[1]吴蔚,杨叶虹,李益明.下丘脑性肥胖临床研究进展[J].国际内分泌代谢杂志,2014,(01):32-35.[doi:10.3760/cma.j.issn.1673-4157.2014.01.009]
　Wu Wei,Yang Yehong,Li Yiming.Clinical progress in hypothalamic obesity[J].International Journal of Endocrinology and Metabolism,2014,(01):32-35.[doi:10.3760/cma.j.issn.1673-4157.2014.01.009]
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下丘脑性肥胖临床研究进展()
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《国际内分泌代谢杂志》[ISSN:1673-4157/CN:12-1383/R]

卷:
期数:
2014年01期
页码:
32-35
栏目:
综述
出版日期:
2014-02-28

文章信息/Info

Title:
Clinical progress in hypothalamic obesity
作者:
吴蔚; 杨叶虹; 李益明
200040　上海,复旦大学附属华山医院内分泌代谢科
Author(s):
Wu Wei; Yang Yehong; Li Yiming．
Department of Endocrinology and Metabolism,Huashan Hospital,Fudan University,Shanghai 200040,China Corresponding author：Li Yiming,Email：yimingli@fudan.edu.cn
关键词:
下丘脑性肥胖; 下丘脑; 能量稳态; 颅咽管瘤
Keywords:
Hypothalamic obesity; Hypothalamus; Energy homeostasis; Craniopharyngioma
DOI:
10.3760/cma.j.issn.1673-4157.2014.01.009
摘要:
下丘脑性肥胖是指下丘脑能量稳态调节系统结构或功能损伤引起的食欲亢进和短期内体重显著增加综合征。其临床特征还包括能量消耗下降、合并多种下丘脑-垂体功能减退以及血糖、血脂、血压等代谢改变,部分可合并昼夜节律、体温、渴感及情绪调节异常。发病机制涉及下丘脑能量调节通路受损,胰岛素、瘦素、ghrelin等体液因子在中枢作用异常,自主神经功能紊乱等方面。其治疗包括常规生活方式干预、药物治疗及减重手术等。
Abstract:
Hypothalamic obesity is defined as the significant polyphagia and rapid weight gain due to a variety of structural or functional damage to the hypothalamic regulatory centers of energy homeostasis. Its clinical characteristics also include reduced energy expenditure, multiple deficits of hypothalamic-pituitary function and metabolic disturbances of blood glucose, lipid profile and blood pressure. Some patients may as well develop abnormal circadian rhythms, impaired regulation of body temperature, thirst perception and mood. The pathogenetic mechanisms underlying hypothalamic obesity include defects in the hypothalamic weight-regulating pathways, dysfunction of afferent peripheral humoral signals in the central nervous system, such as leptin, insulin,ghrelin,etc,and autonomic imbalance.The treatment of hypothalamic obesity includes conventional lifestyle modifications,several agents and bariatric surgery.

参考文献/References:

