Testosterone Restores Testicular Inhibin Content in Cryptorchid Rats
Autor: | Saeko Nakamura, Emi Odagiri, Kazuo Shizume, Hiroshi Demura, Tomoharu Suzuki, Hiromi Komatsu, Kazuko Jibiki, Reiko Demura |
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Rok vydání: | 1988 |
Předmět: |
Male
endocrine system medicine.medical_specialty endocrine system diseases medicine.drug_class Peptide hormone Biology Andrology Follicle-stimulating hormone Endocrinology Atrophy Internal medicine Cryptorchidism Testis medicine Animals Inhibins Testosterone Sertoli Cells Leydig cell urogenital system General Engineering Rats Inbred Strains Testosterone (patch) Organ Size Luteinizing Hormone medicine.disease Androgen Sertoli cell Rats medicine.anatomical_structure Follicle Stimulating Hormone Luteinizing hormone hormones hormone substitutes and hormone antagonists |
Zdroj: | Endocrinologia Japonica. 35:385-390 |
ISSN: | 2185-6370 0013-7219 |
DOI: | 10.1507/endocrj1954.35.385 |
Popis: | The effects of testosterone administration on testicular inhibin content and histology were studied in bilaterally cryptorchid rats, in which a marked decrease in testicular inhibin content had been observed. Mature male Wistar rats weighing approximately 300 g were made bilaterally cryptorchid by placing the testes in the abdominal cavity. Testosterone in oil, 0.1, 1.0 or 10 mg, was given i.m. each week. Testicular inhibin and testosterone content, histology and plasma LH, FSH and testosterone were studied 2 weeks later. Abnormally decreased testicular inhibin in cryptorchidism was restored toward normal by testosterone in a dose dependent manner in 2 weeks after surgery. Sertoli cell structure also recovered toward normal with increasing amount of testosterone. Decreased testicular testosterone content and Leydig cell atrophy were observed with suppressed plasma LH and FSH after testosterone. These results showed that the increased plasma concentration of testosterone had a stimulatory effect on the Sertoli cell function in cryptorchidism, in which compensated Leydig cell failure was demonstrated. |
Databáze: | OpenAIRE |
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