多食症 - 维基百科，自由的百科全书

多食症
多食症
类型	进食障碍、醫學徵象[]、症狀、营养、代谢和发育症状[]
分类和外部资源
醫學專科	內分泌學, 精神病学
ICD-11	MG43.1
ICD-10	R63.2
ICD-9-CM	783.6
DiseasesDB	29453
MeSH	D006963
	[编辑此条目的维基数据]

多食症（英語：polyphagia或hyperphagia），也作食欲过旺，是指极度的饥饿或食欲的增加。^[1]

医学

在医学中，多食症是一个醫學徵象，暗示着极度的饥饿饥饿状态，以及反常食用固体食物，可由糖尿病、克萊恩-萊文症候群^{[來源請求]}、基因紊乱的普瑞德威利症候群和巴德-畢德氏症候群引发。^[2]此外，破坏迷走神经的接收器也可造成多食症。^[3]

病因

多食症的成因有：^[4]

通常在糖尿病酮症酸中毒早期会出现多食症的症状。^[5]然而，在胰岛素越来越匮乏时、糖尿病酮症酸中毒进一步发展时，食欲就能控制住了。^[6]

参见

参考资料

^ Berthoud HR, Lenard NR, Shin AC. Food reward, hyperphagia, and obesity.. Am J Physiol Regul Integr Comp Physiol. 2011, 300 (6): R1266–77. PMC 3119156 . PMID 21411768. doi:10.1152/ajpregu.00028.2011.
^ OMIM::Prader-Willi （页面存档备份，存于互联网档案馆）OMIM::Bardet-Biedl （页面存档备份，存于互联网档案馆）
^ de Lartigue G, Ronveaux CC, Raybould HE. Deletion of leptin signaling in vagal afferent neurons results in hyperphagia and obesity. MOLECULAR METABOLISM. 2014, 3 (6): 595–607 [2017-09-01]. PMC 4142400 . PMID 25161883. doi:10.1016/j.molmet.2014.06.003. （原始内容存档于2022-08-02）.
^ 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. [2017-09-01]. （原始内容存档于2016-07-05）.
^ Elliott RE, Jane JA, Wisoff JH. Surgical management of craniopharyngiomas in children: meta-analysis and comparison of transcranial and transsphenoidal approaches.. Neurosurgery. 2011, 69 (3): 630–43; discussion 643. PMID 21499159. doi:10.1227/NEU.0b013e31821a872d.
^ Masuzaki H, Tanaka T, Ebihara K, Hosoda K, Nakao K. Hypothalamic melanocortin signaling and leptin resistance--perspective of therapeutic application for obesity-diabetes syndrome.. Peptides. 2009, 30 (7): 1383–6 [2020-10-05]. PMID 19394382. doi:10.1016/j.peptides.2009.04.008. （原始内容存档于2020-03-14）.

外部链接

Diseases and conditions associated with Polyphagia （页面存档备份，存于互联网档案馆）

[pmid21411768-1] Berthoud HR, Lenard NR, Shin AC. Food reward, hyperphagia, and obesity.. Am J Physiol Regul Integr Comp Physiol. 2011, 300 (6): R1266–77. PMC 3119156 . PMID 21411768. doi:10.1152/ajpregu.00028.2011.

[2] OMIM::Prader-Willi （页面存档备份，存于互联网档案馆）OMIM::Bardet-Biedl （页面存档备份，存于互联网档案馆）

[pmid25161883-3] Lartigue G, Ronveaux CC, Raybould HE. Deletion of leptin signaling in vagal afferent neurons results in hyperphagia and obesity. MOLECULAR METABOLISM. 2014, 3 (6): 595–607 [2017-09-01]. PMC 4142400 . PMID 25161883. doi:10.1016/j.molmet.2014.06.003. （原始内容存档于2022-08-02）.

[4] 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. [2017-09-01]. （原始内容存档于2016-07-05）.

[pmid21499159-5] Elliott RE, Jane JA, Wisoff JH. Surgical management of craniopharyngiomas in children: meta-analysis and comparison of transcranial and transsphenoidal approaches.. Neurosurgery. 2011, 69 (3): 630–43; discussion 643. PMID 21499159. doi:10.1227/NEU.0b013e31821a872d.

[pmid19394382-6] Masuzaki H, Tanaka T, Ebihara K, Hosoda K, Nakao K. Hypothalamic melanocortin signaling and leptin resistance--perspective of therapeutic application for obesity-diabetes syndrome.. Peptides. 2009, 30 (7): 1383–6 [2020-10-05]. PMID 19394382. doi:10.1016/j.peptides.2009.04.008. （原始内容存档于2020-03-14）.

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