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果糖：代谢综合征和高血压发展中的关键因素。

Fructose: a key factor in the development of metabolic syndrome and hypertension.

作者信息

Khitan Zeid, Kim Dong Hyun

机构信息

Marshall University's Joan C. Edwards School of Medicine, 1600 Medical Center Drive, Huntington, WV 25701-3655, USA ; Department of Medicine, Marshall University Joan Edwards School of Medicine, 1600 Medical Center Drive, Huntington, WV 25701-3655, USA.

出版信息

J Nutr Metab. 2013;2013:682673. doi: 10.1155/2013/682673. Epub 2013 May 25.

DOI:10.1155/2013/682673
PMID:23762544
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3677638/
Abstract

Diabetes mellitus and the metabolic syndrome are becoming leading causes of death in the world. Identifying the etiology of diabetes is key to prevention. Despite the similarity in their structures, fructose and glucose are metabolized in different ways. Uric acid, a byproduct of uncontrolled fructose metabolism is known risk factor for hypertension. In the liver, fructose bypasses the two highly regulated steps in glycolysis, glucokinase and phosphofructokinase, both of which are inhibited by increasing concentrations of their byproducts. Fructose is metabolized by fructokinase (KHK). KHK has no negative feedback system, and ATP is used for phosphorylation. This results in intracellular phosphate depletion and the rapid generation of uric acid due to activation of AMP deaminase. Uric acid, a byproduct of this reaction, has been linked to endothelial dysfunction, insulin resistance, and hypertension. We present possible mechanisms by which fructose causes insulin resistance and suggest actions based on this association that have therapeutic implications.

摘要

糖尿病和代谢综合征正成为全球主要的死亡原因。确定糖尿病的病因是预防的关键。尽管果糖和葡萄糖结构相似，但它们的代谢方式不同。尿酸是果糖代谢失控的副产物，是已知的高血压危险因素。在肝脏中，果糖绕过糖酵解中两个高度受调控的步骤，即葡萄糖激酶和磷酸果糖激酶，这两个步骤都会受到其副产物浓度增加的抑制。果糖由果糖激酶（KHK）代谢。KHK没有负反馈系统，ATP用于磷酸化。这导致细胞内磷酸盐耗竭，并由于AMP脱氨酶的激活而迅速产生尿酸。这种反应的副产物尿酸与内皮功能障碍、胰岛素抵抗和高血压有关。我们提出了果糖导致胰岛素抵抗的可能机制，并基于这种关联提出了具有治疗意义的行动建议。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/46f1/3677638/11bbc082ae54/JNUME2013-682673.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/46f1/3677638/8c57db775672/JNUME2013-682673.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/46f1/3677638/2d9e30d21f9a/JNUME2013-682673.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/46f1/3677638/3b4204903bd1/JNUME2013-682673.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/46f1/3677638/ead216fb36d7/JNUME2013-682673.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/46f1/3677638/3a0f16230730/JNUME2013-682673.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/46f1/3677638/11bbc082ae54/JNUME2013-682673.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/46f1/3677638/8c57db775672/JNUME2013-682673.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/46f1/3677638/2d9e30d21f9a/JNUME2013-682673.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/46f1/3677638/3b4204903bd1/JNUME2013-682673.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/46f1/3677638/ead216fb36d7/JNUME2013-682673.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/46f1/3677638/3a0f16230730/JNUME2013-682673.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/46f1/3677638/11bbc082ae54/JNUME2013-682673.006.jpg

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