biedl
^ de Lartigue G, Ronveaux CC, Raybould HE (2014). "Deletion of leptin signaling in vagal afferent neurons results in hyperphagia and obesity". MOLECULAR METABOLISM. 3 (6): 595–607. PMC 4142400 . PMID 25161883. doi:10.1016/j.molmet.2014.06.003.
^ Updated by: Linda J. Vorvick, MD, Medical Director and Director of Didactic Curriculum, MEDEX Northwest Division of Physician Assistant Studies, Department of Family Medicine, UW Medicine, School of Medicine, University of Washington, Seattle, WA. Also reviewed David Zieve, MD, MHA, Isla Ogilvie, PhD, and the A.D.A.M. Editorial team. "Appetite - increased". nih.gov.
^ Elliott RE, Jane JA, Wisoff JH (2011). "Surgical management of craniopharyngiomas in children: meta-analysis and comparison of transcranial and transsphenoidal approaches.". Neurosurgery. 69 (3): 630–43; discussion 643. PMID 21499159. doi:10.1227/NEU.0b013e31821a872d.
^ Masuzaki H, Tanaka T, Ebihara K, Hosoda K, Nakao K (2009). "Hypothalamic melanocortin signaling and leptin resistance--perspective of therapeutic application for obesity-diabetes syndrome.". Peptides. 30 (7): 1383–6. PMID 19394382. doi:10.1016/j.peptides.2009.04.008.

External links

Diseases and conditions associated with Polyphagia

UpToDate Contents

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1. プラダーウィリ症候群の臨床的特徴、診断、および治療 clinical features diagnosis and treatment of prader willi syndrome
2. クライネ・レビン症候群（反復性過眠症） kleine levin syndrome recurrent hypersomnia
3. 成人における肥満：病因および自然経過 obesity in adults etiology and natural history
4. 肥満の小児や青年の臨床的評価 clinical evaluation of the obese child and adolescent
5. レプチンの生理学 physiology of leptin

English Journal

Higher plasma orexin A levels in children with Prader-Willi syndrome compared with healthy unrelated sibling controls.

Manzardo AM1, Johnson L1, Miller JL2, Driscoll DJ2, Butler MG1,3.
American journal of medical genetics. Part A.Am J Med Genet A.2016 Aug;170(8):2097-102. doi: 10.1002/ajmg.a.37749. Epub 2016 May 23.
Prader-Willi syndrome (PWS) is a rare genetic neurodevelopmental disorder associated with maladaptive social behavior, hyperphagia, and morbid obesity. Orexin A is a hypothalamic neuropeptide important as a homeostatic regulator of feeding behavior and in energy metabolism through actions in the lat
PMID 27214028

Social change and access to a palatable diet produces differences in reward neurochemistry and appetite in female monkeys.

Michopoulos V1, Diaz MP2, Wilson ME3.
Physiology & behavior.Physiol Behav.2016 Aug 1;162:102-11. doi: 10.1016/j.physbeh.2016.04.023. Epub 2016 Apr 14.
Understanding factors that contribute to the etiology of obesity is critical for minimizing the effects of obesity-related adverse physical health outcomes. Emotional eating or the inability to control intake of calorically dense diets (CDD) under conditions of psychosocial stress exposure is a pote
PMID 27090229

Oligonucleotide-induced alternative splicing of serotonin 2C receptor reduces food intake.

Zhang Z1, Shen M1, Gresch PJ2, Ghamari-Langroudi M3, Rabchevsky AG4, Emeson RB3, Stamm S5.
EMBO molecular medicine.EMBO Mol Med.2016 Jul 12. pii: e201506030. doi: 10.15252/emmm.201506030. [Epub ahead of print]
The serotonin 2C receptor regulates food uptake, and its activity is regulated by alternative pre-mRNA splicing. Alternative exon skipping is predicted to generate a truncated receptor protein isoform, whose existence was confirmed with a new antiserum. The truncated receptor sequesters the full-len
PMID 27406820

Japanese Journal

Physiology : Free Access to Running Wheels Abolishes Hyperphagia in Human Growth Hormone Transgenic Rats

KOMATSUDA Mugiko,YAMANOUCHI Keitaro,MATSUWAKI Takashi [他]
The journal of veterinary medical science 76(7), 993-999, 2014-07
NAID 40020175208

Liraglutide as a Potentially Useful Agent for Regulating Appetite in Diabetic Patients with Hypothalamic Hyperphagia and Obesity

Ando Takao,Haraguchi Ai,Matsunaga Tomoe,Natsuda Shoko,Yamasaki Hironori,Usa Toshiro,Kawakami Atsushi
Internal Medicine 53(16), 1791-1795, 2014
… Hypothalamic hyperphagia and obesity are characterized by a lack of satiety and an abnormally high appetite that is difficult to control. … We herein report the cases of two patients with hypothalamic hyperphagia and obesity with MRI-detectable hypothalamic lesions. …
NAID 130004678398

Human brown adipose tissue: regulation and anti-obesity potential [Review]

Saito Masayuki
Endocrine Journal 61(5), 409-416, 2014
… Brown adipose tissue (BAT) is the site of sympathetically activated adaptive thermognenesis during cold exposure and after hyperphagia, thereby controlling whole-body energy expenditure (EE) and body fat. …
NAID 130004443969