Division of Renal Diseases and Hypertension, University of Colorado Denver, Aurora, CO;
Laboratory of Renal Physiopathology, INC Ignacio Chávez, Mexico City, Mexico; and.
Adv Nutr. 2017 May 15;8(3):412-422. doi: 10.3945/an.116.014654. Print 2017 May.
Fructose-containing added sugars, such as sucrose and high-fructose corn syrup, have been experimentally, epidemiologically, and clinically shown to be involved in the current epidemics of obesity and diabetes. Here we track this history of intake of sugar as it relates to these epidemics. Key experimental studies that have identified mechanisms by which fructose causes obesity and diabetes are reviewed, as well as the evidence that the uricase mutation that occurred in the mid-Miocene in ancestral humans acted as a "thrifty gene" that increases our susceptibility for fructose-associated obesity today. We briefly review recent evidence that obesity can also be induced by nondietary sources of fructose, such as from the metabolism of glucose (from high-glycemic carbohydrates) through the polyol pathway. These studies suggest that fructose-induced obesity is driven by engagement of a "fat switch" and provide novel insights into new approaches for the prevention and treatment of these important diseases.
含果糖的添加糖，如蔗糖和高果糖玉米糖浆，已通过实验、流行病学和临床研究表明与当前肥胖和糖尿病的流行有关。在这里，我们跟踪糖的摄入历史，了解其与这些流行病的关系。本文回顾了确定果糖导致肥胖和糖尿病的机制的关键实验研究，以及中更新世在人类祖先中发生的尿酸酶突变作为一种“节俭基因”的证据，这种基因增加了我们今天对果糖相关肥胖的易感性。我们简要回顾了最近的证据，表明肥胖也可以由果糖的非饮食来源引起，例如通过多元醇途径代谢葡萄糖（来自高血糖碳水化合物）。这些研究表明，果糖引起的肥胖是由“脂肪开关”的激活驱动的，并为预防和治疗这些重要疾病提供了新的见解。
