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本文引用的文献

1
Polymorphism of CD36 gene, carbohydrate metabolism and plasma CD36 concentration in obese children. A preliminary study.肥胖儿童CD36基因多态性、碳水化合物代谢与血浆CD36浓度:一项初步研究
Postepy Hig Med Dosw (Online). 2012 Nov 22;66:954-8. doi: 10.5604/17322693.1021112.
2
Genetic polymorphisms in carnitine palmitoyltransferase 1A gene are associated with variation in body composition and fasting lipid traits in Yup'ik Eskimos.卡尼汀棕榈酰转移酶 1A 基因的遗传多态性与尤皮克爱斯基摩人体成分和空腹血脂特征的变化有关。
J Lipid Res. 2012 Jan;53(1):175-84. doi: 10.1194/jlr.P018952. Epub 2011 Nov 1.
3
Factors regulating fat oxidation in human skeletal muscle.调节人体骨骼肌脂肪氧化的因素。
Obes Rev. 2011 Oct;12(10):852-8. doi: 10.1111/j.1467-789X.2011.00898.x.
4
CD36 genetics and the metabolic complications of obesity.CD36 基因与肥胖的代谢并发症。
Curr Opin Clin Nutr Metab Care. 2011 Nov;14(6):527-34. doi: 10.1097/MCO.0b013e32834bbac9.
5
Effect of β(3)-adrenergic receptor gene polymorphism on body weight change in middle-aged, overweight women.β(3)-肾上腺素能受体基因多态性对中年超重女性体重变化的影响。
Environ Health Prev Med. 2006 Mar;11(2):69-74. doi: 10.1007/BF02898145.
6
A CD36-dependent pathway enhances macrophage and adipose tissue inflammation and impairs insulin signalling.一条依赖CD36的信号通路会加剧巨噬细胞和脂肪组织的炎症反应,并损害胰岛素信号传导。
Cardiovasc Res. 2011 Feb 15;89(3):604-13. doi: 10.1093/cvr/cvq360. Epub 2010 Nov 18.
7
Lack of association of CD36 SNPs with early onset obesity: a meta-analysis in 9,973 European subjects.CD36 单核苷酸多态性与早发性肥胖无关:9973 例欧洲受试者的荟萃分析。
Obesity (Silver Spring). 2011 Apr;19(4):833-9. doi: 10.1038/oby.2010.226. Epub 2010 Oct 21.
8
Tissue-specific functions in the fatty acid-binding protein family.脂肪酸结合蛋白家族的组织特异性功能。
J Biol Chem. 2010 Oct 22;285(43):32679-32683. doi: 10.1074/jbc.R110.135210. Epub 2010 Aug 17.
9
A general introduction to the biochemistry of mitochondrial fatty acid β-oxidation.线粒体脂肪酸β-氧化的生物化学概论。
J Inherit Metab Dis. 2010 Oct;33(5):469-77. doi: 10.1007/s10545-010-9061-2. Epub 2010 Mar 2.
10
High dietary fat exacerbates weight gain and obesity in female liver fatty acid binding protein gene-ablated mice.高膳食脂肪会加剧肝脏脂肪酸结合蛋白基因敲除雌性小鼠的体重增加和肥胖。
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脂肪酸氧化的遗传变异与肥胖:文献综述

Genetic Variation of Fatty Acid Oxidation and Obesity, A Literature Review.

作者信息

Freitag Luglio Harry

机构信息

Department of Nutrition and Health, Faculty of Medicine, Universitas Gadjah Mada, Indonesia.

出版信息

Int J Biomed Sci. 2016 Mar;12(1):1-8.

PMID:27127449
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4841982/
Abstract

Modulation of fat metabolism is an important component of the etiology of obesity as well as individual response to weight loss program. The influence of lipolysis process had receives many attentions in recent decades. Compared to that, fatty acid oxidation which occurred after lipolysis seems to be less exposed. There are limited publications on how fatty acid oxidation influences predisposition to obesity, especially the importance of genetic variations of fatty acid oxidation proteins on development of obesity. The aim of this review is to provide recent knowledge on how polymorphism of genes related fatty acid oxidation is obtained. Studies in human as well as animal model showed that disturbance of genes related fatty acid oxidation process gave impact on body weight and risks to obesity. Several polymorphisms on CD36, CPT, ACS and FABP had been shown to be related to obesity either by regulating enzymatic activity or directly influence fatty acid oxidation process.

摘要

脂肪代谢的调节是肥胖病因以及个体对减肥计划反应的重要组成部分。近几十年来,脂解过程的影响受到了许多关注。相比之下,脂解后发生的脂肪酸氧化似乎较少受到关注。关于脂肪酸氧化如何影响肥胖易感性的出版物有限,尤其是脂肪酸氧化蛋白的基因变异对肥胖发展的重要性。本综述的目的是提供有关如何获得与脂肪酸氧化相关基因多态性的最新知识。对人类以及动物模型的研究表明,与脂肪酸氧化过程相关的基因紊乱会影响体重和肥胖风险。已表明CD36、CPT、ACS和FABP上的几种多态性通过调节酶活性或直接影响脂肪酸氧化过程与肥胖有关。