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Am J Physiol Renal Physiol (February 20, 2007). doi:10.1152/ajprenal.00482.2006
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Submitted on December 6, 2006
Accepted on February 12, 2007

Testosterone treatment promotes tubular damage in experimental diabetes in pre-pubertal rats

Jianhong Sun1, Kay Devish2, William J Langer2, Pamela Carmines3, and Pascale H Lane2*

1 Internal Medicine, University of Nebraska Medical Center, Omaha, Nebraska, United States
2 Pediatrics, University of Nebraska Medical Center, Omaha, Nebraska, United States
3 Physiology, University of Nebraska College of Medicine, United States

* To whom correspondence should be addressed. E-mail: phlane{at}unmc.edu.

Puberty unmasks or accelerates progressive kidney diseases, including diabetes mellitus (DM), perhaps through effects of sex steroids. To test the hypothesis that rising androgen levels at puberty permit diabetic kidney damage, we studied 4 groups of male rats with and without streptozocin-induced DM: adult-onset (A), adult-onset after castration (AC), juvenile-onset (J), and juvenile-onset with testosterone treatment (JT). Profibrotic markers were measured after 6 weeks with blood glucose levels 300-450 mg/dl. JT permitted increased expression of mRNA for two isoforms of transforming growth factor {beta} and connective tissue growth factor compared to J animals with DM; prior castration did not provide protection in adult-onset DM. JT also permitted greater tubular staining for {alpha} smooth muscle actin and fibroblast specific protein, two markers of cell damage and potential epithelial mesenchymal transition. Once again, castration was not protective for these effects of DM in the AC group. These data indicate that puberty permits detrimental effects in the tubulointerstitium in the diabetic kidney, an effect mimicked by testosterone treatment of juvenile animals and partially blunted by castration of adults, but damage does not correlate with testosterone levels, suggesting a less direct mechanism.




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