INHIBITORY EFFECTS ON GONADOTROPHIN SECRETION AND GONADAL FUNCTION IN MEN DURING CHRONIC TREATMENT WITH A POTENT STIMULATORY LUTEINIZING HORMONE-RELEASING HORMONE ANALOGUE

1979 ◽  
Vol 91 (3) ◽  
pp. 601-608 ◽  
Author(s):  
Christer Bergquist ◽  
Sven Johan Nillius ◽  
Torbjörn Bergh ◽  
Göran Skarin ◽  
Leif Wide
Keyword(s):  
Luteinizing Hormone ◽  
Treatment Period ◽  
Chronic Treatment ◽  
Seminal Fluid ◽  
Gonadal Function ◽  
Luteinizing Hormone Releasing Hormone ◽  
Healthy Men ◽  
Releasing Hormone ◽  
Gonadotrophin Secretion ◽  
Long Term Treatment

ABSTRACT Long-term treatment with the potent and long-acting stimulatory luteinizing hormone-releasing hormone (LRH) analogue D-Ser(TBU)6-EA10-LRH was given to 4 healthy men to study its effects on pituitary gonadotrophin secretion and gonadal function. Five μg of the LRH agonist was self-administered sc once daily over 17 weeks. Weekly basal blood samples were obtained for determination of follicle-stimulating hormone (FSH), luteinizing hormone (LH), prolactin (PRL) and testosterone. The gonadotrophin responses to the LRH analogue were also determined during the treatment period. LRH tests were performed after treatment. Seminal fluid specimens were collected during and after treatment. A reduction of the basal serum gonadotrophin and testosterone levels were observed during the treatment period. The FSH and LH responses to the analogue were also diminished. After discontinuation of treatment the gonadotrophin and testosterone concentrations returned to pre-treatment levels within a week. The PRL levels and the seminal fluid specimens did not show any significant changes during the study period. The results suggest that chronic treatment with D-Ser(TBU)6-EA10-LRH has an inhibitory effect on the pituitary gonadotrophin secretion in healthy men. It seems likely that the reduced testosterone level is secondary to the diminished gonadotrophin secretion.

scholarly journals Possible Relevance of Soluble Luteinizing Hormone Receptor during Development and Adulthood in Boys and Men

Cancers ◽  
2021 ◽  
Vol 13 (6) ◽  
pp. 1329
Author(s):  
Li Juel Mortensen ◽  
Mette Lorenzen ◽  
Anne Jørgensen ◽  
Jakob Albrethsen ◽  
Niels Jørgensen ◽  
...  
Keyword(s):  
Luteinizing Hormone ◽  
Hormone Receptor ◽  
Adrenal Glands ◽  
Seminal Fluid ◽  
Body Fluids ◽  
Luteinizing Hormone Receptor ◽  
Gonadal Function ◽  
Fetal Kidney ◽  
Healthy Men ◽  
Human Fetal Kidney

Luteinizing hormone (LH) and human chorionic gonadotropin (hCG) are agonists for the luteinizing hormone receptor (LHCGR) which regulates male reproductive function. LHCGR may be released into body fluids. We wish to determine whether soluble LHCGR is a marker for gonadal function. Cross-sectional, longitudinal, and intervention studies on 195 healthy boys and men and 396 men with infertility, anorchia, or Klinefelter Syndrome (KS) were used to correlate LHCGR measured in serum, seminal fluid, urine, and hepatic/renal artery and vein with gonadal function. LHCGR was determined in fluids from in vitro and in vivo models of human testicular tissue and cell lines, xenograft mouse models, and human fetal kidney and adrenal glands. Western blot showed LHCGR fragments in serum and gonadal tissue of similar size using three different antibodies. The LHCGR-ELISA had no species cross-reactivity or unspecific reaction in mouse serum even after human xenografting. Instead, sLHCGR was released into the media after the culture of a human fetal kidney and adrenal glands. Serum sLHCGR decreased markedly during puberty in healthy boys (p = 0.0001). In healthy men, serum sLHCGR was inversely associated with the Inhibin B/FSH ratio (β −0.004, p = 0.027). In infertile men, seminal fluid sLHCGR was inversely associated with serum FSH (β 0.006, p = 0.009), sperm concentration (β −3.5, p = 0.003) and total sperm count (β −3.2, p = 0.007). The injection of hCG lowered sLHCGR in serum and urine of healthy men (p < 0.01). In conclusion, sLHCGR is released into body-fluids and linked with pubertal development and gonadal function. Circulating sLHCGR in anorchid men suggests that sLHCGR in serum may originate from and possibly exert actions in non-gonadal tissues. (ClinicalTrials: NTC01411527, NCT01304927, NCT03418896).

