Endocrine profile and testicular histomorphometry in adult rat offspring of diabetic mothers

Department of Physiology, Shiraz University, P.O. Box 71345, 1731, Shiraz, Iran.
The Journal of Physiological Sciences (Impact Factor: 1.9). 06/2009; 59(5):377-82. DOI: 10.1007/s12576-009-0045-7
Source: PubMed


This investigation was conducted to evaluate the effect of maternal diabetes on fetal testicular structure and function, and reproductive hormones levels. Sixteen female rats were divided into two groups. Diabetes was induced in one group by alloxan. Blood was collected from 90-day-old male offspring of both groups, and the level of blood glucose, testosterone, FSH and LH in their serum was measured. Weight, volume and various histological parameters of testes were determined. A significant increase in blood glucose and decrease in LH, FSH and testosterone in sera of offspring of diabetic mothers (ODM) were observed. The weight and volume of testes in the ODM were 22.7 and 22.9% higher, respectively, than those of the control group (P < 0.05), while the ratio of testes to body weight did not change significantly. The number of seminiferous tubules increased (+21%) significantly (P < 0.05), while thickness of the testicular capsule (-25%), number of Leydig cells (-15.6%), number of Sertoli cells (-14.9%), number of spermatogonia (-26.3%) and diameter of seminiferous tubules (-11%) showed significantly reduced values in the ODM compare to the control. In conclusion, maternal hyperglycemia has a deleterious effect on testicular parameters during fetal life, which will affect reproductive endocrine during postpuberty.

10 Reads
  • Source
    • "Severe germ-cell depletion [85] Serum testosterone [85] [87] Disruption of seminiferous tubular morphology [85] [87] Sertoli-cell vacuolization [85] Sperm production [87] Fertility [84] [87] GK rat T2D Sperm production [91] Chemically-induced models STZ rat T1D Testis weight [86] [90] Disruption of epididymis morphology and density [89] LH, FSH and testosterone serum levels [86] [88] [90] Sperm production [88] [89] Sperm counts and motility [86,88,90–92] Erectile dysfunction [70] Ejaculation dysfunction [88] [90] Mating behavior [88] [90] Fertility [90] [92] ALX rat T2D LH, FSH and testosterone serum levels [93] Disruption of seminiferous tubular morphology [93] Number of Leydig and Sertoli cells [93] Number of spermatogonia [93] Clinical studies T1D Disruption of seminiferous tubular morphology [78] Germ-cell depletion and Sertoli-cell vacuolization [78] Disruption of blood–testis barrier [78] Erectile dysfunction [70] [76] Ejaculation dysfunction [73] [74] Semen volume [76] [77] Sperm counts, motility and morphology [75] [76] [77] T2D Erectile dysfunction [69] Semen volume [5] [79] Sperm motility [79] Sperm DNA fragmentation [79] Legend: BB rat — BioBreeding genetic rodent model; GK rats — Goto–Kakizaki genetic rodent model; STZ rat — Streptozotocin-induced rodent model; ALX rat — Alloxan-induced rodent model. T1D — type 1 diabetes; T2D — type 2 diabetes; — increase; — decrease; superscript numbers are references as indicated in references section. "
    [Show abstract] [Hide abstract]
    ABSTRACT: Diabetes Mellitus (DM) is one of the greatest public health threats in modern societies. Although during a few years it was suggested that DM had no significant effect in male reproductive function, this view has been challenged in recent years. The increasing incidence of DM worldwide will inevitably result in a higher prevalence of this pathology in men of reproductive age and subfertility or infertility associated with DM is expected to dramatically rise in upcoming years. From a clinical perspective, the evaluation of semen parameters, as well as spermatozoa DNA integrity, are often studied due to their direct implications in natural and assisted conception. Nevertheless, recent studies based on the molecular mechanisms beyond glucose transport in testicular cells provide new insights in DM-induced alterations in male reproductive health. Testicular cells have their own glucose sensing machinery that react to hormonal fluctuations and have several mechanisms to counteract hyper- and hypoglycemic events. Moreover, the metabolic cooperation between testicular cells is crucial for normal spermatogenesis. Sertoli cells (SCs), which are the main components of blood-testis barrier, are not only responsible for the physical support of germ cells but also for lactate production that is then metabolized by the developing germ cells. Any alteration in this tied metabolic cooperation may have a dramatic consequence in male fertility potential. Therefore, we present an overview of the clinical significance of DM in the male reproductive health with emphasis on the molecular mechanisms beyond glucose fluctuation and transport in testicular cells.
    Biochimica et Biophysica Acta 01/2013; 1832(5). DOI:10.1016/j.bbadis.2013.01.011 · 4.66 Impact Factor
  • Source
    • "Finally, Jelodar and colleagues (2009) evaluated the effect of maternal diabetes on reproductive hormone levels in rats. A significant increase in blood glucose and decreased serum levels of LH, FSH, and testosterone were observed in the offspring of the diabetic mothers (Jelodar et al, 2009). "
    [Show abstract] [Hide abstract]
    ABSTRACT: Because of the paucity of studies and inconsistencies regarding the impact of diabetes mellitus (DM) on semen quality, this disease is seldom looked for in the infertile patient. Recently, this view has been challenged by findings showing that DM induces subtle molecular changes that are important for sperm quality and function. This brief review shows the main sperm parameters in patients with DM and presents the mechanisms hypothesized to explain the changes observed in these patients. The data available suggest that DM alters conventional sperm parameters. In addition, DM causes histologic damage of the epididymis, with a negative impact on sperm transit. Various mechanisms may explain the sperm damage observed in patients with DM. These include endocrine disorders, neuropathy, and increased oxidative stress. Many authors suggest that DM decreases serum testosterone levels. This is associated with a steroidogenetic defect in Leydig cells. In addition, diabetic neuropathy seems to cause atonia of seminal vesicles, bladder, and urethra. Furthermore, DM is associated with an increased oxidative stress, which damages sperm nuclear and mitochondrial DNA. Finally, spermatogenesis derangement and germ cell apoptosis in type 1 DM may relate to a local autoimmune damage, whereas insulin resistance, obesity, and other related comorbidities may impair sperm parameters and decrease testosterone serum levels in patients with type 2 DM.
    Journal of Andrology 04/2011; 33(2):145-53. DOI:10.2164/jandrol.111.013193 · 2.47 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: The current study showed that the daily oral treatment of fenugreek steroids, designated F(steroids), to diabetic rats during 30 days demonstrated a significant (p < 0.05) decrease of blood glucose level and a considerable increase of the area of insulin-immunoreactive beta-cells in diabetic rats. Interestingly, this study showed that F(steroids) potentially unregulated the key steroidogenesis enzymes such as 3-hydroxy-3-methyl-glutaryl-CoA reductase (HMG-CoA reductase), malic enzyme, 3beta-hydroxysteroid dehydrogenase (3beta-HSD) and glucose-6-phosphate dehydrogenase (G6P-DH) activities as cholesterol rate in testis, which considerably enhanced testosterone and estradiol levels in the plasma of surviving diabetic rats. More interestingly, F(steroids) obviously prevented the alteration of the key carbohydrate enzymes such as hexokinase and pyruvate kinase activities as well as testicular glycogen and seminal fructose contents in surviving diabetic rats. Furthermore, F(steroids) administration to surviving diabetic rats significantly decreased the sperm shape abnormality and improved the sperm count. Above all, the potential protective action of reproductive systems was approved by the histological study of testis and epididymis.
    Archives of Physiology and Biochemistry 07/2010; 116(3):146-55. DOI:10.3109/13813455.2010.486405 · 1.76 Impact Factor
Show more