Effect of Streptozotocin Diabetes on the Pituitary-Testicular Axis in the Rat

Díaz, Julio Pérez; Benítez, Alfi Contreras; Galaz, Carmen Fernandez

doi:10.1055/s-2007-1019052

Cited by 31 publications

(13 citation statements)

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“…Two hypotheses may be discussed: (1) is it possible that decreased epididymal ABP levels are due to decreased serum FSH levels? Serum FSH concentrations have been reported to be decreased in streptozotocin-diabetic animals [2], but this finding has not been confirmed by other authors [3,7]. FSH has been proposed to enhance both testicular and epididymal ABP concentrations [8,9,11] as well as the ABP production by cultured Sertoli cells from immature rats [12].…”

Section: Discussionmentioning

confidence: 42%

“…Numerous studies have demonstrated impairment of fertility [1] and testicular endocrine function [1-4] to be late complications of streptozotocin-treated hypoinsulinaemic, hyperglycaemic male rats. In addition to reports on defective spermatogenesis [5][6] and indications of disturbances of pituitary gonadotropin secretion [1][2][3][5][6][7], dysfunction of the Leydig cells resulting in diminished testosterone formation in these diabetic animals seems to be the most extensively investigated problem in this field [1][2][3][4]. …”

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confidence: 99%

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Effect of streptozotocin-induced hyperglycaemia on androgen-binding protein in rat testis and epididymis

1984

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Summary. In adult male rats treated with streptozotocin 6weeks before the experiments, androgen-binding protein concentration was increased in testicular tissue by 33% (p< 0.01) and reduced in epididymal tissue by 25% (p < 0.005) in animals exhibiting severe hyperglycaemia as compared with animals remaining in normoglycaemia or moderate hyperglycaemia. Androgen-binding protein content was diminished in epididymal tissue by 40% (p< 0.0005) but not changed in testicular tissue. If related to constant body weight, the sum of testicular and epididymal androgen-binding protein was identical in both norrno-and hyperglycaemic animals. This disturbance in androgen-binding protein distribution may be the consequence of altered testicular secretion or impaired transport of androgen-binding protein from testes to epididymides. Numerous studies have demonstrated impairment of fertility [1] and testicular endocrine function [1-4] to be late complications of streptozotocin-treated hypoinsulinaemic, hyperglycaemic male rats. In addition to reports on defective spermatogenesis [5][6] and indications of disturbances of pituitary gonadotropin secretion [1][2][3][5][6][7], dysfunction of the Leydig cells resulting in diminished testosterone formation in these diabetic animals seems to be the most extensively investigated problem in this field [1][2][3][4]. Key words:In contrast, less attention has been drawn to Sertoli cell function in diabetic animals. Although a specific androgen-binding protein (ABP) was shown several years ago to be a marker of Sertoli cell function [8][9][10][11][12][13], ABP measurements in diabetic rats have been reported in only one study [2]. A paradoxical increase of ABP content (expressed as lxl-equivalent of epididymal cytosol standard) of the testes (the site of production) but no change of ABP content of the epididymis (a possible site of action) has been found in rats 4 weeks after streptozotocin injection [2].The aims of the present study on streptozotocintreated male rats were to re-evaluate those results, to distinguish between ABP concentrations and ABP content of testes and epididymides by consideration of changes in organ weights and to make correlations between testicular or epididymal ABP and blood glucose levels in order to prove possible diabetes-induced changes in testicular ABP secretion. Materials and methodsEighteen male Han: Wistar rats, weighing 214 + 5 g (mean + SEM) at the beginning of the study, received 65 mg streptozotocin (2-desoxy-2-(3-methyl-3-nitrosurea)-la-glucopyranose; Calbiochem, Giel3en, FRG)/kg body weight, i.p. (experimental group). One rat died during week 3. Five animals (205 ___ 5 g initial body weight) were injected with citrate buffer only and served as a control group. All animals were allowed food (Altromin 1314; Altromin, Lage, FRG) and tap water ad libitum.Post-prandial blood glucose levels were examined routinely (seven times during the 6-week period of the experiment) using the Eyetone reflectometer system (Dextrostix; Ames-Miles, Frankfurt/Main, FRG). Urin...

