Genetically determined dosage of Follicle-Stimulating Hormone (FSH) affects male reproductive parameters
dc.contributor.author | Grigorova, Marina | |
dc.contributor.author | Punab, Margus | |
dc.contributor.author | Ẑilaitiene, Birute | |
dc.contributor.author | Erenpreiss, Juris | |
dc.contributor.author | Ausmees, Kristo | |
dc.contributor.author | Matuleviĉius, Valentinas | |
dc.contributor.author | Tsarev, Igor | |
dc.contributor.author | Jørgensen, Niels | |
dc.contributor.author | Laan, Maris | |
dc.contributor.institution | Rīga Stradiņš University | |
dc.date.accessioned | 2021-07-14T08:05:01Z | |
dc.date.available | 2021-07-14T08:05:01Z | |
dc.date.issued | 2011-09 | |
dc.description.abstract | Context: The detailed role of FSH in contributing to male testicular function and fertility has been debated. We have previously identified the association between the T-allele of the FSHB promoter polymorphism (rs10835638; G/T, -211 bp from the mRNA start) and significantly reduced male serum FSH. Objective: In the current study, the T-allele carriers of the FSHB -211 G/T single nucleotide polymorphism represented a natural model for documenting downstream phenotypic consequences of insufficient FSH action. Design and Subjects: We genotyped rs10835638 in the population-based Baltic cohort of young men (n=1054; GG carriers, n=796; GT carriers, n=244; TT carriers, n=14) recruited by Andrology Centres in Tartu, Estonia; Riga, Latvia; and Kaunas, Lithuania. Marker-trait association testing was performed using linear regression (additive, recessive models) adjusted by age, body mass index, smoking, and recruitment center. Results: Serum hormones directly correlated with the T-allele dosage of rs10835638 included FSH (additive model, P=1.11×10 -6; T-allele effect, -0.41 IU/liter), inhibin-B (P=2.16×10 -3; T-allele effect, -14.67 pg/ml), and total testosterone (P = 9.30 × 10 -3; T-allele effect, -1.46 nmol/liter). Parameters altered only among TT homozygotes were reduced testicular volume (recessive model, P = 1.19 × 10 -4; TT genotype effect, -9.47 ml) and increased serum LH (P = 2.25 × 10 -2; TT genotype effect, 1.07 IU/liter). The carrier status of rs10835638 alternative genotypes did not affect sperm motility and morphology, calculated free testosterone, serum SHBG, and estradiol concentrations. Conclusion: We showed for the first time that genetically determined low FSH may have wider downstream effects on the male reproductive system, including impaired testes development, altered testicular hormone levels (inhibin-B, total testosterone, LH), and affected male reproductive potential. | en |
dc.description.status | Peer reviewed | |
dc.format.extent | 442066 | |
dc.identifier.citation | Grigorova, M, Punab, M, Ẑilaitiene, B, Erenpreiss, J, Ausmees, K, Matuleviĉius, V, Tsarev, I, Jørgensen, N & Laan, M 2011, 'Genetically determined dosage of Follicle-Stimulating Hormone (FSH) affects male reproductive parameters', Journal of Clinical Endocrinology and Metabolism, vol. 96, no. 9, pp. E1534-E1541. https://doi.org/10.1210/jc.2011-0632 | |
dc.identifier.doi | 10.1210/jc.2011-0632 | |
dc.identifier.issn | 0021-972X | |
dc.identifier.uri | https://dspace.rsu.lv/jspui/handle/123456789/5874 | |
dc.identifier.url | http://www.scopus.com/inward/record.url?scp=80052521669&partnerID=8YFLogxK | |
dc.language.iso | eng | |
dc.relation.ispartof | Journal of Clinical Endocrinology and Metabolism | |
dc.rights | info:eu-repo/semantics/openAccess | |
dc.subject | 1.6 Biological sciences | |
dc.subject | 3.2 Clinical medicine | |
dc.subject | 1.1. Scientific article indexed in Web of Science and/or Scopus database | |
dc.subject | Endocrinology, Diabetes and Metabolism | |
dc.subject | Biochemistry | |
dc.subject | Endocrinology | |
dc.subject | Clinical Biochemistry | |
dc.subject | Biochemistry, medical | |
dc.subject | SDG 3 - Good Health and Well-being | |
dc.title | Genetically determined dosage of Follicle-Stimulating Hormone (FSH) affects male reproductive parameters | en |
dc.type | /dk/atira/pure/researchoutput/researchoutputtypes/contributiontojournal/article |
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