Department of Nephrology, Rakuwakai Otowa Hospital, Kyoto, Japan
Department of Biochemistry, Shiga University of Medical Science, Shiga, Japan.
J Am Soc Nephrol. 2020 May;31(5):898-906. doi: 10.1681/ASN.2019101015. Epub 2020 Apr 6.
Understanding fructose metabolism might provide insights to renal pathophysiology. To support systemic glucose concentration, the proximal tubular cells reabsorb fructose as a substrate for gluconeogenesis. However, in instances when fructose intake is excessive, fructose metabolism is costly, resulting in energy depletion, uric acid generation, inflammation, and fibrosis in the kidney. A recent scientific advance is the discovery that fructose can be endogenously produced from glucose under pathologic conditions, not only in kidney diseases, but also in diabetes, in cardiac hypertrophy, and with dehydration. Why humans have such a deleterious mechanism to produce fructose is unknown, but it may relate to an evolutionary benefit in the past. In this article, we aim to illuminate the roles of fructose as it relates to gluconeogenesis and fructoneogenesis in the kidney.
了解果糖代谢可能为肾脏病理生理学提供新的见解。为了维持全身葡萄糖浓度,近端肾小管细胞将果糖作为糖异生的底物重吸收。然而,当果糖摄入过多时,果糖代谢代价高昂,导致肾脏内能量耗竭、尿酸生成、炎症和纤维化。最近的科学进展是发现果糖在病理条件下可以从葡萄糖内源性产生,不仅在肾脏疾病中如此,而且在糖尿病、心脏肥大和脱水时也是如此。为什么人类有如此有害的产生果糖的机制尚不清楚,但它可能与过去的进化优势有关。在本文中,我们旨在阐明果糖在肾脏中与糖异生和果糖生成相关的作用。