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Publication

Diabetic nephropathy is accelerated by farnesoid X receptor deficiency and inhibited by farnesoid X receptor activation in a type 1 diabetes model.

Xiaoxin X Wang | Tao Jiang | Yan Shen | Yupanqui Caldas | Shinobu Miyazaki-Anzai | Hannah Santamaria | Cydney Urbanek | Nathaniel Solis | Pnina Scherzer | Linda Lewis | Frank J Gonzalez | Luciano Adorini | Mark Pruzanski | Jeffrey B Kopp | Jill W Verlander | Moshe Levi
Diabetes | 2010

The pathogenesis of diabetic nephropathy is complex and involves activation of multiple pathways leading to kidney damage. An important role for altered lipid metabolism via sterol regulatory element binding proteins (SREBPs) has been recently recognized in diabetic kidney disease. Our previous studies have shown that the farnesoid X receptor (FXR), a bile acid-activated nuclear hormone receptor, modulates renal SREBP-1 expression. The purpose of the present study was then to determine if FXR deficiency accelerates type 1 diabetic nephropathy in part by further stimulation of SREBPs and related pathways, and conversely, if a selective FXR agonist can prevent the development of type 1 diabetic nephropathy.

Pubmed ID: 20699418

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Associated grants

  • Agency: NIA NIH HHS, United States
    Id: R01 AG026529
  • Agency: NIDDK NIH HHS, United States
    Id: R01 DK098336
  • Agency: NIA NIH HHS, United States
    Id: R01AG-026529
  • Agency: NIDDK NIH HHS, United States
    Id: U01 DK076134
  • Agency: NIDDK NIH HHS, United States
    Id: U01 DK-076134

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