Visfatin

A new player in mesangial cell physiology and diabetic nephropathy

Kyoung Song Hye, Hwa Lee Mi, Kyung Kim Bo, Yun Gyu Park, Gang Jee Ko, Young Sun Kang, Young Han Jee, Youb Han Sang, Hyun Han Kum, Kyu Kim Hyoung, Dae-Ryong Cha

Research output: Contribution to journalArticle

70 Citations (Scopus)

Abstract

Visfatin is an adipocytokine that improves insulin resistance and has an antidiabetic effect. However, the role of visfatin in the kidney has not yet been reported. In this experiment, the synthesis and physiological action of visfatin in cultured mesangial cells (MCs) were studied to investigate the role of visfatin in diabetic nephropathy. Visfatin was found synthesized in MCs as well as adipocytes. Visfatin synthesis was markedly increased, not by angiotensin II, but by high glucose stimuli. In addition, visfatin treatment induced a rapid uptake of glucose, peaking at 20 min after visfatin treatment in a dose-dependent manner. A small inhibiting RNA against insulin receptor significantly blocked visfatin-mediated glucose uptake. Visfatin stimuli also enhanced intracellular NAD levels, and treatment with FK866, which is a specific inhibitor of nicotinamide phosphoribosyltransferase (Nampt), significantly inhibited visfatin-induced NAD synthesis and glucose uptake. Visfatin treatment increased glucose transporter-1 (GLUT-1) protein expression in isolated cellular membranes, and pretreatment with cytochalasin B completely inhibited visfatin-induced glucose uptake. Moreover, immunofluorescent microscopy showed the migration of cytosolic GLUT-1 into cellular membranes after visfatin treatment. In accordance with these results, the activation of protein kinase B was detected after visfatin treatment. Furthermore, visfatin treatment dramatically increased the synthesis of profibrotic molecules including transforming growth factor-β1, plasminogen activator inhibitor-1, and type I collagen, and pretreatment with cytochalasin B completely inhibited visfatin-induced upregulation of profibrotic molecules. These results suggest that visfatin is produced in MCs, which are a novel target for visfatin, and play an important role in the pathogenesis of diabetic nephropathy.

Original languageEnglish
JournalAmerican Journal of Physiology - Renal Physiology
Volume295
Issue number5
DOIs
Publication statusPublished - 2008 Nov 1

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Nicotinamide Phosphoribosyltransferase
Cell Physiological Phenomena
Mesangial Cells
Diabetic Nephropathies
Glucose
Cytochalasin B
Facilitative Glucose Transport Proteins
NAD

Keywords

  • Glucose transporter-1
  • Glucose uptake
  • Profibrotic molecule
  • Protein kinase B

ASJC Scopus subject areas

  • Physiology
  • Urology

Cite this

Visfatin : A new player in mesangial cell physiology and diabetic nephropathy. / Hye, Kyoung Song; Mi, Hwa Lee; Bo, Kyung Kim; Park, Yun Gyu; Ko, Gang Jee; Kang, Young Sun; Jee, Young Han; Sang, Youb Han; Kum, Hyun Han; Hyoung, Kyu Kim; Cha, Dae-Ryong.

In: American Journal of Physiology - Renal Physiology, Vol. 295, No. 5, 01.11.2008.

Research output: Contribution to journalArticle

Hye, Kyoung Song ; Mi, Hwa Lee ; Bo, Kyung Kim ; Park, Yun Gyu ; Ko, Gang Jee ; Kang, Young Sun ; Jee, Young Han ; Sang, Youb Han ; Kum, Hyun Han ; Hyoung, Kyu Kim ; Cha, Dae-Ryong. / Visfatin : A new player in mesangial cell physiology and diabetic nephropathy. In: American Journal of Physiology - Renal Physiology. 2008 ; Vol. 295, No. 5.
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AU - Ko, Gang Jee

AU - Kang, Young Sun

AU - Jee, Young Han

AU - Sang, Youb Han

AU - Kum, Hyun Han

AU - Hyoung, Kyu Kim

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AB - Visfatin is an adipocytokine that improves insulin resistance and has an antidiabetic effect. However, the role of visfatin in the kidney has not yet been reported. In this experiment, the synthesis and physiological action of visfatin in cultured mesangial cells (MCs) were studied to investigate the role of visfatin in diabetic nephropathy. Visfatin was found synthesized in MCs as well as adipocytes. Visfatin synthesis was markedly increased, not by angiotensin II, but by high glucose stimuli. In addition, visfatin treatment induced a rapid uptake of glucose, peaking at 20 min after visfatin treatment in a dose-dependent manner. A small inhibiting RNA against insulin receptor significantly blocked visfatin-mediated glucose uptake. Visfatin stimuli also enhanced intracellular NAD levels, and treatment with FK866, which is a specific inhibitor of nicotinamide phosphoribosyltransferase (Nampt), significantly inhibited visfatin-induced NAD synthesis and glucose uptake. Visfatin treatment increased glucose transporter-1 (GLUT-1) protein expression in isolated cellular membranes, and pretreatment with cytochalasin B completely inhibited visfatin-induced glucose uptake. Moreover, immunofluorescent microscopy showed the migration of cytosolic GLUT-1 into cellular membranes after visfatin treatment. In accordance with these results, the activation of protein kinase B was detected after visfatin treatment. Furthermore, visfatin treatment dramatically increased the synthesis of profibrotic molecules including transforming growth factor-β1, plasminogen activator inhibitor-1, and type I collagen, and pretreatment with cytochalasin B completely inhibited visfatin-induced upregulation of profibrotic molecules. These results suggest that visfatin is produced in MCs, which are a novel target for visfatin, and play an important role in the pathogenesis of diabetic nephropathy.

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