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Abstract: FR-PO452

The Differential Roles of Leptin, Adiponectin, and Omentin on Phenotype Transition of Human Peritoneal Mesothelial Cells

Session Information

Category: Dialysis

  • 702 Dialysis: Home Dialysis and Peritoneal Dialysis


  • Kang, Hyun-Jung, Ewha Womans University, Seoul, Korea (the Republic of)
  • Kim, Dal-Ah, Ewha Womans University, Seoul, Korea (the Republic of)
  • Her, Ye rim, Ewha Womans University, Seoul, Korea (the Republic of)
  • Kang, Duk-Hee, Ewha Womans University, Seoul, Korea (the Republic of)

Functional and structural integrity of peritoneal membrane is essential for successful peritoneal dialysis (PD). Residential cells in peritoneal cavity are mesothelial cells (MCs), endothelial cells, fibroblasts, and adipocytes (ACs) located in submesothelial tissue. Previous studies focused on the role of peritoneal MCs in the development of peritoneal fibrosis, however the role of neighboring adipose tissue and adipokines released from ACs has not been investigated. Since there are now compelling evidences suggesting that ACs exert important metabolic and proinflammatory effects on peripheral tissue, we examined the effect of representative adipokines, leptin, adiponectin, and omentin on phenotype transition of MCs.


The effect of co- and pre-treatment of leptin (10~100 ng/mL) or adiponectin (1~2 μg/mL) or omentin (0.5~1 μg/mL) on epithelial-to-mesenchymal transition (EMT) of cultured human peritoneal MCs was investigated. The effect of leptin, adiponectin, and omentin gene silencing using siRNA technique on TGF-β-induced EMT was examined. EMT was assessed by the changes in morphology and markers of epithelial and mesenchymal cells both in mRNA and protein levels. Activation of Smad2/3, Erk1/2 MAPK, p38 MAPK phosphorylation was also assessed.


Leptin, adiponectin or omentin per se did not alter the expression of the markers of EMT of MCs up to 72 hours. Leptin (100 ng/mL) aggravated TGF-β (1 ng/mL)-induced EMT whereas adiponectin (2 μg/mL) and omentin (1 μg/mL) ameliorated TGF-β-induced EMT of MCs at 48 hours of stimulation. Leptin gene silencing alleviated TGF-β-induced EMT and adiponectin or omentin siRNA treatment enhanced TGF-β-induced EMT. EMT induced by 24-hour exposure to TGF-β was reversible upon the removal of TGF-β, and this reversal of EMT was further accentuated with co-treatment of adiponectin for additional 48 hours. Reversibility of EMT after removal of TGF-β stimulation was blocked by leptin treatment. Leptin gene silencing ameliorated TGF-β-induced activation of Smad2/3 in MCs.


Our results suggest the differential role of leptin, adiponectin and omentin in phenotype transition of MCs and peritoneal fibrosis. Modulation of the expression/activity of adipokines can be a novel target for prevention and treatment of peritoneal fibrosis.