Fructose metabolism and metabolic disease

被引：403

作者：

Hannou, Sarah A. ^{[1
,2
]}

Haslam, Danielle E. ^{[3
]}

McKeown, Nicola M. ^{[3
]}

Herman, Mark A. ^{[1
,2
]}

机构：

[1] Duke Univ, Med Ctr, Div Endocrinol & Metab, Durham, NC 27705 USA

[2] Duke Univ, Med Ctr, Duke Mol Physiol Inst, Durham, NC 27705 USA

[3] Tufts Univ, Nutr Epidemiol Program, Jean Mayer US Dept Agr, Human Nutr Res Ctr Aging, Boston, MA 02111 USA

来源：

JOURNAL OF CLINICAL INVESTIGATION | 2018年 / 128卷 / 02期

关键词：

SWEETENED BEVERAGE CONSUMPTION; ELEMENT-BINDING PROTEIN; HEPATIC INSULIN-RESISTANCE; CORONARY-HEART-DISEASE; DE-NOVO LIPOGENESIS; GROWTH-FACTOR; 21; URIC-ACID; DIETARY FRUCTOSE; OXIDATIVE STRESS; ALDOSE REDUCTASE;

D O I：

10.1172/JCI96702

中图分类号：

R-3 [医学研究方法]; R3 [基础医学];

学科分类号：

1001 ;

摘要：

Increased sugar consumption is increasingly considered to be a contributor to the worldwide epidemics of obesity and diabetes and their associated cardiometabolic risks. As a result of its unique metabolic properties, the fructose component of sugar may be particularly harmful. Diets high in fructose can rapidly produce all of the key features of the metabolic syndrome. Here we review the biology of fructose metabolism as well as potential mechanisms by which excessive fructose consumption may contribute to cardiometabolic disease.

引用

页码：545 / 555

页数：11

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