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Related Experiment Videos

Decrease in tetrahydrobiopterin as a possible cause of nephropathy in type II diabetic rats.

M Okumura1, M Masada, Y Yoshida

  • 1Department of Internal Medicine, Osaka City General Hospital, Osaka, Japan.

Kidney International
|June 16, 2006
PubMed
Summary
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Diabetic nephropathy is linked to reduced nitric oxide (NO) synthesis. This study shows (6R)-5,6,7,8-tetrahydrobiopterin (BH4) deficiency contributes to kidney disease in type II diabetes, and BH4 supplementation or benidipine treatment may offer renoprotection.

Area of Science:

  • Nephrology
  • Endocrinology
  • Biochemistry

Background:

  • Diabetic nephropathy is associated with decreased renal nitric oxide (NO) synthesis.
  • (6R)-5,6,7,8-tetrahydrobiopterin (BH4), an essential cofactor for NO synthase, may be deficient in diabetic kidney disease.

Purpose of the Study:

  • To investigate the role of BH4 deficiency in the pathogenesis of diabetic nephropathy.
  • To evaluate the renoprotective effects of BH4 supplementation and benidipine treatment in a type II diabetes rat model.

Main Methods:

  • Otsuka Long-Evans Tokushima Fatty (OLETF) rats (type II diabetes model) and Long-Evans Tokushima Otsuka (LETO) rats (controls) were used.
  • OLETF rats were treated with BH4 or benidipine, or left untreated.
  • Proteinuria, renal BH4 levels, and GTP cyclohydrolase I (GTPCH) activity were measured.

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Main Results:

  • Proteinuria worsened with age in OLETF rats, but was reduced by BH4 supplementation.
  • BH4 levels and GTPCH activity were decreased in OLETF rats' kidneys and plasma.
  • Benidipine treatment improved proteinuria and preserved BH4 levels without lowering blood pressure, and reduced glomerulosclerosis.

Conclusions:

  • Renal BH4 deficiency plays a critical role in type II diabetic nephropathy.
  • BH4 supplementation and benidipine show renoprotective effects.
  • Benidipine may exert therapeutic benefits by preserving BH4 levels.