Here's a few papers for Sunday morning perusal, I've highlighted a few points of interest, but no spoon feeding today as it's my only day off:
Int J Sports Med. 2004 May;25(4):257-63.
?Concomitant abuse of anabolic androgenic steroids and human chorionic gonadotropin impairs spermatogenesis in power athletes? (Karila T, Hovatta O, Sepp?l? T.)
18 power athletes who were contemporarily using AAS and hCG were followed. At the end of the AAS the mean sperm count was 33 +/- 49 x 10 (6) /ml, with only one subject having azoospermia. The conclusions of the study were that the use of hCG maintains spermatogenesis, but they found a significant correlation between the dose of hCG and the number of morphologically abnormal spermatozoa.
http://www.ncbi.nlm.nih.gov/pubmed/6833460
Mol Reprod Dev. 2009 Nov;76(11):1076-83. doi: 10.1002/mrd.21074.
?Adverse effects associated with persistent stimulation of Leydig cells with hCG in vitro? (Matsumoto AM, Paulsen CA, Hopper BR, Rebar RW, Bremner WJ.)
This study highlighted how persistent hCG stimulation induces oxidative stress and cell apoptosis in Leydig cells.
http://www.ncbi.nlm.nih.gov/pubmed/20824644
Int J Androl. 1985 Feb;8(1):28-36.
?Effects of short- and long-term administration of tamoxifen on hCG-induced testicular steroidogenesis in man: no evidence for an oestradiol-induced steroidogenic lesion? (van Bergeijk L, Gooren LJ, van der Veen EA, de Vries CP.)
This study found that the hCG induced block of the C-17, 20-lyase enzyme isn?t due to endogenous E2.
http://www.ncbi.nlm.nih.gov/pubmed/4079381
Mol Cell Endocrinol. 1977 Jul;8(1):73-80.
?hCG suppression of LH receptors and responsiveness of testicular tissue to hCG? (Purvis K, Torjesen PA, Haug E, Hansson V.)
This study demonstrated how a relatively high dose (75IU of hCG in adult male rats)
caused a dramatic reduction in the concentration of membrane receptors for LH in the testis. 3 days after the injection it gradually returned to normal. Reduction in the number of LH binding sites in the testis was associated with a decreased responsiveness of the testicular tissue to hCG as measured by hCG-stimulated endogenous testosterone production.
http://press.endocrine.org/doi/abs/1...51/6/1395&
The Journal of Clinical Endocrinology & Metabolism
?Resensitization of Testosterone Production in Men after Human Chorionic Gonadotropin-Induced Desensitization? (ALLAN R. GLASS, and ROBERT A. VIGERSKY)
Article states how 24 hour exposure to hCG can lead to a loss of testicular LH receptors and/or a decrease in the ability of the testis to produce testosterone in response to LH (i.e. desensitisation). They relate the desensitisation as being caused by block in the conversion of 17-hydroxyprogesterone to testosterone. In humans the desensitisation is characterised by a plateau in serum T (after an initial rise) for 4-24 hours after hCG administration despite high serum hCG and rising serum 17-hydroxyprogesterone. After 72-hour exposure to hCG, serum testosterone doubles, suggesting testis re-sensitisation to gonadotropin. Ten days after a single injection of hCG, serum testosterone was below baseline but serum 17-hydroxyprogesterone was still greater than baseline, thus suggesting a prolonged block in the conversion of the latter to testosterone. They suggest a shift in the pathway of endogenous testosterone production from A4 to A5.
http://www.ncbi.nlm.nih.gov/pubmed/221476
J Biol Chem. 1979 Jul 10;254(13):5613-7.
?Testicular steroidogenesis after human chorionic gonadotropin desensitization in rats? (Chasalow F, Marr H, Haour F, Saez JM.)
This study shows an initial acute rise in both lyase and 17 alpha-hydroxylase activities following a single injection of hCG. Thereafter plasma and testicular testosterone decline and do not increase after a second injection of hCG. During this period of desensitisation isolated Leydig cells were insensitive to effect of hCG. This block was correlated with a decrease in both lyase and 17 alphy-hydroxylase activities of the Leydig cells. Within 60 to 96 hours after the hCG injection there was in increase of both plasma and testicular testosterone together with a rise in activity of lyase and 17 alpha-hydroxylase.
http://www.ncbi.nlm.nih.gov/pubmed/3747510
J Clin Endocrinol Metab. 1980 May;50(5):879-81.
?Lack of a biphasic steroid response to single human chorionic gonadotropin administration in patients with isolated gonadotropin deficiency? (Smals AG, Pieters GF, Kloppenborg PW, Lozekoot DC, Benraad TJ.)
This study suggested that
hCG temporarily depresses the conversion of 17-OHP to testosterone.
http://www.ncbi.nlm.nih.gov/pubmed/23260550
Biology of Reproduction March 1, 1980 vol. 22 no. 2 383-391
?Increase in Leydig Cell Number in Testes of Adult Rats Treated Chronically with an Excess of Human Chorionic Gonadotropin? (A. KENT CHRISTENSEN and KENNETH C. PEACOCK)
This very interesting study found that
the number of Leydig cells increased in rats treated with 100IU hCG per day for 5 weeks.
http://www.ncbi.nlm.nih.gov/pubmed/3497025
The paper I posted up recently:
Human Chorionic Gonadotropin Up-Regulates Insulin- Like Growth Factor-I Receptor Gene Expression of Leydig Cells*
MADAN L. NAGPAL, DELI WANG, JO H. CALKINS, WEIWEI CHANG, AND TU LIN
Medical and Research Services, W. J. B. Dorn Veterans Hospital, and Department of Medicine, University of South Carolina School of Medicine, Columbia, South Carolina 29208
ABSTRACT. The effects of hCG, 8-bromo-cAMP, 4/3-phorbol 12/3-myristate 13a-acetate, and forskolin on insulin-like growth factor-I (IGF-I) receptor gene expression of Leydig cells were studied. The treatment of purified Leydig cells with hCG caused a dose-dependent increase in [125I]IGF-I binding to Leydig cells without changes in binding affinity, indicating that the increased binding was due to increased receptor numbers and not to increased affinity. The minimal time required for hCG to induce IGF-I binding was 6 h, and it had reached a plateau at 16 h. 8- Bromo-cAMP (1 mM) increased IGF-I binding about 2-fold, and forskolin (10 /*M) increased binding about 51%. Using the ribonuclease protection assay, we found that hCG and 8-bromo-cAMP could increase IGF-I receptor mRNA expression as early as 2 h before the increase in IGF-I binding. The induction by hCG was over 3.5-fold at 4 h and decreased to about 2-fold at 6 h. 4/3- Phorbol 12/3-myristate 13a-acetate had a very small effect on IGF-I receptor mRNA levels (1.5-fold increase at 2 h and no changes at 4 and 6 h).
In conclusion, IGF-I receptors can be upregulated by hCG, 8-bromo-cAMP, and forskolin. The up-regulation of IGF-I receptor number is associated with transient increases in IGF-I receptor mRNA levels.
This could be a mechanism by which hCG and IGF-I interact to enhance Leydig cell steroidogenesis. {Endocrinology 129: 2820-2826,1991)
