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Effects of insulin replacement on ejaculatory dysfunction in streptozotocin-induced diabetic rats
Akihiko Yonezawa1, Manabu Ebiko, Masaru Yoshizumi
1Department of Physiology and Anatomy, Tohoku Pharmaceutical University, Sendai, Miyagi, Japan. yonezawa@tohoku-pharm.ac.jp
Objectives:
To investigate the effects of insulin replacement on ejaculatory dysfunction in streptozotocin (STZ)-induced diabetic rats.
Methods:
Rats were divided into three groups: (i) STZ-treated group; (ii) STZ-treated + insulin replacement (5 and 2 international units [IU]) group; and (iii) control group. The ejaculatory function in rats was evaluated using the spontaneous seminal emission (SSE) test. The amount of seminal vesicle fluid (SVF) stored in seminal vesicle was measured after the SSE test. Blood glucose was measured using a simplified blood glucose meter.
Results:
In the SSE test, the ejaculatory capacity in STZ-induced diabetic rats deteriorated with time after the onset of diabetes, and the incidence of SSE and the amount of ejaculated seminal material (SM) were significantly decreased from 5 weeks after STZ administration. Likewise, the amount of SVF was also significantly decreased in a time-dependent manner. One week after STZ administration when ejaculatory capacity had not yet diminished, insulin replacement (for 4 weeks) completely prevented the decrease in frequency of SSE, the amount of SM and SVF. However, insulin replacement after the dysfunction had occurred (5 or 15 weeks after STZ administration) did not allow all parameters for ejaculatory function to be restored to the levels of the control group.
Conclusion:
This study demonstrates that at an early stage following the onset of diabetes, insulin replacement can prevent ejaculatory dysfunction in STZ-induced diabetic rats, but once the dysfunction occurs, treatment with insulin alone does not restore the ejaculatory capacity to normal levels. In addition, this study suggests that the loss of seminal emission that results from a decrease in SVF may be involved in the mechanism of ejaculatory dysfunction in diabetic rats.
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