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本文引用的文献

1
Variants in ADCY5 and near CCNL1 are associated with fetal growth and birth weight.ADCY5 和 CCNL1 附近的变异与胎儿生长和出生体重有关。
Nat Genet. 2010 May;42(5):430-5. doi: 10.1038/ng.567. Epub 2010 Apr 6.
2
New genetic loci implicated in fasting glucose homeostasis and their impact on type 2 diabetes risk.新的遗传位点与空腹血糖稳态有关,及其对 2 型糖尿病风险的影响。
Nat Genet. 2010 Feb;42(2):105-16. doi: 10.1038/ng.520. Epub 2010 Jan 17.
3
Type 2 diabetes gene TCF7L2 polymorphism is not associated with fetal and postnatal growth in two birth cohort studies.两项出生队列研究表明,2型糖尿病基因TCF7L2多态性与胎儿及出生后生长无关。
BMC Med Genet. 2009 Jul 17;10:67. doi: 10.1186/1471-2350-10-67.
4
Examination of type 2 diabetes loci implicates CDKAL1 as a birth weight gene.对2型糖尿病基因座的研究表明,CDKAL1是一个影响出生体重的基因。
Diabetes. 2009 Oct;58(10):2414-8. doi: 10.2337/db09-0506. Epub 2009 Jul 10.
5
A rare variant in the visfatin gene (NAMPT/PBEF1) is associated with protection from obesity.内脂素基因(烟酰胺磷酸核糖转移酶/前B细胞克隆增强因子1)中的一种罕见变异与预防肥胖有关。
Obesity (Silver Spring). 2009 Aug;17(8):1549-53. doi: 10.1038/oby.2009.75. Epub 2009 Mar 19.
6
Type 2 diabetes risk alleles are associated with reduced size at birth.2型糖尿病风险等位基因与出生时体型较小有关。
Diabetes. 2009 Jun;58(6):1428-33. doi: 10.2337/db08-1739. Epub 2009 Feb 19.
7
Interaction between prenatal growth and high-risk genotypes in the development of type 2 diabetes.产前生长与高危基因型在2型糖尿病发生发展中的相互作用。
Diabetologia. 2009 May;52(5):825-9. doi: 10.1007/s00125-009-1291-1. Epub 2009 Feb 19.
8
Two British women studies replicated the association between the Val66Met polymorphism in the brain-derived neurotrophic factor (BDNF) and BMI.两项针对英国女性的研究重复了脑源性神经营养因子(BDNF)中的Val66Met基因多态性与体重指数(BMI)之间的关联。
Eur J Hum Genet. 2009 Aug;17(8):1050-5. doi: 10.1038/ejhg.2008.272. Epub 2009 Feb 11.
9
Genome-wide association study for early-onset and morbid adult obesity identifies three new risk loci in European populations.针对早发性和病态成人肥胖的全基因组关联研究在欧洲人群中发现了三个新的风险基因座。
Nat Genet. 2009 Feb;41(2):157-9. doi: 10.1038/ng.301. Epub 2009 Jan 18.
10
Six new loci associated with body mass index highlight a neuronal influence on body weight regulation.六个与体重指数相关的新基因座凸显了神经元对体重调节的影响。
Nat Genet. 2009 Jan;41(1):25-34. doi: 10.1038/ng.287. Epub 2008 Dec 14.

肥胖和糖尿病基因与胎儿生长受限有关:奥克兰出生体重协作研究的结果。

Obesity and diabetes genes are associated with being born small for gestational age: results from the Auckland Birthweight Collaborative study.

机构信息

Discipline of Nutrition, Faculty of Medical and Health Sciences, The University of Auckland, Auckland, New Zealand.

出版信息

BMC Med Genet. 2010 Aug 16;11:125. doi: 10.1186/1471-2350-11-125.

DOI:10.1186/1471-2350-11-125
PMID:20712903
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2928774/
Abstract

BACKGROUND

Individuals born small for gestational age (SGA) are at increased risk of rapid postnatal weight gain, later obesity and diseases in adulthood such as type 2 diabetes, hypertension and cardiovascular diseases. Environmental risk factors for SGA are well established and include smoking, low pregnancy weight, maternal short stature, maternal diet, ethnic origin of mother and hypertension. However, in a large proportion of SGA, no underlying cause is evident, and these individuals may have a larger genetic contribution.

METHODS

In this study we tested the association between SGA and polymorphisms in genes that have previously been associated with obesity and/or diabetes. We undertook analysis of 54 single nucleotide polymorphisms (SNPs) in 546 samples from the Auckland Birthweight Collaborative (ABC) study. 227 children were born small for gestational age (SGA) and 319 were appropriate for gestational age (AGA).

RESULTS AND CONCLUSION

The results demonstrated that genetic variation in KCNJ11, BDNF, PFKP, PTER and SEC16B were associated with SGA and support the concept that genetic factors associated with obesity and/or type 2 diabetes are more prevalent in those born SGA compared to those born AGA. We have previously determined that environmental factors are associated with differences in birthweight in the ABC study and now we have demonstrated a significant genetic contribution, suggesting that the interaction between genetics and the environment are important.

摘要

背景

出生体重小于胎龄儿(SGA)个体在出生后体重快速增加、成年后肥胖以及罹患 2 型糖尿病、高血压和心血管疾病等疾病的风险增加。SGA 的环境危险因素已得到充分证实,包括吸烟、低妊娠体重、母亲身材矮小、母亲饮食、母亲种族和高血压。然而,在很大一部分 SGA 中,没有明显的潜在原因,这些个体可能有更大的遗传贡献。

方法

本研究检测了先前与肥胖和/或糖尿病相关的基因中的单核苷酸多态性(SNP)与 SGA 之间的关联。我们对来自奥克兰出生体重协作研究(ABC)的 546 个样本中的 54 个单核苷酸多态性(SNP)进行了分析。227 名儿童出生体重小于胎龄(SGA),319 名儿童出生体重符合胎龄(AGA)。

结果与结论

结果表明,KCNJ11、BDNF、PFKP、PTER 和 SEC16B 中的遗传变异与 SGA 相关,支持这样的概念,即与肥胖和/或 2 型糖尿病相关的遗传因素在 SGA 出生儿中比 AGA 出生儿中更为普遍。我们之前已经确定环境因素与 ABC 研究中的出生体重差异相关,现在我们已经证明了遗传因素的显著贡献,这表明遗传与环境之间的相互作用很重要。