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1.
Asian Journal of Andrology ; (6): 319-323, 2018.
Article in English | WPRIM | ID: wpr-1009591

ABSTRACT

Pulsatile gonadotropin-releasing hormone (GnRH) may induce spermatogenesis in most patients with congenital hypogonadotropic hypogonadism (CHH) by stimulating gonadotropin production, while the predictors for a pituitary response to pulsatile GnRH therapy were rarely investigated. Therefore, the aim of our study is to investigate predictors of the pituitary response to pulsatile GnRH therapy. This retrospective cohort study included 82 CHH patients who received subcutaneous pulsatile GnRH therapy for at least 1 month. Patients were categorized into poor or normal luteinizing hormone (LH) response subgroups according to their LH level (LH <2 IU l-1 or LH ≥2 IU l-1) 1 month into pulsatile GnRH therapy. Gonadotropin and testosterone levels, testicular size, and sperm count were compared between the two subgroups before and after GnRH therapy. Among all patients, LH increased from 0.4 ± 0.5 IU l-1 to 7.5 ± 4.4 IU l-1 and follicle-stimulating hormone (FSH) increased from 1.1 ± 0.9 IU l-1 to 8.8 ± 5.3 IU l-1. A Cox regression analysis showed that basal testosterone level (β = 0.252, P = 0.029) and triptorelin-stimulated FSH60min(β = 0.518, P = 0.01) were two favorable predictors for pituitary response to GnRH therapy. Nine patients (9/82, 11.0%) with low LH response to GnRH therapy were classified into the poor LH response subgroup. After pulsatile GnRH therapy, total serum testosterone level was 39 ± 28 ng dl-1 versus 248 ± 158 ng dl-1 (P = 0.001), and testicular size was 4.0 ± 3.1 ml versus 7.9 ± 4.5 ml (P = 0.005) in the poor and normal LH response subgroups, respectively. It is concluded that higher levels of triptorelin-stimulated FSH60minand basal total serum testosterone are favorable predictors of pituitary LH response to GnRH therapy.


Subject(s)
Adult , Humans , Male , Young Adult , Cohort Studies , Follicle Stimulating Hormone/blood , Gonadotropin-Releasing Hormone/therapeutic use , Gonadotropins/blood , History, 16th Century , Hypogonadism/pathology , Luteinizing Hormone/blood , Pituitary Gland/pathology , Predictive Value of Tests , Retrospective Studies , Sperm Count , Testis/pathology , Testosterone/blood , Treatment Outcome , Triptorelin Pamoate/therapeutic use
2.
National Journal of Andrology ; (12): 587-592, 2015.
Article in Chinese | WPRIM | ID: wpr-276054

ABSTRACT

<p><b>OBJECTIVE</b>To investigate the effects of different concentrations of lipopolysaccharide (LPS), tumor necrosis factor α (TNFα), interleukin-6 (IL-6), dexamethasone (Dex), and insulin on the mRNA and protein expressions of GPR54 in the MCF7 cell line in vitro.</p><p><b>METHODS</b>MCF7 breasr cancer cells were cultured and treated with different concentrations of LPS (10 and 20 µg/ml), TNFα (20 and 100 ng/ml), IL-6 (10 and 20 ng/ml), Dex (10(-6) and 10(-7) mol/L), and insulin (0.01 and 0.1 IU/L). Those treated with culture fluid only served as controls. The mRNA and protein expressions of GPR54 were measured by real-time PCR and Western blot, respectively, after 6, 24, 48, and 72 hours of treatment.</p><p><b>RESULTS</b>Compared with the blank con- trol, LPS (10 and 20 µg/ml), TNFα (20 and 100 ng/ml), IL-6 (10 and 20 ng/ml), Dex (10(-6) and 10(-7) mol/L), and insulin (0.01 and 0.1 IU/L) significantly increased the expressions of GPR54 mRNA (P < 0.05) and protein (P < 0.05).</p><p><b>CONCLUSION</b>LPS, TNFα, IL-6, Dex, and insulin evidently increase the expression of GPR54 in the MCF7 cell line, indicating their influence on the function of gonads by regulating the GPR54 level.</p>


Subject(s)
Humans , Blotting, Western , Dexamethasone , Pharmacology , Glucocorticoids , Pharmacology , Gonads , Metabolism , Hypoglycemic Agents , Pharmacology , Insulin , Pharmacology , Interleukin-6 , Pharmacology , Lipopolysaccharides , Pharmacology , MCF-7 Cells , RNA, Messenger , Metabolism , Real-Time Polymerase Chain Reaction , Receptors, G-Protein-Coupled , Genetics , Metabolism , Receptors, Kisspeptin-1 , Time Factors , Tumor Necrosis Factor-alpha , Pharmacology
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