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Dysfunctions of the epididymis as a result of primary carnitine deficiency in juvenile visceral steatosis mice
Author(s) -
Toshimori Kiyotaka,
Kuwajima Masamichi,
Yoshinaga Kazuya,
Wakayama Tomohiko,
Shima Kenji
Publication year - 1999
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/s0014-5793(99)00241-0
Subject(s) - epididymis , steatosis , obstructive azoospermia , medicine , endocrinology , infertility , carnitine , juvenile , duct (anatomy) , azoospermia , mesonephric duct , cholangiocyte , biology , anatomy , andrology , sperm , kidney , pregnancy , genetics
The juvenile visceral steatosis mutant mice serve as an animal model of primary carnitine deficiency, classified as the sudden infant death syndrome. The defect in carnitine uptake was recently found to be due to a defect in the carnitine transporter gene. We herein report, for the first time, the characteristics of epididymal dysfunction in juvenile visceral steatosis mice. At 8–9 weeks of age, the epididymis was deformed and weight was significantly increased. Histologically, the duct of the proximal epididymis was dilated due to the accumulation of an unusually high level of spermatozoa. Spermatozoa were extravasated from the epididymal duct into the stroma. In contrast, the duct of the distal epididymis was constricted and contained no spermatozoa. Thus, the epididymal disorder causes obstructive azoospermia, leading to infertility.