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<p>The kidney is a high-energy-consuming organ, and glucose is one of its principal fuel sources. It has been documented that disturbed renal glucose metabolism occurs in acute kidney injury (AKI), but whether these disturbances are consistent in different types of AKI, and how they change during the transition from AKI to chronic kidney disease (CKD), remain to be addressed. In this study, we used AKI models induced by cisplatin (20&#xa0;mg/kg, 48&#xa0;h), lipopolysaccharide (10&#xa0;mg/kg, 48&#xa0;h), and ischemia–reperfusion (48&#xa0;h) to mimic distinct etiologies, and the catalytic enzymes involved in glucose transport, gluconeogenesis, and glycolysis were evaluated at both mRNA and protein levels by qPCR and immunofluorescence, respectively. In AKI, sodium-glucose cotransporter 2 (SGLT2) and fructose-1,6-bisphosphatase 1 (FBP1) protein levels were decreased, whereas the glycolytic enzymes hexokinase 2 (HK2), phosphofructokinase muscle type (PFKM), and pyruvate kinase M2 (PKM2) protein levels were increased. During the AKI-to-CKD transition, SGLT2 remained low; HK2, PFKM, PKM2, and FBP1 displayed a biphasic pattern (early rise, late fall) that varied with injury dose and time. These findings describe the expression changes of glucose metabolic enzymes during AKI and the AKI-to-CKD transition. Direct measurements of glycolytic activity were not performed; therefore, the relationship between these expression changes and actual metabolic function remains to be determined. This study provides a descriptive foundation for future investigations of glucose metabolism during the AKI-to-CKD transition.</p>

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Renal glucose metabolic enzyme expression during AKI-to-CKD transition

  • 期刊论文

  • 发表日期：

    2026年7月8日

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  • Chaoyan Yan,
  • Yuting Zhu,
  • Mingming Liu,
  • Die Yang,
  • Yan Zha,
  • Yanjun Long,
  • Rong Dong

摘要

The kidney is a high-energy-consuming organ, and glucose is one of its principal fuel sources. It has been documented that disturbed renal glucose metabolism occurs in acute kidney injury (AKI), but whether these disturbances are consistent in different types of AKI, and how they change during the transition from AKI to chronic kidney disease (CKD), remain to be addressed. In this study, we used AKI models induced by cisplatin (20 mg/kg, 48 h), lipopolysaccharide (10 mg/kg, 48 h), and ischemia–reperfusion (48 h) to mimic distinct etiologies, and the catalytic enzymes involved in glucose transport, gluconeogenesis, and glycolysis were evaluated at both mRNA and protein levels by qPCR and immunofluorescence, respectively. In AKI, sodium-glucose cotransporter 2 (SGLT2) and fructose-1,6-bisphosphatase 1 (FBP1) protein levels were decreased, whereas the glycolytic enzymes hexokinase 2 (HK2), phosphofructokinase muscle type (PFKM), and pyruvate kinase M2 (PKM2) protein levels were increased. During the AKI-to-CKD transition, SGLT2 remained low; HK2, PFKM, PKM2, and FBP1 displayed a biphasic pattern (early rise, late fall) that varied with injury dose and time. These findings describe the expression changes of glucose metabolic enzymes during AKI and the AKI-to-CKD transition. Direct measurements of glycolytic activity were not performed; therefore, the relationship between these expression changes and actual metabolic function remains to be determined. This study provides a descriptive foundation for future investigations of glucose metabolism during the AKI-to-CKD transition.