Testosterone treatment promotes tubular damage in experimental diabetes in prepubertal rats
| Autor: | Pascale H. Lane, Kay Devish, William J. Langer, Pamela K. Carmines, Jianhong Sun |
|---|---|
| Rok vydání: | 2007 |
| Předmět: |
Male
medicine.medical_specialty Tissue Fixation Physiology medicine.drug_class Urinary system medicine.medical_treatment Connective tissue Biology Diabetes Mellitus Experimental Immediate-Early Proteins Kidney Tubules Proximal Rats Sprague-Dawley Transforming Growth Factor beta1 Transforming Growth Factor beta2 chemistry.chemical_compound Transforming Growth Factor beta3 Internal medicine Diabetes mellitus medicine Animals Diabetic Nephropathies Testosterone Sexual Maturation Kidney Tubules Distal Kidney Reverse Transcriptase Polymerase Chain Reaction Growth factor Connective Tissue Growth Factor Androgen medicine.disease Rats Kidney Tubules medicine.anatomical_structure Castration Endocrinology chemistry Intercellular Signaling Peptides and Proteins |
| Zdroj: | American Journal of Physiology-Renal Physiology. 292:F1681-F1690 |
| ISSN: | 1522-1466 1931-857X |
| DOI: | 10.1152/ajprenal.00482.2006 |
| Popis: | 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 four 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 wk with blood glucose levels 300–450 mg/dl. JT permitted increased expression of mRNA for two isoforms of transforming growth factor-β and connective tissue growth factor compared with J animals with DM; prior castration did not provide protection in adult-onset DM. JT also permitted greater tubular staining for α-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. |
| Databáze: | OpenAIRE |
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