Evidence for Testicular Impairment After Long-Term Treatment with a Luteinizing Hormone-Releasing Hormone Agonist in Elderly Men

1989 ◽  
Vol 142 (5) ◽  
pp. 1235-1238 ◽  
Author(s):  
Andrea U. Decensi ◽  
Domenico Guarneri ◽  
Paola Marroni ◽  
Liborio Di Cristina ◽  
Michela Paganuzzi ◽  
...  
Keyword(s):  
Luteinizing Hormone ◽  
Term Treatment ◽  
Elderly Men ◽  
Luteinizing Hormone Releasing Hormone ◽  
Releasing Hormone ◽  
Long Term Treatment ◽  
Testicular Impairment

Suppression of Pituitary-Gonadal Function by a Potent New Luteinizing Hormone-Releasing Hormone Antagonist in Normal Men*

1987 ◽  
Vol 64 (5) ◽  
pp. 931-936 ◽  
Author(s):  
SPYROS N. PAVLOU ◽  
GAIL B. WAKEFIELD ◽  
DONALD P. ISLAND ◽  
PHILIP G. HOFFMAN ◽  
MARY E. LEPAGE ◽  
...  
Keyword(s):  
Luteinizing Hormone ◽  
Gonadal Function ◽  
Luteinizing Hormone Releasing Hormone ◽  
Releasing Hormone ◽  
Normal Men

Myotonia Dystrophica: Studies on Gonadal Function Using Luteinizing Hormone-Releasing Hormone (LRH)

1975 ◽  
Vol 40 (6) ◽  
pp. 1110-1113 ◽  
Author(s):  
JULIUS SAGEL ◽  
LARRY A. DISTILLER ◽  
JOHN E. MORLEY ◽  
HYAM ISAACS ◽  
G. KAY ◽  
...  
Keyword(s):  
Luteinizing Hormone ◽  
Gonadal Function ◽  
Luteinizing Hormone Releasing Hormone ◽  
Releasing Hormone ◽  
Myotonia Dystrophica

Effects of chronic treatment with oestrogen, an oestrogen antagonist and a potent luteinizing hormone releasing hormone agonist analogue on pituitary responsiveness to luteinizing hormone releasing hormone in the rat

1983 ◽  
Vol 98 (3) ◽  
pp. 313-321 ◽  
Author(s):  
J. M. Hall ◽  
S. A. Whitehead
Keyword(s):  
Luteinizing Hormone ◽  
Chronic Treatment ◽  
Ex Vivo ◽  
Significant Rise ◽  
Luteinizing Hormone Releasing Hormone ◽  
Releasing Hormone ◽  
Serum Lh ◽  
Lh Release ◽  
Lh Releasing Hormone

The rise in gonadotrophin release which occurs after ovariectomy is caused by steroid withdrawal resulting in an enhanced pituitary responsiveness to LH releasing hormone (LHRH) associated with increased LHRH release and pituitary LHRH binding. The effects of oestrogen replacement after ovariectomy and chronic treatment of intact rats with an oestrogen antagonist, tamoxifen, on LH release and in-vitro pituitary responses to LHRH have been investigated. Capsules containing crystalline oestradiol, implanted at the time of ovariectomy, completely inhibited the rise in LH release although pituitary responsiveness was greater after 10 days in the oestrogen-treated rats than in untreated ovariectomized controls. On day 4 after ovariectomy pituitary responses to LHRH were comparable in both treated and untreated groups although in both groups the responses were greater than those measured in intact dioestrous rats. Treatment with tamoxifen over a 4-day period also augmented pituitary responsiveness but only at the lowest dose (0·5 mg/kg); no effect on serum LH concentrations was observed. Higher doses of the antagonist (1 and 2 mg/kg) did not affect pituitary responses, although the highest dose did cause a significant rise in serum LH. Treatment with a daily dose of 50 ng [d-Ser(But)6]LHRH(1–9)nonapeptide-ethylamide, starting on the day of ovariectomy, markedly attenuated the LH responses to LHRH ex vivo at days 2, 4 and 10 after ovariectomy. In contrast, the analogue treatment did not abolish the rise in LH release but this was proportionately less than in controls.

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