Serial Inhibin B Measurements in Boys with Congenital Monorchism Indicate Compensatory Testicular Hypertrophy in Early Infancy

Aim Congenital monorchism is considered a condition in which an initially normal testis has existed but subsequently atrophied and disappeared due to a third trimester catastrophe (presumably torsion). Since inhibin B concentrations appear related to Sertoli and germ cells number, we evaluated pre- and postoperative inhibin B of boys with congenital monorchism to determine whether the well-known hypertrophy of the contralateral testis was reflected in inhibin B concentrations. Materials and Methods Twenty-seven boys consecutively diagnosed with congenital monorchism (median age 12 months) underwent follow-up with reproductive hormones 1 year postoperatively (median age 25 months). The results were compared with inhibin B of 225 boys with congenital nonsyndromic unilateral cryptorchidism, by converting values to multiple of the median (MoM) for age in normal boys. Results Ten boys (37%) had blind-ending vessels and ductus deferens (vanished testis) and the remaining (63%) had testicular remnants. At the time of diagnostic procedure, monorchid boys did not have significantly lower inhibin B (median 114, range 20–208) than unilateral cryptorchid boys (136, 47–393) (p = 0.27). During follow-up, MoM values of inhibin B increased in monorchid boys (median 0.59 to 0.98) and in unilateral cryptorchid boys (0.69 to 0.89) (both p < 0.0001). Compared with the concentration at surgery, an additional 44% monorchid boys had inhibin B MoM values higher than 1.0, whereas only additional 23% of unilateral cryptorchid boys exhibited such values (p = 0.04). Conclusion Generally, inhibin B MoM values were normalized during follow-up in boys with congenital monorchism, reflecting compensatory hypertrophy within the first 2.5 years of life. The compensatory capacity to increase was better in monorchism than in unilateral cryptorchidism.

Serum 25OHD3 of Obese Mice Is Affected by Liver Injury and Correlates with Testosterone Levels and Sperm Motility

<b><i>Introduction:</i></b> The concentration of 25-hydroxycholecalciferol (25OHD₃) in the serum of obese people is low and often accompanied by symptoms of low fertility. Therefore, vitamin D is recommended as a potential treatment option. However, after clinical trials, it was found that vitamin D cannot effectively increase the concentration of 25OHD₃ in the serum of obese people. How obesity causes low 25OHD₃ concentration and low fertility is unclear. <b><i>Methods:</i></b> We analyzed the physiological and pathological changes in obese mice induced by a high-fat diet (HFD) and the changes in mice after supplementing with 25OHD₃. <b><i>Results:</i></b> The concentration of 25OHD₃ in the serum of obese mice induced by HFD was significantly reduced, and these mice showed liver hypertrophy accompanied by abnormal liver injury, testicular hypertrophy, low testosterone levels, high leptin levels, and low sperm motility. The mRNA and protein expression of CYP2R1 of hydroxylated vitamin D₃ was significantly reduced; CYP11A1 and CYP11A2, which synthesize testosterone, were significantly reduced. After supplementing with 25OHD₃, there was an increase in serum 25OHD₃ concentration, testosterone level, and sperm motility, but it cannot improve the degree of obesity, CYP2R1 expression, and liver damage. <b><i>Conclusion:</i></b> Our research shows that there is a metabolic interference mediated by 25OHD₃ and testosterone between obesity and low sperm motility. The results of this study can provide a scientific basis for studying the mechanism of 25OHD₃ and hormone regulation and treating obese people with low sperm motility.

Immunohistochemical Review of Leydig Cell Lesions in Ochratoxin A-Treated Fischer Rats and Controls

Ochratoxin A is best known as a potent renal carcinogen in male rats and mice after necessarily protracted ingestion, although valid extrapolation to any human disease has not been verified. The hypothesis that the toxin is a cause of human testicular cancer was proposed a decade ago and has proliferated since, partly through incomplete study of the scientific literature. Archived tumorous rat testes were available from Fischer F344 rats exposed to continuous dietary exposure for half of or the whole life in London in the 2000s. Renal cancer occurred in some of these cases and testicular tumours were observed frequently, as expected, in both treated and untreated animals. Application of clinical immunohistochemistry has for the first time consistently diagnosed the testicular hypertrophy in toxin-treated rats as Leydig cell tumours. Comparison is made with similar analysis of tumorous testes from control (untreated) rats from U.S. National Toxicology Program studies, both of ochratoxin A (1989) and the more recent one on Ginkgo biloba. All have been found to have identical pathology as being of sex cord-stromal origin. Such are rare in humans, most being of germinal cell origin. The absence of experimental evidence of any specific rat testicular cellular pathology attributable to long-term dietary ochratoxin A exposure discredits any experimental animal evidence of testicular tumorigenicity. Thus, no epidemiological connection between ochratoxin A and the incidence of human testicular cancer can be justified scientifically.

Alterations in the biochemical parameters and the spermatic function generated by obesity in rats

The aim of the present study was to assess the effects of a hyperlipidic diet set before puberty in male Wistar rats’ gonadal weights and testicular func-tions. Males rats were used for the study, they were randomly distributed into 2 groups: Control Group (CG: standard diet (normolipidemic) and the second: Intervention Group (IG: hyperlipidemic diet), after 7 days of experi-mentation, 3 rats were sacrificed per week, blood samples were collected and level of HDL, LDL and triglyceride were analyzed. A significant reduction (p<0.05) in testicular weight in the control group was observed compared with the hyperlipidic diet group, triglyceride levels showed a consistent change over the weeks of the study, HDL levels showed a consistent change during the 5 weeks of the study, Photomicraphie of the testicles of Wistar rats in the hyperlipid diet group for the first week showed Sertoli cell hyper-plasia ,during the second week microscopic examination showed significant testicular hypertrophy the microscopic examination during the fifth week showed hyperplasia of the seminal vesicle characterized by an increase in the number of glandular epithelial cells. The proliferating epithelium may form papillary structures with supporting stroma and with extension into the glandular lumen and total absence of sperm cells. Obesity is associated with many metabolic abnormalities. It has been found that these metabolic ab-normalities induce disorders of spermatogenesis. Our results show that the hyperlipidic diet affects the gonads significantly with hypertrophic testes, the presence of hyperplastic seminiferous tubes, as well as a fine basement membrane.

Hyperreactio luteinalis in association with multiple foetal malformations – a consequence of supra-physiological HCG?

Hyperreactio luteinalis (HL) is characterised by ovarian cystic enlargement that is associated with high levels of human chorionic gonadotropin (hCG). Here the possible effects of abnormally high hCG levels on foetal development are demonstrated.We report a 28-year-old patient who was referred for evaluation of bilateral maternal ovarian enlargement in the second trimester. Abnormally elevated hCG (887,514 IU/L) was found with ultrasound examination identifying various foetal malformations. The karyotype was normal. Spontaneous abortion occurred at 20 weeks. Autopsy showed testicular hypertrophy with marked Leydig cell hyperplasia. The HL resolved with normalisation of the hCG levels following delivery.HL is a rare finding in normal pregnancies; the potential effects of abnormally elevated hCG on the foetus are discussed.