Impaired ³H-Testosterone Uptake and Metabolism in the Accessory Sex Glands of Diabetic Castrated Male Rats

Abstract

The uptake and retention of 1, 2-³H-testosterone in accessory sex glands, muscle and liver of streptozotocin diabetic castrated male rats, insulin-treated diabetic castrated rats and non-diabetic castrated control rats were studied at various time intervals after an intravenous injection. Diabetes reduced the retention of ³H-testosterone in the prostate, the preputial gland and the epididymis. Exogenous insulin slightly increased the retention of ³H-testosterone in these tissues of diabetic rats. No significant differences in the radioactivity in the rectus abdominis muscle, the coagulating glands and the seminal vesicles were found between the various experimental groups. Ventral prostate homogenates obtained from diabetic and control rats were incubated with ³H-testosterone in vitro. The steroids were extracted and thin-layer chromatographs were scanned for radioactivity. In prostatic homogenates taken from diabetic rats, testosterone transformation to dihydrotestosterone was reduced. The results indicate that the impaired function and androgen retention of the accessory sex glands of diabetic male rats is at least partly due to the reduced formation of dihydrotestosterone from testosterone.

Experimental diabetes has adverse effects on the differentiation of ventral prostate during sexual maturation of rats

“…It is therefore suggested that the diabetes‐induced impairment in the availability of testosterone at the level of ventral prostate and its conversion to dihydrotestosterone (DHT) may be responsible for the histological changes recorded in the present study. Further, STZ‐diabetes in adult rats has been shown to reduce androgen receptor content (Tesone et al,1986) and uptake and retention of 3 H‐testosterone in accessory sex glands (Oksanen and Tuohimaa,1975). Therefore, the observed adverse effects in ventral prostate may also be due to the impaired binding of androgen to its receptor.…”

“…Though the adverse effects of diabetes on testicular functions are well established (Handelsman et al,1985; Murray et al,1985; Sudha et al,1999), there is relatively less information on the impact of diabetes on the accessory sex organs (Oksanen and Tuohimaa,1975; Balasubramanian et al,1991), which contribute a major portion of seminal plasma (Brandes,1974; Marker et al,2003). Prostate, an androgen‐dependent accessory sex organ, secretes a complex mixture of nutrients in seminal fluid, which are essential for sperm viability, motility, and fertilizing capacity (Brandes,1974; Cunha et al,1987; Lee,1997).…”

Alteration of α_1A-Adrenoceptor Gene Expression in the Prostate of Streptozotocin-Induced Diabetic Rats

“…The mechanism of how hyperglycemia may affect · 1A -AR gene expression is not clear. In an earlier report, Oksanen and Tuohimaa [31] demonstrated reduced testosterone transformation to dihydrotestosterone in the prostate of diabetic rats. Whether neuroendocrine interaction plays an important part needs further investigations.…”

Effects of puerarin in STZ-induced diabetic rats by oxidative stress and the TGF-β1/Smad2 pathway

“…2,3 Streptozotocin (STZ)-diabetes in adult rats has been shown to reduce the androgen receptor content, 4 uptake and retention of [3H]testosterone in accessory sex glands. 5 Earlier reports from the author's laboratory [6][7][8] and others 9,10 have shown decreased synthesis and availability of testosterone in STZ-induced diabetic rats. Induction of diabetes causes a signicant reduction in the prostatic weight and serum testosterone level in rats.…”