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논문 기본 정보

자료유형
학술저널
저자정보
Nakagawa Takahiko (Rakuwakai Otowa Hospital Kyoto Japan) 강덕희 (이화여자대학교)
저널정보
대한신장학회 Kidney Research and Clinical Practice Kidney Research and Clinical Practice Vol.40 No.4
발행연도
2021.12
수록면
527 - 541 (15page)
DOI
10.23876/j.krcp.21.138

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초록· 키워드

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The Warburg effect is a unique property of cancer cells, in which glycolysis is activated instead of mitochondrial respiration despite ox- ygen availability. However, recent studies found that the Warburg effect also mediates non-cancer disorders, including kidney disease. Currently, diabetes or glucose has been postulated to mediate the Warburg effect in the kidney, but it is of importance that the War- burg effect can be induced under nondiabetic conditions. Fructose is endogenously produced in several organs, including the kidney, under both physiological and pathological conditions. In the kidney, fructose is predominantly metabolized in the proximal tubules; under normal physiologic conditions, fructose is utilized as a substrate for gluconeogenesis and contributes to maintain systemic glu- cose concentration under starvation conditions. However, when present in excess, fructose likely becomes deleterious, possibly due in part to excessive uric acid, which is a by-product of fructose metabolism. A potential mechanism is that uric acid suppresses aconi- tase in the Krebs cycle and therefore reduces mitochondrial oxidation. Consequently, fructose favors glycolysis over mitochondrial respiration, a process that is similar to the Warburg effect in cancer cells. Activation of glycolysis also links to several side pathways, including the pentose phosphate pathway, hexosamine pathway, and lipid synthesis, to provide biosynthetic precursors as fuel for re- nal inflammation and fibrosis. We now hypothesize that fructose could be the mediator for the Warburg effect in the kidney and a po- tential mechanism for chronic kidney disease.

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