Testicular steroidogenesis is suppressed during experimental autoimmune encephalomyelitis in rats
2021
Authors:
Milošević, AnaBjelobaba, Ivana
Božić, Iva
Lavrnja, Irena
Savić, Danijela
Milošević, Katarina
Jakovljević, Marija
Stojilković, Stanko S.
Janjić, Marija
Document Type:
Article (Published version)
Metadata
Show full item recordAbstract:
Multiple sclerosis (MS) is an autoimmune disease that usually occurs during the reproductive years in both sexes. Many male patients with MS show lower blood testosterone levels, which was also observed in male rats during experimental autoimmune encephalomyelitis (EAE), an animal model of MS. To better understand the causes of decreased testosterone production during EAE, we investigated the expression status of genes and proteins associated with steroidogenesis in the testes. No changes in the number of interstitial cells were observed in EAE animals, but the expression of the insulin-like 3 gene was reduced at the peak of the disease, implying that the Leydig cell functional capacity was affected. Consistent with this finding, the expression of most steroidogenic enzyme genes and proteins was reduced during EAE, including StAR, CYP11A1, CYP17A1 and HSD3B. No signs of testicular inflammation were observed. Recovery of steroidogenesis was observed after injection of hCG, the placental gonadotropin, or buserelin acetate, a gonadotropin-releasing hormone analogue, at the peak of EAE. Together, our results are consistent with the hypothesis that impaired testicular steroidogenesis originates upstream of the testes and that low serum LH is the main cause of decreased testosterone levels during EAE.
Keywords:
Endocrinology; Immunology; Neuroscience; PhysiologySource:
Scientific Reports, 2021, 11, 1, 8996-Funding / projects:
- Ministry of Science, Technological Development and Innovation of the Republic of Serbia, institutional funding - 200007 (University of Belgrade, Institute for Biological Research 'Siniša Stanković') (RS-MESTD-inst-2020-200007)
- Intramural Research Program of the National Institute of Child Health and Human Development, NIH
DOI: 10.1038/s41598-021-88305-5
ISSN: 2045-2322
PubMed: 33903635