Gonadotropin-releasing hormone, follicle-stimulating hormone beta, luteinizing hormone beta gene structure in idiopathic hypogonadotropic hypogonadism

Lawrence C Layman, J. T. Wilson, L. O. Huey, K. D. Lanclos, L. Plouffe, Paul G McDonough

Research output: Contribution to journalArticle

28 Citations (Scopus)

Abstract

Objective: To determine if the genes for gonadotropin-releasing hormone (GnRH), follicle-stimulating hormone beta (FSHβ), and luteinizing hormone beta (LHβ) are present, and if so, whether gene structure is normal in patients with idiopathic hypogonadotropic hypogonadism (IHH). Design: Patients with clinical and laboratory characteristics of IHH were studied at the deoxyribonucleic acid (DNA) level to assess gene structure. Setting: This study took place in an academic setting. Patients: Human volunteers with documented IHH and fertile controls were studied. Interventions: Genomic DNAs were extracted from each patient, Southern blots were constructed and hybridized to DNA probes for GnRH, FSHβ, and LHβ. DNA samples were also subjected to polymerase chain reaction analysis. Main Outcome Measures: Gene structure was assessed by analysis of autoradiographs and gel electrophoresis of polymerase chain reaction products in both the study patients and controls. Results: Each analysis for FSHβ, LHβ, and GnRH demonstrated the same sized fragments in both the study group and control group. A 1.2- kilobase fragment containing the coding region for GnRH was present in all patients with IHH and controls by polymerase chain reaction. Conclusions: The genes for GnRH, LHβ, and FSHβ are present in patients with IHH. No large deletions or rearrangements of any of these genes were identified in any of these patients.

Original languageEnglish (US)
Pages (from-to)42-49
Number of pages8
JournalFertility and sterility
Volume57
Issue number1
StatePublished - Jan 1 1992

Fingerprint

Follicle Stimulating Hormone
Luteinizing Hormone
Gonadotropin-Releasing Hormone
Genes
DNA
Polymerase Chain Reaction
Idiopathic Hypogonadotropic Hypogonadism
Gene Rearrangement
Southern Blotting
Electrophoresis
Volunteers
Gels
Outcome Assessment (Health Care)
Control Groups

Keywords

  • FSH
  • GnRH
  • GnRH deficiency
  • Idiopathic hypogonadotropic hypogonadism
  • LH
  • genes

ASJC Scopus subject areas

  • Reproductive Medicine
  • Obstetrics and Gynecology

Cite this

Gonadotropin-releasing hormone, follicle-stimulating hormone beta, luteinizing hormone beta gene structure in idiopathic hypogonadotropic hypogonadism. / Layman, Lawrence C; Wilson, J. T.; Huey, L. O.; Lanclos, K. D.; Plouffe, L.; McDonough, Paul G.

In: Fertility and sterility, Vol. 57, No. 1, 01.01.1992, p. 42-49.

Research output: Contribution to journalArticle

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abstract = "Objective: To determine if the genes for gonadotropin-releasing hormone (GnRH), follicle-stimulating hormone beta (FSHβ), and luteinizing hormone beta (LHβ) are present, and if so, whether gene structure is normal in patients with idiopathic hypogonadotropic hypogonadism (IHH). Design: Patients with clinical and laboratory characteristics of IHH were studied at the deoxyribonucleic acid (DNA) level to assess gene structure. Setting: This study took place in an academic setting. Patients: Human volunteers with documented IHH and fertile controls were studied. Interventions: Genomic DNAs were extracted from each patient, Southern blots were constructed and hybridized to DNA probes for GnRH, FSHβ, and LHβ. DNA samples were also subjected to polymerase chain reaction analysis. Main Outcome Measures: Gene structure was assessed by analysis of autoradiographs and gel electrophoresis of polymerase chain reaction products in both the study patients and controls. Results: Each analysis for FSHβ, LHβ, and GnRH demonstrated the same sized fragments in both the study group and control group. A 1.2- kilobase fragment containing the coding region for GnRH was present in all patients with IHH and controls by polymerase chain reaction. Conclusions: The genes for GnRH, LHβ, and FSHβ are present in patients with IHH. No large deletions or rearrangements of any of these genes were identified in any of these patients.",
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