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Acta Physiologica 2011; Volume 203, Supplement 686
Joint Congress of FEPS and Turkish Society of Physiological Sciences
9/3/2011-9/7/2011
Istanbul, Turkey
CHRONIC CENTRAL INFUSION OF APELIN-13 SUPPRESSES TESTOSTERONE LEVELS BY SUPPRESSING LH RELEASE IN RATS
Abstract number: OC38
Tekin1 Suat, Sandal1 Süleyman, Beytur2 Ali, Seker3 Burcu, Yildiz1 Sedat, Yilmaz3 Bayram
1Department of Physiology, Faculty of Medicine, Inonu University, Malatya, TURKEY
2Department of Urology, Faculty of Medicine, Inonu University, Malatya, TURKEY
3Department of Physiology, Faculty of Medicine, Yeditepe University, Istanbul, TURKEY
Objective:
Expression of apelin and its receptor, APJ, both in the hypothalamus and testes implicates a role apelin in reproduction. Therefore, the present study was designed to investigate the effects of chronic central infusion of apelin-13 on luteinizing hormone (LH), follicle stimulating hormone (FSH) and testosterone levels.
Methods:
Male Wistar rats (n=21) were divided into three groups and received either artificial cerebrospinal fluid (vehicle) or apelin-13 at concentrations of 1 or 10 nmol for seven days (via ALZET osmotic mini pumps, 10 ml/h). At the last 90 min of the infusion period, blood samples were collected at 15 min intervals (0, 15, 30, 45, 60, 75 and 90 min.) for LH and FSH analysis. At the last sampling point (90 min), blood samples were analysed for testosterone levels.
Results:
Infusion of high dose apelin-13 significantly suppressed LH release compared with the vehicle values at 30, 60 and 75 min. (p<0.05). However, FSH levels did not significantly differ among the groups. Plasma testosterone levels in high dose apelin-13 group were statistically lower than the control group (p<0.05).
Conclusions:
In conclusion, central administration of apelin-13 reduced testosterone release by suppressing LH secretion. Thus, it is suggested that use of apelin receptor antagonists may bring new approaches for the treatment of infertility.
Acknowledgement: This study was supported by Inonu University BAP (Project # 2010/140).
To cite this abstract, please use the following information:
Acta Physiologica 2011; Volume 203, Supplement 686 :OC38