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Visceral Adiposity Genetic Susceptibility and Risk of Complications Among Individuals with Crohn’s Disease

机译：克罗恩病患者的内脏肥胖遗传易感性和并发症风险

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IntroductionAdipose tissue in mesenteric fat plays a key role in systemic and luminal inflammation. However, little is known about the role of visceral adipose tissue (VAT) and its interaction with genetic predisposition in Crohn’s disease (CD) progression.

机译：简介肠系膜脂肪中的脂肪组织在全身和腔内炎症中起关键作用。但是，关于内脏脂肪组织（VAT）的作用及其与克罗恩病（CD）进展中遗传易感性的相互作用了解甚少。

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期刊名称 Inflammatory Bowel Diseases
作者
Kimberley W.J. Van Der Sloot; Amit D. Joshi; Danielle R. Bellavance; Katherine K. Gilpin; Kathleen O. Stewart; Paul Lochhead; John J Garber; Cosmas Giallourakis; Vijay Yajnik; Ashwin N. Ananthakrishnan; Behrooz Z. Alizadeh; Ramnik J Xavier; Hamed Khalili;
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年(卷),期 -1(23),1
年度 -1
页码 82–88
总页数 14
原文格式 PDF
正文语种
中图分类肠道病毒与肝炎病毒;肝及胆疾病;肠疾病;
关键词
Visceral adipose tissue Obesity Crohn’s Disease Complications Genetic Predisposition;

机译：内脏脂肪组织;肥胖;克罗恩病并发症;遗传易感性;

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专利

1. Body Mass Index, Genetic Susceptibility, and Risk of Complications Among Individuals with Crohn's Disease [J] . Pringle Patricia L., Stewart Kathleen O., Peloquin Joanna M., Inflammatory bowel diseases . 2015,第10期

机译：克罗恩病患者的体重指数，遗传易感性和并发症风险
2. Depot- and obesity-related differences in adipogenesisAdipocyte hypertrophy and hyperplasia are known to facilitate lipid storage in adipose tissues by increasing adipocyte cell size and number, respectively. Adipogenesis is the process resulting in adipose tissue hyperplasia. Although depot-specific differences and obesity-related modulation of adipocyte size are well documented, available data on adipogenesis and adipose tissue hyperplasia are less conclusive. Most studies support a reduction of adipogenesis in the obese state. Preadipocytes of the subcutaneous fat depot appear to be more responsive to adipogenic stimulation compared with those from visceral fat compartments in most studies. A number of studies support the notion that adipose tissue expansion through hyperplasia reduces ectopic lipid excess and obesity-related complications. Several genetic variants have been identified in the genes coding for adipogenesis-regulating proteins. While some of these variants have been clearly associated with the phenotypes of obesity and obesity-related alterations, available data highlight the importance of considering gene–gene and gene–diet interactions. [J] . Julie. Lessard, André. Tchernof Clinical lipidology. . 2012,第5期

机译：脂肪形成与肥胖相关的差异已知脂肪细胞肥大和增生分别通过增加脂肪细胞的大小和数量来促进脂质在脂肪组织中的存储。脂肪形成是导致脂肪组织增生的过程。尽管已经有很多文献记载了贮库特异性差异和肥胖相关的脂肪细胞大小调节，但有关脂肪形成和脂肪组织增生的可用数据尚无定论。大多数研究支持在肥胖状态下减少脂肪形成。在大多数研究中，与来自内脏脂肪区室的脂肪细胞相比，皮下脂肪库的前脂肪细胞似乎对脂肪刺激更为敏感。许多研究支持这样的观点，即通过增生的脂肪组织扩张可以减少异位脂质过多和肥胖相关的并发症。在编码脂肪形成调节蛋白的基因中已经鉴定出几种遗传变异。尽管其中一些变异与肥胖症的表型和与肥胖有关的改变明显相关，但现有数据突出了考虑基因-基因和基因-饮食相互作用的重要性。
3. Identifying genetic susceptibilities to diabetes-related complications among individuals at low risk of complications: An application of tree-structured survival analysis. [J] . Costacou T, Chang Y, Ferrell RE, American Journal of Epidemiology . 2006,第9期

机译：在并发症风险低的个体中鉴定对糖尿病相关并发症的遗传易感性：树状存活分析的应用。
4. Gene-environment interactions between arsenic exposure from drinking water and genetic susceptibility in cardiovascular disease risk and carotid artery intima-media thickness in Bangladesh [C] . F. Wu, M.L. Liu, X. Cheng International Congress on Arsenic in the Environment . 2014

机译：孟加拉国心血管疾病风险饮用水和遗传易感性砷的基因环境相互作用及孟加拉国颈动脉内膜介质厚度
5. Epigenetics of Crohn's Disease, Ulcerative Colitis, and Phenotypically Normal Individuals [D] . Phillips, Delisa L. 2017

机译：克罗恩病，溃疡性结肠炎和表型正常个体的表观遗传
6. Body Mass Index Genetic Susceptibility and Risk of Complications Among Individuals with Crohns Disease [O] . Patricia L Pringle, Kathleen O Stewart, Joanna M Peloquin, -1

机译：克罗恩病患者的体重指数遗传易感性和并发症风险
7. Visceral Adiposity, Genetic Susceptibility, and Risk of Complications Among Individuals with Crohn's Disease [O] . van der Sloot, Kimberley, Ziad Alizadeh, Behrooz 2017

机译：克罗恩病患者的内脏肥胖，遗传易感性和并发症风险

Visceral Adiposity Genetic Susceptibility and Risk of Complications Among Individuals with Crohn’s Disease

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