Suppr超能文献

小鼠模型中的代谢综合征组成部分。

Metabolic syndrome components in murine models.

作者信息

Lawson Heather A, Cheverud James M

机构信息

The Department of Anatomy and Neurobiology, Washington University School of Medicine in St Louis, MO, USA.

出版信息

Endocr Metab Immune Disord Drug Targets. 2010 Mar;10(1):25-40. doi: 10.2174/187153010790827948.

Abstract

Animal models have enriched understanding of the physiological basis of metabolic disorders and advanced identification of genetic risk factors underlying the metabolic syndrome (MetS). Murine models are especially appropriate for this type of research, and are an excellent resource not only for identifying candidate genomic regions, but also for illuminating the possible molecular mechanisms or pathways affected in individual components of MetS. In this review, we briefly discuss findings from mouse models of metabolic disorders, particularly in light of issues raised by the recent flood of human genome-wide association studies (GWAS) results. We describe how mouse models are revealing that genotype interacts with environment in important ways, indicating that the underlying genetics of MetS is highly context dependant. Further we show that epistasis, imprinting and maternal effects each contribute to the genetic architecture underlying variation in metabolic traits, and mouse models provide an opportunity to dissect these aspects of the genetic architecture that are difficult if not impossible to ascertain in humans. Finally we discuss how knowledge gained from mouse models can be used in conjunction with comparative genomic methods and bioinformatic resources to inform human MetS research.

摘要

动物模型丰富了我们对代谢紊乱生理基础的理解,并推动了对代谢综合征(MetS)潜在遗传风险因素的识别。小鼠模型尤其适合此类研究,不仅是识别候选基因组区域的优秀资源,也是阐明MetS各个组成部分中可能受影响的分子机制或途径的良好工具。在这篇综述中,我们简要讨论代谢紊乱小鼠模型的研究结果,特别是鉴于近期大量人类全基因组关联研究(GWAS)结果所引发的问题。我们描述了小鼠模型如何揭示基因型与环境以重要方式相互作用,表明MetS的潜在遗传学高度依赖背景。此外,我们表明上位性、印记和母体效应均对代谢性状变异的遗传结构有贡献,并且小鼠模型为剖析遗传结构中这些在人类中难以(如果不是不可能)确定的方面提供了机会。最后,我们讨论如何将从小鼠模型中获得的知识与比较基因组方法和生物信息资源结合起来,为人类MetS研究提供信息。

相似文献

1
Metabolic syndrome components in murine models.
Endocr Metab Immune Disord Drug Targets. 2010 Mar;10(1):25-40. doi: 10.2174/187153010790827948.
3
Trends in metabolic syndrome and gene networks in human and rodent models.
Endocr Metab Immune Disord Drug Targets. 2008 Sep;8(3):198-207. doi: 10.2174/187153008785700145.
5
Genetics of metabolic syndrome: is there a role for phenomics?
Curr Atheroscler Rep. 2008 Jun;10(3):201-8. doi: 10.1007/s11883-008-0032-0.
7
Genome-wide association study identifies African-ancestry specific variants for metabolic syndrome.
Mol Genet Metab. 2015 Dec;116(4):305-13. doi: 10.1016/j.ymgme.2015.10.008. Epub 2015 Oct 23.
8
9
Genetics of metabolic syndrome: potential clues from wild-derived inbred mouse strains.
Physiol Genomics. 2018 Jan 1;50(1):35-51. doi: 10.1152/physiolgenomics.00059.2017. Epub 2017 Nov 10.

引用本文的文献

1
Spontaneous restoration of functional β-cell mass in obese SM/J mice.
Physiol Rep. 2020 Oct;8(20):e14573. doi: 10.14814/phy2.14573.
3
Genetic background and diet affect brown adipose gene coexpression networks associated with metabolic phenotypes.
Physiol Genomics. 2020 Jun 1;52(6):223-233. doi: 10.1152/physiolgenomics.00003.2020. Epub 2020 Apr 27.
4
Genome wide association analysis in a mouse advanced intercross line.
Nat Commun. 2018 Dec 4;9(1):5162. doi: 10.1038/s41467-018-07642-8.
5
Glucose dysregulation and response to common anti-diabetic agents in the FATZO/Pco mouse.
PLoS One. 2017 Jun 22;12(6):e0179856. doi: 10.1371/journal.pone.0179856. eCollection 2017.
6
Genetics of glucose homeostasis: implications for insulin resistance and metabolic syndrome.
Arterioscler Thromb Vasc Biol. 2012 Sep;32(9):2091-6. doi: 10.1161/ATVBAHA.112.255463.
7
Obesity-insulin targeted genes in the 3p26-25 region in human studies and LG/J and SM/J mice.
Metabolism. 2012 Aug;61(8):1129-41. doi: 10.1016/j.metabol.2012.01.008. Epub 2012 Mar 3.
8
Dark matter: are mice the solution to missing heritability?
Front Genet. 2011 Jun 13;2:32. doi: 10.3389/fgene.2011.00032. eCollection 2011.
9

本文引用的文献

1
Calpain-10 is a component of the obesity-related quantitative trait locus Adip1.
J Lipid Res. 2010 May;51(5):907-13. doi: 10.1194/jlr.M900128.
2
Fine-mapping of obesity-related quantitative trait loci in an F9/10 advanced intercross line.
Obesity (Silver Spring). 2010 Jul;18(7):1383-92. doi: 10.1038/oby.2009.411. Epub 2009 Nov 12.
3
TCF7L2 polymorphisms and inflammatory markers before and after treatment with fenofibrate.
Diabetol Metab Syndr. 2009 Oct 12;1(1):16. doi: 10.1186/1758-5996-1-16.
4
Type 2 Diabetes Mellitus: New Genetic Insights will Lead to New Therapeutics.
Curr Genomics. 2009 Apr;10(2):110-8. doi: 10.2174/138920209787847023.
5
Mouse models of diabetic nephropathy.
J Am Soc Nephrol. 2009 Dec;20(12):2503-12. doi: 10.1681/ASN.2009070721. Epub 2009 Sep 3.
6
Obesity and genetics regulate microRNAs in islets, liver, and adipose of diabetic mice.
Mamm Genome. 2009 Aug;20(8):476-85. doi: 10.1007/s00335-009-9217-2.
7
The effects of ABCG5/G8 polymorphisms on HDL-cholesterol concentrations depend on ABCA1 genetic variants in the Boston Puerto Rican Health Study.
Nutr Metab Cardiovasc Dis. 2010 Oct;20(8):558-66. doi: 10.1016/j.numecd.2009.05.005. Epub 2009 Aug 18.
8
Identification of the UBP1 locus as a critical blood pressure determinant using a combination of mouse and human genetics.
PLoS Genet. 2009 Aug;5(8):e1000591. doi: 10.1371/journal.pgen.1000591. Epub 2009 Aug 7.
9
Genetic analysis of blood pressure in 8 mouse intercross populations.
Hypertension. 2009 Oct;54(4):802-9. doi: 10.1161/HYPERTENSIONAHA.109.134569. Epub 2009 Aug 3.
10
Copy number variation influences gene expression and metabolic traits in mice.
Hum Mol Genet. 2009 Nov 1;18(21):4118-29. doi: 10.1093/hmg/ddp360. Epub 2009 Jul 31.

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