Effects of Long-Term Testosterone Replacement on Copulatory Activity in Old Male Rats

Gerontology ◽  
1986 ◽  
Vol 32 (1) ◽  
pp. 10-17 ◽  
Author(s):  
H.K. Hsu ◽  
C. Hsu ◽  
John Y.L. Yu ◽  
M.T. Peng
1998 ◽  
Vol 160 (4) ◽  
pp. 1572-1575 ◽  
Author(s):  
YOSHIKAZU SATO ◽  
AKIHIKO SHIBUYA ◽  
HIDEKI ADACHI ◽  
RYU-ICHI KATO ◽  
HIROKI HORITA ◽  
...  

2019 ◽  
Vol 110 (11-12) ◽  
pp. 914-928 ◽  
Author(s):  
Charity Smith ◽  
Jo Contreras-Garza ◽  
Rebecca L. Cunningham ◽  
Jessica M. Wong ◽  
Philip H. Vann ◽  
...  

Introduction: An increasing number of middle-aged men are being screened for low testosterone levels and the number of prescriptions for various forms of testosterone replacement therapy (TRT) has increased dramatically over the last 10 years. However, the safety of TRT has come into question with some studies suggesting increased morbidity and mortality. Objective: Because the benefits of estrogen replacement in postmenopausal women and ovariectomized rodents are lost if there is an extended delay between estrogen loss and replacement, we hypothesized that TRT may also be sensitive to delayed replacement. Methods: We compared the effects of testosterone replacement after short-term (2 weeks) and long-term testosterone deprivation (LTTD; 10 weeks) in middle-aged male rats on cerebral ischemia, oxidative stress, and cognitive function. We hypothesized that LTTD would increase oxidative stress levels and abrogate the beneficial effects of TRT. Results: Hypogonadism itself and TRT after short-term castration did not affect stroke outcome compared to intact rats. However, after long-term hypogonadism in middle-aged male Fischer 344 rats, TRT exacerbated the detrimental behavioral effects of experimental focal cerebral ischemia, whereas this detrimental effect was prevented by administration of the free-radical scavenger tempol, suggesting that TRT exacerbates oxidative stress. In contrast, TRT improved cognitive performance in non-stroked rats regardless of the length of hypogonadism. In the Morris water maze, peripheral oxidative stress was highly associated with decreased cognitive ability. Conclusions: Taken together, these data suggest that TRT after long-term hypogonadism can exacerbate functional recovery after focal cerebral ischemia, but in the absence of injury can enhance cognition. Both of these effects are modulated by oxidative stress levels.


2018 ◽  
Vol 30 (3) ◽  
pp. 122-128 ◽  
Author(s):  
Jung Sik Huh ◽  
Byung Ha Chung ◽  
Chang Hee Hong ◽  
Ji Kan Ryu ◽  
Jang Hwan Kim ◽  
...  

1998 ◽  
pp. 1572-1575 ◽  
Author(s):  
YOSHIKAZU SATO ◽  
AKIHIKO SHIBUYA ◽  
HIDEKI ADACHI ◽  
RYU-ICHI KATO ◽  
HIROKI HORITA ◽  
...  

2021 ◽  
Vol 54 (1) ◽  
Author(s):  
Mayarling Francisca Troncoso ◽  
Mario Pavez ◽  
Carlos Wilson ◽  
Daniel Lagos ◽  
Javier Duran ◽  
...  

Abstract Background Testosterone regulates nutrient and energy balance to maintain protein synthesis and metabolism in cardiomyocytes, but supraphysiological concentrations induce cardiac hypertrophy. Previously, we determined that testosterone increased glucose uptake—via AMP-activated protein kinase (AMPK)—after acute treatment in cardiomyocytes. However, whether elevated glucose uptake is involved in long-term changes of glucose metabolism or is required during cardiomyocyte growth remained unknown. In this study, we hypothesized that glucose uptake and glycolysis increase in testosterone-treated cardiomyocytes through AMPK and androgen receptor (AR). Methods Cultured cardiomyocytes were stimulated with 100 nM testosterone for 24 h, and hypertrophy was verified by increased cell size and mRNA levels of β-myosin heavy chain (β-mhc). Glucose uptake was assessed by 2-NBDG. Glycolysis and glycolytic capacity were determined by measuring extracellular acidification rate (ECAR). Results Testosterone induced cardiomyocyte hypertrophy that was accompanied by increased glucose uptake, glycolysis enhancement and upregulated mRNA expression of hexokinase 2. In addition, testosterone increased AMPK phosphorylation (Thr172), while inhibition of both AMPK and AR blocked glycolysis and cardiomyocyte hypertrophy induced by testosterone. Moreover, testosterone supplementation in adult male rats by 5 weeks induced cardiac hypertrophy and upregulated β-mhc, Hk2 and Pfk2 mRNA levels. Conclusion These results indicate that testosterone stimulates glucose metabolism by activation of AMPK and AR signaling which are critical to induce cardiomyocyte hypertrophy.


2013 ◽  
Vol 56 (5) ◽  
pp. 1102-1109 ◽  
Author(s):  
Xiujing Cao ◽  
Shenghai Huang ◽  
Jiejie Cao ◽  
Tingting Chen ◽  
Ping Zhu ◽  
...  

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