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Section: Discussionmentioning

confidence: 42%

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confidence: 99%

Effect of streptozotocin-induced hyperglycaemia on androgen-binding protein in rat testis and epididymis

1984

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“…Various reports have suggested that the diminished sexual behavior in STZ-induced diabetic rats is related to changes in hypothalamic-pituitary gonadal axis (27,29). However, gonadectomy did not change the urethrogenital reflexes, suggesting that androgen changes are unlikely as the cause of the sexual dysfunction in this model (10).…”

Section: Discussionmentioning

confidence: 91%

Lack of central nitric oxide triggers erectile dysfunction in diabetes

Zheng¹,

Bidasee²,

Mayhan³

et al. 2007

American Journal of Physiology-Regulatory, Integrative and Comp

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Erectile dysfunction is a serious and common complication of diabetes mellitus. The proposed mechanisms for erectile dysfunction in diabetes include central and autonomic neuropathy, endothelial dysfunction, and smooth muscle dysfunction. The paraventricular nucleus (PVN) of the hypothalamus is known to be involved in centrally mediated penile erection. This study was designed to examine the role of nitric oxide (NO) within the central nervous system component of the behavioral responses including erection in diabetic rats. N-methyl-D-aspartic acid (NMDA)-induced erection, yawning, and stretch through the PVN can be blocked by prior administration of NO synthase (NOS) blocker, L-NMMA, in freely moving, conscious male normal rats. Four weeks after streptozotocin (STZ) and vehicle injections, NMDA-induced erection, yawning, and stretch responses through the PVN are significantly blunted in diabetic rats compared with control rats. Examination of neuronal NOS (nNOS) protein by Western blot analysis indicated a reduced amount of nNOS protein in the PVN of rats with diabetes compared with control rats. Furthermore, restoring nNOS within the PVN by gene transfer using adenoviral transfection significantly restored the erectile and yawning responses to NMDA in diabetic rats. These data demonstrate that a blunted NO mechanism within the PVN may contribute to NMDA-induced erectile dysfunction observed in diabetes mellitus.

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“…There is a wide disparity regarding the effects of insulin treatment on gonadotrophin levels in diabetic individuals with reports ranging from a total recovery of both LH and FSH (Seethalakshmi et al 1987), to the recovery of just one (Perez Diaz et al 1982, Hutson et al 1983, Benitez & Perez Diaz 1985, Sudha et al 2000 or even the absence of effects (Steger & Kienast 1990), suggesting that testicular function regulation is the result of a complex process in which several players are involved. Other studies have explored these aspects in more detail, and insulin treatment was observed to totally reverse all parameters of pulsatile LH secretion, which were reduced in diabetic rats and, at least partially, due to a decreased responsiveness of the pituitary to GnRH (Dong et al 1991).…”

Section: Pre-testicular Levelmentioning

confidence: 99%

“…In early experiments, it was shown that untreated diabetes caused a reduction in serum LH, testosterone levels and steroidogenic activity and that these parameters were restored by insulin treatment (Tesone et al 1976, Murray et al 1981, Perez Diaz et al 1982, Benitez & Perez Diaz 1985, raising the question on whether the effects of insulin are directly in the testis or induced through alterations in LH secretion. Furthermore, it was observed that Leydig cells' LH receptors were decreased in diabetic rats, though the binding capacity was restored after insulin administration (Charreau et al 1978).…”

Section: Testicular Levelmentioning

confidence: 99%

Antidiabetic therapies and male reproductive function: where do we stand?

Tavares¹,

Escada-Rebelo²,

Silva³

et al. 2018

Reproduction

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Diabetes mellitus has been increasing at alarming rates in recent years, thus jeopardizing human health worldwide. Several antidiabetic drugs have been introduced in the market to manage glycemic levels, and proven effective in avoiding, minimizing or preventing the appearance or development of diabetes mellitus-related complications. However, and despite the established association between such pathology and male reproductive dysfunction, the influence of these therapeutic interventions on such topics have been scarcely explored. Importantly, this pathology may contribute toward the global decline in male fertility, giving the increasing preponderance of diabetes mellitus in young men at their reproductive age. Therefore, it is mandatory that the reproductive health of diabetic individuals is maintained during the antidiabetic treatment. With this in mind, we have gathered the available information and made a critical analysis regarding the effects of several antidiabetic drugs on male reproductive function. Unlike insulin, which has a clear and fundamental role on male reproductive function, the other antidiabetic therapies' effects at this level seem incoherent. In fact, studies are highly controversial possibly due to the different experimental study approaches, which, in our opinion, suggests caution when it comes to prescribing such drugs to young diabetic patients. Overall, much is still to be determined and further studies are needed to clarify the safety of these antidiabetic strategies on male reproductive system. Aspects such as the effects of insulin levels variations, consequent of insulin therapy, as well as what will be the impact of the side effect hypoglycemia, common to several therapeutic strategies discussed, on the male reproductive system are still to be addressed.Reproduction (2018) 155 R13-R37

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Effect of Streptozotocin Diabetes on the Pituitary-Testicular Axis in the Rat

Cited by 31 publications

References 0 publications

Effect of streptozotocin-induced hyperglycaemia on androgen-binding protein in rat testis and epididymis

Effect of streptozotocin-induced hyperglycaemia on androgen-binding protein in rat testis and epididymis

Lack of central nitric oxide triggers erectile dysfunction in diabetes

Antidiabetic therapies and male reproductive function: where do we stand?

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