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Absence of testosterone exacerbates diabetic renal disease
Author(s) -
Maric Christine,
Wells Corinne C,
Xu Qin
Publication year - 2007
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.21.6.a1417-a
Subject(s) - medicine , endocrinology , testosterone (patch) , streptozotocin , diabetes mellitus , castration , diabetic nephropathy , kidney , hormone , glomerulosclerosis , proteinuria
Background: Studies suggest that testosterone exacerbates and that absence of testosterone (castration) protects from development of non‐diabetic renal disease. However, the contribution of testosterone to diabetic renal disease has not been studied. Objectives: We examined the effects of castration on diabetes‐associated renal disease. Methods: The study was performed in 10 week‐old male Sprague‐Dawley non‐diabetic (ND), streptozotocin (STZ)‐induced diabetic (D) and STZ‐castrated (Dcas) rats (n=5/group) for 14 weeks. Results: D was associated with increased albumin excretion (UAE; ND, 13.5±1.5; D, 77.5±14.9; p<0.001), glomerulosclerosis (GSI; ND, 0.07±0.01; D, 0.71±0.10 AU; p<0.01), tubulointerstitial fibrosis (TIFI, 0.20±0.03; D, 1.19±0.12 AU; p<0.01) and increased TGF‐β protein expression (ND, 2.0±0.1; D, 2.6±0.1 ROD; p<0.01). Castration did not improve UAE (67.6±7.4 mg/day) or GSI (0.83±0.08 AU) and interestingly, exacerbated TIFI (1.91±0.24 AU; p<0.05 vs D) and TGF‐β protein expression (3.2±0.2; p<0.05 vs D). Conclusion: Our results suggest that in the diabetic kidney, absence of testosterone exacerbates the disease, suggesting that sex hormones may be differently regulated thus resulting in differential effects in the diabetic vs. non‐diabetic kidney. Most importantly, our results suggest an important role for testosterone in the pathophysiology of diabetic renal complications.