Testicular Lesions of Streptozotocin Diabetic Rats

Oksanen, Aulikki

doi:10.1159/000178671

Cited by 75 publications

(65 citation statements)

References 8 publications

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“…Among other complications, impairment of testicular function and fertility occurs in these diabetic animals: a spermatogenic arrest at step 7 spermatids was seen similar to that found in hypophysectomized animals [2]. Diminution of testicular androgen production in vivo as well as in vitro (incubation of interstitial cells) was described for streptozotocin-diabetic rats [3,4].…”

supporting

confidence: 62%

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Evaluation of steroid biosynthetic lesions in isolated Leydig cells from the testes of streptozotocin-diabetic rats

1982

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Summary.In streptozotocin-treated adult male rats, the mechanisms of reduced response of testicular Leydig cells in vitro to stimulation with human chorionic gonadotropin was investigated. A decrease in testosterone formation by 70% after 6 weeks of diabetes mellitus is combined with diminished intracellular cyclic AMP accumulation as well as with a disturbance in progesterone conversion to androgens. The latter is also reflected by reduced progesterone binding to the cytochrome P-450 moiety of the steroid-17a-hydroxylase system.Key words: Streptozotocin-diabetes, Leydig cells, human chorionic gonadotropin, cyclic AMP, testosterone production, steroid metabolism, progesterone binding to cytochrome P-450.Disturbances of spermatogenesis are well-known complications of diabetes mellitus in male patients, but there are only few and contradictory data concerning their hormonal state [1].Streptozotocin-induced diabetes mettitus in rats is frequently used as a model for studying late effects of the diabetic state. Among other complications, impairment of testicular function and fertility occurs in these diabetic animals: a spermatogenic arrest at step 7 spermatids was seen similar to that found in hypophysectomized animals [2]. Diminution of testicular androgen production in vivo as well as in vitro (incubation of interstitial cells) was described for streptozotocin-diabetic rats [3,4]. This depression of endocrine testicular function was reported to be the consequence of the small amounts of luteinizing hormone releasing hormone (LHRH) secreted by the hypothalamus and of a reduction of blood lutropin (LH) levels [3]. Testicular functions and fertility could be improved by insulin treatment [4] and restored by means of a combined insulinhuman chorionic gonadotropin (HCG) therapy [5].The present study was undertaken to answer the question (1) can the probable loss of LH receptors on the surface of Leydig cells [6] alone explain diminished testosterone synthesis in testes from streptozotocindiabetic rats ? (2) are there additional disturbances within the steroidogenic pathways which could also be responsible for diabetic testicular injury? Materials and MethodsMale Wistar rats, weighing 190-210 g at the beginning of the experiment, were used. Diabetes was induced by intraperitoneal injection of 100 mg streptozotocin/kg body weight (Calbiochem, GieBen, FRG; freshly prepared in 0.01 mol/l citrate buffer, pH 4.5). The diabetic state was verified by glucosuria 24 h later; venous blood levels of glucose were controlled at least twice weekly using the Ames reflectometer system. Animals exhibiting post prandial blood glucose levels < 3 g/1 were excluded from the diabetic group. In all other cases, duration of diabetes was 3 or 6 weeks as indicated. Control rats were given vehicle injection only. Animals were fed pelleted food and tap water ad libitum.With this dose of streptozotocin, a 95% manifestation rate of hyperglycemia and glucosuria was achieved; mortality rate was 8% (n = 43). The body weight gain was + 1% in diabetic a...

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supporting

confidence: 62%

“…(2) are there additional disturbances within the steroidogenic pathways which could also be responsible for diabetic testicular injury?…”

mentioning

confidence: 99%

Evaluation of steroid biosynthetic lesions in isolated Leydig cells from the testes of streptozotocin-diabetic rats

1982

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“…Several studies have demonstrated a stepwise decrease in mean testosterone level per progressive increase in fasting plasma glucose throughout the whole range of plasma glucose [60,62,63]. In laboratory animals, diabetes has been associated with reductions in testicular Leydig cell number [66,67,68] and in testosterone secretion [68,69], possibly due to a direct adverse effect of glycaemia [68].…”

Section: Discussionmentioning

confidence: 99%

Diabetes mellitus and risk of prostate cancer: a meta-analysis

2004

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Aims/hypothesis. The association of diabetes mellitus with prostate cancer has been controversial. This study examines the strength of this association by conducting a detailed meta-analysis of the studies published in peer-reviewed literature on the subject. Methods. A comprehensive search for articles published up to 2003 was performed, reviews of each study were conducted and data were abstracted. Prior to meta-analysis, the studies were evaluated for publication bias and heterogeneity. Pooled relative risk (RR) was calculated using the random-and the fixedeffects models. Subgroup and sensitivity analyses were also performed. Results. We included 14 studies, published between 1971 and 2002, in the meta-analysis (five case-control studies, nine cohort studies). We found no evidence of publication bias (p=0.89) or heterogeneity among the studies (p=0.38). The association of diabetes with prostate cancer was statistically significant, both on the basis of a random-effects model (RR=0.91, 95% CI: 0.86 to 0.96), and on the basis of a fixed-effects model (RR=0.91, 95% CI: 0.88 to 0.94). When the analysis was stratified into subgroups according to study design, the association was inverse in both cohort and case-control studies, but only in the former was it statistically significant. The sensitivity analysis strengthened our confidence in the validity of this association. Conclusions/interpretation. Our meta-analysis findings provide strong evidence that people with diabetes have a significant decrease in risk of developing prostate cancer. There is biological evidence to support this association.

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“…The existence of specific insulin receptors in Leydig cells has been demonstrated, as has a decrease in these receptors in diabetic animals [25]. The seminiferous tubules of diabetic rats undergo degenerative changes until spermatogenesis is arrested [29] with a corresponding decrease in the production of CO, from glucose by the sperm and seminiferous tubules [ 121. In summary, future work should be directed toward clarifying the influence of diabetes mellitus and insulin on the function of the seminiferous tubule, testicular steroidogenesis, and its hypothalamichypophyseal control.…”

Section: Discussionmentioning

confidence: 99%

Semen Characteristics and Diabetes Mellitus: Significance of Insulin in Male Infertility

García-Díez¹,

Corrales²,

Hernandez-Diaz³

et al. 1991

Archives of Andrology

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A study was made of semen quality and serum hormonal profiles (FSH, LH, prolactin, testosterone) of patients with type I diabetes mellitus. Semen parameters and levels of prolactin and testosterone were significantly altered in the diabetic state. The concentration of insulin in serum and seminal plasma and the serum levels of FSH, LH, and testosterone were measured in 80 men classified in the following groups: fertile subjects, infertile normoglycemic subjects, subjects with carbohydrate intolerance, and excretory and secretory azoospermic subjects. In all groups, seminal insulin concentrations were higher than those obtained in serum. The hormone appears to freely cross the blood-testis barrier, there to be concentrated in the semen. The levels of insulin in serum and seminal plasma did not correlate with semen parameters and are not suitable markers of seminal quality. For unknown reasons, the concentrations of insulin in seminal plasma were lower in the subjects suffering from carbohydrate intolerance.

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Testicular Lesions of Streptozotocin Diabetic Rats

Cited by 75 publications

References 8 publications

Evaluation of steroid biosynthetic lesions in isolated Leydig cells from the testes of streptozotocin-diabetic rats

Evaluation of steroid biosynthetic lesions in isolated Leydig cells from the testes of streptozotocin-diabetic rats

Diabetes mellitus and risk of prostate cancer: a meta-analysis

Semen Characteristics and Diabetes Mellitus: Significance of Insulin in Male Infertility

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