scholarly journals QUANTIFICATION OF LEYDIG CELLS AND MEASUREMENT OF LEYDIG-CELL SIZE FOLLOWING ADMINISTRATION OF HUMAN CHORIONIC GONADOTROPHIN TO NORMAL MEN

Reproduction ◽  
1971 ◽  
Vol 25 (2) ◽  
pp. 185-192 ◽  
Author(s):  
C. G. HELLER ◽  
D. R. LEACH
Keyword(s):  
Cell Size ◽  
Leydig Cell ◽  
Leydig Cells ◽  
Chorionic Gonadotrophin ◽  
Human Chorionic Gonadotrophin ◽  
Normal Men

Studies on the testicular source of inhibin and its route of secretion in rams: failure of the Leydig cell to secrete inhibin in response to a human chorionic gonadotrophin/LH stimulus

1991 ◽  
Vol 130 (1) ◽  
pp. 107-114 ◽  
Author(s):  
A. J. Tilbrook ◽  
D. M. de Kretser ◽  
I. J. Clarke
Keyword(s):  
Leydig Cell ◽  
Leydig Cells ◽  
Jugular Vein ◽  
Plasma Concentrations ◽  
Chorionic Gonadotrophin ◽  
Human Chorionic Gonadotrophin ◽  
Spermatic Vein ◽  
Jugular Veins ◽  
Testicular Vein ◽  
Peripheral Plasma

ABSTRACT To determine whether Leydig cells produce inhibin in the ram, Leydig cells were stimulated by administering human chorionic gonadotrophin (hCG) or raising the levels of endogenous LH by an injection of gonadotrophin releasing hormone (GnRH). Plasma concentrations of testosterone increased in the 72 h after either a single injection (P < 0·05) or two injections (P < 0·01) of hCG. Plasma concentrations of inhibin were not significantly influenced by either one or two injections of hCG. Administration of GnRH (1 μg) caused an 11-fold increase in plasma concentrations of LH but did not influence concentrations of inhibin in either the jugular or testicular veins (pampiniform plexus). In contrast, concentrations of testosterone were increased by about fourfold in both jugular (P < 0·01) and testicular (P < 0·05) veins. The concentrations of inhibin in the testicular vein were 1·3-fold higher than in the peripheral plasma (P < 0·05) both before and following treatment with GnRH whereas the concentrations of testosterone were 18- to 21-fold greater than in peripheral concentrations. In view of the difference in concentrations of inhibin between testicular and jugular veins, in a further experiment a sample was taken from the jugular vein, a vein located in the tunica vasculosa of the testis (testicular vein) and from a vein (spermatic vein) and lymph vessels located in the spermatic cord. The mean (± s.e.m.) concentrations of inhibin were highest in the testicular lymph (45·93±4·21 μg/l; P < 0·001) compared with the peripheral (4·14±0·31 μg/l), spermatic (8·0±1·17 μg/l) or testicular (6·4±0·82 μg/l) plasma. Plasma concentrations of inhibin were significantly higher in the spermatic vein than in the testicular vein (P < 0·05) and jugular vein (P < 0·01), and concentrations of inhibin in the testicular vein were significantly (P < 0·05) higher than in the jugular vein. There were no significant differences in the concentrations of testosterone in the spermatic vein, testicular vein or testicular lymph but the concentrations of testosterone in the peripheral plasma were significantly (P < 0·05) less than in the testicular plasma or lymph. These results suggest that, in the ram, the Leydig cell does not respond to hCG or endogenous LH by secreting inhibin or by influencing other cells within the testis to secrete inhibin within the time-frame of these experiments. The low testicular to jugular differences in the concentration of inhibin and the high concentrations of inhibin in the testicular lymph suggest that the lymph may be an important route of secretion of inhibin from the testis in the ram. Journal of Endocrinology (1991) 130, 107–114

Indirect evidence of chronic Leydig cell desensitization in Klinefelter's syndrome

1981 ◽  
Vol 96 (4) ◽  
pp. 552-556 ◽  
Author(s):  
Anthony G. Smals ◽  
Gerlach F. Pieters ◽  
Peter W. Kloppenborg
Keyword(s):  
Leydig Cells ◽  
Response Pattern ◽  
Indirect Evidence ◽  
Chorionic Gonadotrophin ◽  
Human Chorionic Gonadotrophin ◽  
Klinefelter’S Syndrome ◽  
Klinefelter's Syndrome ◽  
Basal Plasma ◽  
Normal Men ◽  
T Values

