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本文引用的文献

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The wrong white crystals: not salt but sugar as aetiological in hypertension and cardiometabolic disease.错误的白色晶体:不是盐而是糖成为高血压和心脏代谢疾病的病因。
Open Heart. 2014 Nov 3;1(1):e000167. doi: 10.1136/openhrt-2014-000167. eCollection 2014.
2
Added fructose: a principal driver of type 2 diabetes mellitus and its consequences.添加的果糖:2 型糖尿病及其并发症的主要驱动因素。
Mayo Clin Proc. 2015 Mar;90(3):372-81. doi: 10.1016/j.mayocp.2014.12.019. Epub 2015 Jan 29.
3
Uric acid induces endothelial dysfunction by vascular insulin resistance associated with the impairment of nitric oxide synthesis.尿酸通过血管胰岛素抵抗导致一氧化氮合成受损,从而引起内皮功能障碍。
FASEB J. 2014 Jul;28(7):3197-204. doi: 10.1096/fj.13-247148. Epub 2014 Mar 20.
4
Impact of sugar-sweetened beverages on blood pressure.含糖饮料对血压的影响。
Am J Cardiol. 2014 May 1;113(9):1574-80. doi: 10.1016/j.amjcard.2014.01.437. Epub 2014 Feb 12.
5
High dietary salt decreases antioxidant defenses in the liver of fructose-fed insulin-resistant rats.高盐饮食可降低果糖喂养的胰岛素抵抗大鼠肝脏的抗氧化防御能力。
J Nutr Biochem. 2013 Dec;24(12):2016-22. doi: 10.1016/j.jnutbio.2013.06.006. Epub 2013 Oct 14.
6
Uric acid induces hepatic steatosis by generation of mitochondrial oxidative stress: potential role in fructose-dependent and -independent fatty liver.尿酸通过产生线粒体氧化应激诱导肝脂肪变性:果糖依赖性和非依赖性脂肪肝中的潜在作用。
J Biol Chem. 2012 Nov 23;287(48):40732-44. doi: 10.1074/jbc.M112.399899. Epub 2012 Oct 3.
7
The effects of fructose intake on serum uric acid vary among controlled dietary trials.果糖摄入对血清尿酸的影响在对照饮食试验中有所不同。
J Nutr. 2012 May;142(5):916-23. doi: 10.3945/jn.111.151951. Epub 2012 Mar 28.
8
Sympathetic overactivity precedes metabolic dysfunction in a fructose model of glucose intolerance in mice.在小鼠果糖型葡萄糖耐量异常模型中,交感神经活性亢进先于代谢功能障碍。
Am J Physiol Regul Integr Comp Physiol. 2012 Apr 15;302(8):R950-7. doi: 10.1152/ajpregu.00450.2011. Epub 2012 Feb 8.
9
Fructose-induced steatosis in mice: role of plasminogen activator inhibitor-1, microsomal triglyceride transfer protein and NKT cells.果糖诱导的小鼠脂肪变性:纤溶酶原激活物抑制剂-1、微粒体甘油三酯转移蛋白和 NKT 细胞的作用。
Lab Invest. 2011 Jun;91(6):885-95. doi: 10.1038/labinvest.2011.44. Epub 2011 Mar 21.
10
Sugar-sweetened beverage, sugar intake of individuals, and their blood pressure: international study of macro/micronutrients and blood pressure.含糖饮料、个体糖摄入量及其血压:宏量/微量营养素与血压国际研究。
Hypertension. 2011 Apr;57(4):695-701. doi: 10.1161/HYPERTENSIONAHA.110.165456. Epub 2011 Feb 28.

高果糖摄入对健康的影响及当前研究

Health implications of high-fructose intake and current research.

作者信息

Dornas Waleska C, de Lima Wanderson G, Pedrosa Maria L, Silva Marcelo E

机构信息

Research in Biological Sciences-Center for Research in Biological Sciences (NUPEB),

Research in Biological Sciences-Center for Research in Biological Sciences (NUPEB), Department of Biological Sciences, Institute of Exact and Biological Sciences, and.

出版信息

Adv Nutr. 2015 Nov 13;6(6):729-37. doi: 10.3945/an.114.008144. Print 2015 Nov.

DOI:10.3945/an.114.008144
PMID:26567197
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4642413/
Abstract

Although fructose consumption has dramatically increased and is suspected to be causally linked to metabolic abnormalities, the mechanisms involved are still only partially understood. We discuss the available data and investigate the effects of dietary fructose on risk factors associated with metabolic disorders. The evidence suggests that fructose may be a predisposing cause in the development of insulin resistance in association with the induction of hypertriglyceridemia. Experiments in animals have shown this relation when they are fed diets very high in fructose or sucrose, and human studies also show this relation, although with conflicting results due to the heterogeneity of the studies. The link between increased fructose consumption and increases in uric acid also has been confirmed as a potential risk factor for metabolic syndrome, and insulin resistance/hyperinsulinemia may be causally related to the development of hypertension. Collectively, these results suggest a link between high fructose intake and insulin resistance, although future studies must be of reasonable duration, use defined populations, and improve comparisons regarding the effects of relevant doses of nutrients on specific endpoints to fully understand the effect of fructose intake in the absence of potential confounding factors.

摘要

尽管果糖的摄入量急剧增加,并且被怀疑与代谢异常存在因果关系,但其中涉及的机制仍仅被部分理解。我们讨论现有数据,并研究膳食果糖对与代谢紊乱相关的风险因素的影响。证据表明,果糖可能是与高甘油三酯血症的诱导相关联的胰岛素抵抗发展的一个诱发因素。动物实验表明,当给它们喂食果糖或蔗糖含量非常高的饮食时会出现这种关系,人体研究也显示了这种关系,不过由于研究的异质性,结果相互矛盾。果糖摄入量增加与尿酸升高之间的联系也已被确认为代谢综合征的一个潜在风险因素,并且胰岛素抵抗/高胰岛素血症可能与高血压的发展存在因果关系。总体而言,这些结果表明高果糖摄入量与胰岛素抵抗之间存在联系,不过未来的研究必须有合理的时长,使用特定人群,并改善关于相关剂量营养素对特定终点影响的比较,以便在不存在潜在混杂因素的情况下充分理解果糖摄入的影响。