An Overview of Mongenic and Syndromic Obesities in Humans

被引：38
作者：
Chung, Wendy K. [1 ,2 ]
机构：
[1] Columbia Univ, Coll Med, Div Mol Genet, New York, NY 10032 USA
[2] Columbia Univ, Coll Med, Naomi Berrie Diabet Ctr, New York, NY 10032 USA
来源：
PEDIATRIC BLOOD & CANCER | 2012年 / 58卷 / 01期
关键词：
16p11.2; deletion; Alstrom syndrome; Bardet-Biedl syndrome; leptin; leptin receceptor; melanocortin; 4; receptor; Prader Willi syndrome; EARLY-ONSET OBESITY; MELANOCORTIN-4 RECEPTOR GENE; CONGENITAL LEPTIN DEFICIENCY; PRADER-WILLI-SYNDROME; BARDET-BIEDL-SYNDROME; ALSTROM-SYNDROME; MORBID-OBESITY; MISSENSE MUTATION; ADULTS; PROOPIOMELANOCORTIN;
D O I：
10.1002/pbc.23372
中图分类号：
R73 [肿瘤学];
学科分类号：
100214 ;
摘要：
Obesity is increasing in prevalence in the United States with over 65% of adults considered overweight and 16% of children with BMI > 95 percentile. The heritability of obesity is estimated between 40% and 70%, but the genetics of obesity for most individuals are complex and involve the interaction of multiple genes and environment. There are however several syndromic and non-syndromic forms of obesity that are monogenic and oligogenic that provide insight into the underlying molecular control of food intake and the neural networks that control ingestive behavior and satiety to regulate body weight and which may interact with treatment exposures to produce or exacerbate obesity in childhood cancer survivors. Pediatr Blood Cancer 2012; 58: 122 128. (C) 2011 Wiley Periodicals, Inc.
引用
收藏
页码：122 / 128
页数：7
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