Abstract. The basal plasma 17α-hydroxyprogesterone (17-OHP) and testosterone (T) levels were proportionally decreased in 10 hypergonadotropic patients with Klinefelter's syndrome. The ratio 17-OHP to T was however about twice as high as in 10 eugonadal male controls, suggesting the presence of a block in the conversion of 17-hydroxylated steroids to androgens in the Klinefelter patients under basal circumstances. Administration of human chorionic gonadotrophin (hCG, 1500 IU im daily for 3 days) to the Klinefelter patients disclosed a response pattern quite different from that observed in controls. In the control subjects 17-OHP and the ratio 17-OHP/T sharply rose to maximum values at 24 h after the first injection. Thereafter both progressively fell to lowest values at 72 h, when T levels reached their maximum. In the Klinefelter patients the T response to hCG administration was greatly diminished but the 17-OHP response was similar to that in the controls. Maximum 17-OHP and 17-OHP/T values however were not achieved until 72 h after the first injection when T levels also reached their maximum. Unlike in the controls in the Klinefelter patients maximum 17-OHP and T increments and the 17-OHP and T levels 48 and 72 h after the injection were positively correlated. Together the findings of a decreased T synthesis and reserve in the presence of relative 17-OHP accumulation, further increasing after acute hCG administration in a pattern quite different from that in normal men, suggest that in Klinefelter's syndrome the Leydig cells may be chronically desensitized by the persistent endogenous hypergonadotropism.

Proliferation and differentiation of possible Leydig cell precursors after destruction of the existing Leydig cells with ethane dimethyl sulphonate: the role of LH/human chorionic gonadotrophin

1989 ◽  
Vol 122 (3) ◽  
pp. 689-NP ◽  
Author(s):  
K. J. Teerds ◽  
D. G. de Rooij ◽  
F. F. G. Rommerts ◽  
R. van den Hurk ◽  
C. J. G. Wensing
Keyword(s):  
Leydig Cell ◽  
Proliferative Activity ◽  
Leydig Cells ◽  
Precursor Cells ◽  
Chorionic Gonadotrophin ◽  
Human Chorionic Gonadotrophin ◽  
Adult Rats ◽  
Proliferation And Differentiation ◽  
Endocrine Factors

ABSTRACT The influence of LH levels on the proliferation and differentiation of possible Leydig cell precursors was investigated in adult rats, after the destruction of the existing Leydig cells with the cytotoxic drug ethane dimethyl sulphonate (EDS). In rats bearing a testosterone implant which prevented the rise in plasma LH levels and kept them within the normal range after the destruction of the Leydig cells, the proliferative activity of possible Leydig cell precursors still increased seven- to eightfold 2 days after EDS administration. Apparently, in this situation, locally produced factors, and not LH, may play a role in the stimulation of proliferation. The proliferative activity of the possible precursor cells could be further stimulated by treating rats with daily injections of human chorionic gonadotrophin (hCG) following EDS administration. It was concluded that the proliferative activity of possible Leydig cell precursors is probably regulated by both paracrine and endocrine factors. Almost no Leydig cells were formed in the rats bearing a testosterone implant during the first 4 weeks after EDS administration. When these rats were treated with hCG, starting 28 days after administration of EDS, a substantial number of Leydig cells was found after 2 days, and these cells also showed 3β-hydroxysteroid dehydrogenase (3β-HSD) and α-naphtyl esterase (α-NE) activity. When hCG treatment was started at 14 or 21 days after EDS administration, some cells with the nuclear characteristics of Leydig cells were present after 2 days, but no 3β-HSD or α-NE activity could be detected. Finally, when hCG treatment was started directly after EDS administration, a considerable number of Leydig cells was found 14 days after EDS, and some of these cells already showed 3β-HSD and α-NE activity. It is concluded that precursor cells are able to develop into advanced precursor cells at normal LH levels, and that the rate of development of new Leydig cells strongly depends upon LH/hCG levels. Journal of Endocrinology (1989) 122, 689–696

Effects of hypophysectomy and human chorionic gonadotrophin on Leydig cell function in mature rats