　[1]　Luquet S,Magnan C．The central nervous system at the core of the regulation of energy homeostasis[J]．Front Biosci（Schol Ed）,2009,1：448-465． 　
[2]　Hochberg I,Hochberg Z．Expanding the definition of hypotha-lamic obesity[J]．Obes Rev,2010,11（10）：709-721． 　
[3]　Lin LL,El Naqa I,Leonard JR,et al．Long-term outcome in chil-dren treated for craniopharyngioma with and without radio-therapy[J]．J Neurosurg Pediatr,2008,1（2）：126-130. 　
[4]　Crowley RK,Hamnvik OP,O'Sullivan EP,et al．Morbidity and mortality in patients with craniopharyngioma after surgery[J]．Clin Endocrinol（Oxf）,2010,73（4）：516-521. 　
[5]　Holmer H,Pozarek G,Wirf?覿lt E,et al．Reduced energy expendi-ture and impaired feeding-related signals but not high energy intake reinforces hypothalamic obesity in adults with childhood onset craniopharyngioma[J]．J Clin Endocrinol Metab,2010,95（12）：5395-5402. 　
[6]　Shaikh MG,Grundy RG,Kirk JM．Reductions in basal metabolic rate and physical activity contribute to hypothalamic obesity[J]．J Clin Endocrinol Metab,2008,93（7）：2588-2593. 　
[7]　Van Gompel JJ,Nippoldt TB,Higgins DM,et al．Magnetic resonance imaging-graded hypothalamic compression in surgically treated adult craniopharyngiomas determining postopera-tive obesity[J]．Neurosurg Focus,2010,28（4）：E3. 　
[8]　Cohen M,Syme C,McCrindle BW,et al．Autonomic nervous system balance in children and adolescents with craniopharyn-gioma and hypothalamic obesity[J]．Eur J Endocrinol,2013,168（6）：845-852. 　
[9]　Emerick JE,Vogt KS．Endocrine manifestations and management of Prader-Willi syndrome[J]．Int J Pediatr Endocrinol,2013,2013（1）：14.
[10]　Shaikh MG,Grundy RG,Kirk JM．Hyperleptinaemia rather than fasting hyperinsulinaemia is associated with obesity following hypothalamic damage in children[J]．Eur J Endocrinol,2008,159（6）：791-797.
[11]　Guran T,Turan S,Bereket A,et al．The role of leptin,soluble leptin receptor, resistin,and insulin secretory dynamics in the pathogenesis of hypothalamic obesity in children[J]．Eur J Pediatr,2009,168（9）：1043-1048.
[12]　Feigerlová E,Diene G,Conte-Auriol F,et al．Hyperghrelinemia precedes obesity in Prader-Willi syndrome[J]．J Clin Endocrinol Metab, 2008,93（7）：2800-2805.
[13]　Marino JS,Xu Y,Hill JW．Central insulin and leptin-mediated autonomic control of glucose homeostasis[J]．Trends Endocrinol Metab, 2011,22（7）：275-285.
[14]　Haskell-Luevano C,Schaub JW,Andreasen A,et al．Voluntary exercise prevents the obese and diabetic metabolic syndrome of the melanocortin-4 receptor knockout mouse[J]．FASEB J,2009,23（2）： 642-655.
[15]　Bereket A,Kiess W,Lustig RH,et al．Hypothalamic obesity in children[J]．Obes Rev,2012,13（9）：780-798.
[16]　De Waele K,Ishkanian SL,Bogarin R,et al．Long-acting octreotide treatment causes a sustained decrease in ghrelin concentrations but does not affect weight,behaviour and appetite in subjects with Prader-Willi syndrome[J]．Eur J Endocrinol,2008,159（4）：381-388.
[17]　Greenway FL,Bray GA．Treatment of hypothalamic obesity with caffeine and ephedrine[J]．Endocr Pract,2008,14（6）：697-703.
[18]　Paz-Filho G,Wong ML,Licinio J．Ten years of leptin replace-ment therapy[J]．Obes Rev,2011,12（5）：e315-e323.
[19]　Hayes MR,Skibicka KP,Grill HJ．Caudal brainstem processing is sufficient for behavioral,sympathetic,and parasympathetic responses driven by peripheral and hindbrain glucagon-like-peptide-1 receptor stimulation[J]．Endocrinology,2008,149（8）：4059-4068.
[20]　Elfers CT,Simmons JH,Roth CL．Glucagon-like peptide-1 agonist exendin-4 leads to reduction of weight and caloric intake in a rat model of hypothalamic obesity[J]．Horm Res Paediatr,2012,78（1）：47-53.
[21]　Simmons JH,Shoemaker AH,Roth CL．Treatment with glucagon-like Peptide-1 agonist exendin-4 in a patient with hypothalamic obesity secondary to intracranial tumor[J]．Horm Res Paediatr,2012,78（1）：54-58.
[22]　Thondam SK,Cuthbertson DJ,Aditya BS,et al．A glucagon-like peptide-1（GLP-1）receptor agonist in the treatment for hypothalamic obesity complicated by type 2 diabetes mellitus[J]．Clin Endocrinol（Oxf）, 2012,77（4）：635-637.
[23]　Zoicas F,Droste M,Mayr B,et al．GLP-1 analogues as a new treatment option for hypothalamic obesity in adults：report of nine cases[J]． Eur J Endocrinol,2013,168（5）：699-706.
[24]　Lustig RH．Hypothalamic obesity after craniopharyngioma：mechanisms,diagnosis,and treatment[J]．Front Endocrinol （Lausanne）,2011,2： 60.
[25]　Bretault M,Boillot A,Muzard L,et al．Clinical review：bariatric surgery following treatment for craniopharyngioma：a systematic review and individual-level data meta-analysis[J]．J Clin Endocrinol Metab, 2013,98（6）：2239-2246.

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备注/Memo

备注/Memo:
通信作者：李益明,Email: yimingli@fudan.edu.cn
更新日期/Last Update: 2014-01-20