ASN's Mission

To create a world without kidney diseases, the ASN Alliance for Kidney Health elevates care by educating and informing, driving breakthroughs and innovation, and advocating for policies that create transformative changes in kidney medicine throughout the world.

learn more

Contact ASN

1401 H St, NW, Ste 900, Washington, DC 20005


The Latest on X

Kidney Week

Abstract: FR-PO401

Metabolomics and In Vitro Validation Study to Identify the Preventive Effect of Sodium-Glucose Cotransporter 2 Inhibitor on the Progression of Diabetic Nephropathy

Session Information

Category: Development‚ Stem Cells‚ and Regenerative Medicine

  • 500 Development‚ Stem Cells‚ and Regenerative Medicine


  • Jo, Hyung Ah, Inje University Ilsan Paik Hospital, Goyang, Korea (the Republic of)
  • Yang, Seung Hee, Seoul National University College of Medicine, Seoul, Korea (the Republic of)

We aimed to determine the metabolic profile of kidney resident cells under hyperglycemic conditions and following SGLT2 inhibitor treatment. The targeted metabolomics using the Absolute IDQ-p180 kit was applied to quantify metabolites in the kidney resident cells stimulated by high glucose (25, 50 µM) and following SGLT2 inhibitor, dapagliflozin treatment.


The primary cultured human tubular epithelial cells (TECs), podocytes, and glomerular endothelial cells (GECs) were used to identify metabolomic patterns according to hyperglycemic conditions following dapagliflozin treatment.


The metabolomic pattern of kidney resident cells is distinctly depicted in the hyperglycemic stimuli compared to control (Figure 1).
The levels of Asparagine, PC aa C38:4, and PC ae C34:1 were elevated in the TECs stimulated with 50 µM of glucose and significantly decreased after dapagliflozin treatment. The metabolite level of PC aa C28:1 was decreased in the TECs according to 50 µM of glucose treatment, and dapagliflozin treatment elevated its level. The level C18:1-OH was significantly decreased after 50 µM of glucose compared with control and its level was significantly increased after dapagliflozin treatment in podocytes. The level of C12 in the GECs was decreased after treatment with 50 µM of glucose, whereas dapagliflozin treatment significantly elevated its level. In vitro analysis showed that the treatment with glucose significantly increased the expression of fibronectin dose-dependently assessed by Western blot in the TECs, podocytes, and GECs. Dapagliflozin treatment significantly abrogated the high-glucose-induced increased expression of fibronectin (Figure 2).


The metabolic pattern of renal resident cells after SGLT2 inhibitor treatment is thought to originate from pathways associated with renal anti-fibrosis in diabetic conditions.