Suppr超能文献

肥胖诱导物、干细胞与肥胖的发育编程

Obesogens, stem cells and the developmental programming of obesity.

作者信息

Janesick A, Blumberg B

机构信息

Departments of Developmental and Cell Biology, University of California, Irvine, CA 92697-2300, USA.

出版信息

Int J Androl. 2012 Jun;35(3):437-48. doi: 10.1111/j.1365-2605.2012.01247.x. Epub 2012 Feb 28.

Abstract

Obesogens are chemicals that directly or indirectly lead to increased fat accumulation and obesity. Obesogens have the potential to disrupt multiple metabolic signalling pathways in the developing organism that can result in permanent changes in adult physiology. Prenatal or perinatal exposure to obesogenic endocrine disrupting chemicals has been shown to predispose an organism to store more fat from the beginning of its life. For example, excess oestrogen or cortisol exposure in the womb or during early life resulted in an increased susceptibility to obesity and metabolic syndrome later in life. This review focuses on the effects of environmental chemicals, such as the model obesogen, tributyltin (TBT), on the development of obesity. We discuss evidence linking the obesogenic effects of TBT with its ability to activate the peroxisome proliferator-activated receptor gamma and stimulate adipogenesis. We also discuss how TBT and other environmental obesogens may lead to epigenetic changes that predispose exposed individuals to subsequent weight gain and obesity. This suggests that humans, who have been exposed to obesogenic chemicals during sensitive windows of development, might be pre-programmed to store increased amounts of fat, resulting in a lifelong struggle to maintain a healthy weight and exacerbating the deleterious effects of poor diet and inadequate exercise.

摘要

致肥胖物是直接或间接导致脂肪堆积增加和肥胖的化学物质。致肥胖物有可能扰乱发育中生物体的多种代谢信号通路,从而导致成年生理机能发生永久性变化。已表明,产前或围产期接触致肥胖的内分泌干扰化学物质会使生物体从生命伊始就更易储存脂肪。例如,子宫内或生命早期接触过量雌激素或皮质醇会导致日后对肥胖和代谢综合征的易感性增加。本综述聚焦于环境化学物质,如典型致肥胖物三丁基锡(TBT),对肥胖发展的影响。我们讨论了将TBT的致肥胖作用与其激活过氧化物酶体增殖物激活受体γ及刺激脂肪生成的能力相联系的证据。我们还讨论了TBT和其他环境致肥胖物如何可能导致表观遗传变化,使接触者更易随后体重增加和肥胖。这表明,在发育的敏感窗口期接触致肥胖化学物质的人类可能会被预先设定为储存更多脂肪,导致终生为维持健康体重而挣扎,并加剧不良饮食和运动不足的有害影响。

相似文献

1
Obesogens, stem cells and the developmental programming of obesity.
Int J Androl. 2012 Jun;35(3):437-48. doi: 10.1111/j.1365-2605.2012.01247.x. Epub 2012 Feb 28.
2
Endocrine disrupting chemicals and the developmental programming of adipogenesis and obesity.
Birth Defects Res C Embryo Today. 2011 Mar;93(1):34-50. doi: 10.1002/bdrc.20197.
3
Transgenerational inheritance of prenatal obesogen exposure.
Mol Cell Endocrinol. 2014 Dec;398(1-2):31-5. doi: 10.1016/j.mce.2014.09.002. Epub 2014 Sep 16.
4
Endocrine Disruptors and Obesity.
Curr Obes Rep. 2017 Mar;6(1):18-27. doi: 10.1007/s13679-017-0240-4.
5
The Role of Epigenetics in the Latent Effects of Early Life Exposure to Obesogenic Endocrine Disrupting Chemicals.
Endocrinology. 2015 Oct;156(10):3466-72. doi: 10.1210/en.2015-1434. Epub 2015 Aug 4.
7
Minireview: PPARγ as the target of obesogens.
J Steroid Biochem Mol Biol. 2011 Oct;127(1-2):4-8. doi: 10.1016/j.jsbmb.2011.01.005. Epub 2011 Jan 18.
9
Environmental obesogens: organotins and endocrine disruption via nuclear receptor signaling.
Endocrinology. 2006 Jun;147(6 Suppl):S50-5. doi: 10.1210/en.2005-1129. Epub 2006 May 11.

引用本文的文献

2
Adipose tissue dysfunction disrupts metabolic homeostasis: mechanisms linking fat dysregulation to disease.
Front Endocrinol (Lausanne). 2025 Jun 24;16:1592683. doi: 10.3389/fendo.2025.1592683. eCollection 2025.
3
Endocrine Disruptors in Child Obesity and Related Disorders: Early Critical Windows of Exposure.
Curr Nutr Rep. 2025 Jan 8;14(1):14. doi: 10.1007/s13668-024-00604-1.

本文引用的文献

1
Obesogens, stem cells and the maternal programming of obesity.
J Dev Orig Health Dis. 2011 Feb;2(1):3-8. doi: 10.1017/S2040174410000589.
2
Developmental exposure to bisphenol A leads to cardiometabolic dysfunction in adult mouse offspring.
J Dev Orig Health Dis. 2012 Aug;3(4):287-92. doi: 10.1017/S2040174412000153.
3
Association of prenatal exposure to polybrominated diphenyl ethers and infant birth weight.
Am J Epidemiol. 2011 Oct 15;174(8):885-92. doi: 10.1093/aje/kwr212. Epub 2011 Aug 30.
6
Urinary bisphenol A and obesity: NHANES 2003-2006.
Environ Res. 2011 Aug;111(6):825-30. doi: 10.1016/j.envres.2011.05.014. Epub 2011 Jun 14.
7
Bisphenol A: an endocrine disruptor with widespread exposure and multiple effects.
J Steroid Biochem Mol Biol. 2011 Oct;127(1-2):27-34. doi: 10.1016/j.jsbmb.2011.05.002. Epub 2011 May 13.
8
Increase in metabolic syndrome-related hospitalizations in relation to environmental sources of persistent organic pollutants.
Int J Environ Res Public Health. 2011 Mar;8(3):762-76. doi: 10.3390/ijerph8030762. Epub 2011 Mar 4.
9
PPAR-γ action: it's all in your head.
Nat Med. 2011 May;17(5):544-5. doi: 10.1038/nm0511-544.
10
Brain PPAR-γ promotes obesity and is required for the insulin-sensitizing effect of thiazolidinediones.
Nat Med. 2011 May;17(5):618-22. doi: 10.1038/nm.2332. Epub 2011 May 1.

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验