小柯机器人

美国威尔康奈尔医学中心Marcus D. Goncalves小组发现，饮食中的果糖能改善肠道细胞的生存和营养吸收。相关论文于2021年8月18日在线发表在《自然》杂志上。

研究人员表明，饮食中的果糖能提高肠道细胞的存活率，并增加几种小鼠模型的肠绒毛长度。绒毛长度的增加扩大了肠道的表面积，并增加了高脂肪饮食的小鼠的营养吸收和脂肪含量。在缺氧的肠道细胞中，1-磷酸果糖抑制丙酮酸激酶的M2异构体来促进细胞存活。遗传上敲除己糖激酶或刺激丙酮酸激酶可防止绒毛伸长，并废除用高果糖玉米糖浆喂养小鼠所诱发的营养吸收和肿瘤生长的现象。因此，果糖通过一种异生代谢物促进细胞生存的能力提供了对西方饮食产生过量脂肪的新见解，也是对高果糖玉米糖浆促进肿瘤生长的一种解释。

据介绍，果糖消费与肥胖和癌症发病率的上升有关，而肥胖和癌症是全球发病率和死亡率的两个主要原因。饮食中的果糖代谢始于小肠上皮，在那里果糖被5型葡萄糖转运器（GLUT5；由SLC2A5编码）运输，并被酮六激酶磷酸化形成1-磷酸果糖，在细胞中积累到高水平。尽管这一途径与肥胖和肿瘤的促进有关，但在肠道中驱动这些病变的确切机制仍不清楚。

附：英文原文

Title: Dietary fructose improves intestinal cell survival and nutrient absorption

Author: Taylor, Samuel R., Ramsamooj, Shakti, Liang, Roger J., Katti, Alyna, Pozovskiy, Rita, Vasan, Neil, Hwang, Seo-Kyoung, Nahiyaan, Navid, Francoeur, Nancy J., Schatoff, Emma M., Johnson, Jared L., Shah, Manish A., Dannenberg, Andrew J., Sebra, Robert P., Dow, Lukas E., Cantley, Lewis C., Rhee, Kyu Y., Goncalves, Marcus D.

Issue&Volume: 2021-08-18

Abstract: Fructose consumption is linked to the rising incidence of obesity and cancer, which are two of the leading causes of morbidity and mortality globally1,2. Dietary fructose metabolism begins at the epithelium of the small intestine, where fructose is transported by glucose transporter type 5 (GLUT5; encoded by SLC2A5) and phosphorylated by ketohexokinase to form fructose 1-phosphate, which accumulates to high levels in the cell3,4. Although this pathway has been implicated in obesity and tumour promotion, the exact mechanism that drives these pathologies in the intestine remains unclear. Here we show that dietary fructose improves the survival of intestinal cells and increases intestinal villus length in several mouse models. The increase in villus length expands the surface area of the gut and increases nutrient absorption and adiposity in mice that are fed a high-fat diet. In hypoxic intestinal cells, fructose 1-phosphate inhibits the M2 isoform of pyruvate kinase to promote cell survival5,6,7. Genetic ablation of ketohexokinase or stimulation of pyruvate kinase prevents villus elongation and abolishes the nutrient absorption and tumour growth that are induced by feeding mice with high-fructose corn syrup. The ability of fructose to promote cell survival through an allosteric metabolite thus provides additional insights into the excess adiposity generated by a Western diet, and a compelling explanation for the promotion of tumour growth by high-fructose corn syrup.

DOI: 10.1038/s41586-021-03827-2

Source: https://www.nature.com/articles/s41586-021-03827-2

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