1990 ◽  
Vol 126 (3) ◽  
pp. 367-NP ◽  
Author(s):  
D. M. Stocco ◽  
K. J. Teerds ◽  
M. van Noort ◽  
F. F. G. Rommerts
Keyword(s):  
Leydig Cell ◽  
Leydig Cells ◽  
Cell Function ◽  
Fold Increase ◽  
Specific Protein ◽  
Chorionic Gonadotrophin ◽  
Human Chorionic Gonadotrophin ◽  
Cell Functions ◽  
Complete Restoration ◽  
Hypophysectomized Rats

ABSTRACT The biochemical activities involved in the maintenance of Leydig cell functions, and the effects of hypophysectomy and human chorionic gonadotrophin (hCG) on these functions are largely unknown. In the present study, adult hypophysectomized rats were used as a model to determine the effects of these treatments on a number of biochemical and morphological parameters. After 33 days of hypophysectomy, the morphology of the Leydig cells had been drastically altered. In addition, α-naphthol and β-naphthol esterase activity as well as the steroidogenic capacity of the Leydig cells were greatly reduced at this time. In contrast, the level of sterol carrier protein 2 (SCP2), a Leydig cell-specific protein, was affected by hypophysectomy much less than the other parameters measured. Two daily injections of hCG to rats hypophysectomized for 31 days resulted in no change in the morphology of the Leydig cells, or in their proliferative activity. Non-specific esterase activities were also unaffected by 2 days of treatment with hCG. However, two injections of hCG to rats hypophysectomized for 31 days resulted in nearly complete restoration of steroidogenic capacity, and a 3·5-fold increase in the level of SCP2. These findings indicate that hypophysectomy results in significant morphological and biochemical changes in Leydig cells, and that hCG is capable of restoring some of these capacities within a short time. Journal of Endocrinology (1990) 126, 367–375

BINDING OF HUMAN CHORIONIC GONADOTROPHIN BY RAT TESTIS: EFFECT OF SEXUAL MATURATION, CRYPTORCHIDISM AND HYPOPHYSECTOMY

1975 ◽  
Vol 64 (1) ◽  
pp. 59-66 ◽  
Author(s):  
JOACHIM FROWEIN ◽  
WOLFGANG ENGEL
Keyword(s):  
Dissociation Constant ◽  
Sexual Maturation ◽  
Leydig Cells ◽  
Binding Capacity ◽  
Specific Binding ◽  
Chorionic Gonadotrophin ◽  
Human Chorionic Gonadotrophin ◽  
Scatchard Analysis ◽  
Rat Testis ◽  
Relative Binding

SUMMARY The specific binding of 125I-labelled human chorionic gonadotrophin (HCG) by rat testicular homogenate as compared with isolated Leydig cells differs with respect to total binding capacity but not to the dissociation constant (KD) as revealed by Scatchard analysis. The maximal binding capacity for [125I]HCG of crude testicular homogenate was 95 ng/g rat testis. Hypophysectomy causes a decline in binding capacity within the first three days but on the 20th and 30th day after hypophysectomy the relative binding capacity no longer differs from that of controls. Binding capacity is enhanced in cryptorchid testes relative to normal, and increases during sexual maturation to a peak shortly before puberty.

Regulation of testicular human chorionic gonadotrophin binding in prolactin-deficient Snell dwarf mice

1982 ◽  
Vol 95 (3) ◽  
pp. 301-309 ◽  
Author(s):  
A. G. Amador ◽  
A. Bartke
Keyword(s):  
Leydig Cells ◽  
Chorionic Gonadotrophin ◽  
Human Chorionic Gonadotrophin ◽  
Direct Effects ◽  
Down Regulation ◽  
Drug Induced ◽  
Congenital Deficiency ◽  
Similar Dose ◽  
Snell Dwarf ◽  
Dwarf Mice

The regulation of binding of 125I-labelled human chorionic gonadotrophin (hCG) to testis was studied in mutant mice with congenital deficiency of prolactin (dw/dw), in mice with prolactin deficiency induced by treatment with bromocriptine and in normal untreated mice. After injection of hCG, normal mice showed a dose-related decrease in testicular hCG binding and subsequent recovery from down-regulation, similar to previous findings in the rat. Mice with congenital prolactin deficiency had a similar dose–response curve of receptor loss after hCG administration, but recovered from down-regulation faster than the normal mice. Induction of prolactin deficiency with bromocriptine prevented down-regulation of hCG binding. The differential effects of congenital and drug-induced prolactin deficiency could be related to a difference in the duration of the deficiency or to its severity. However, this difference could also suggest direct effects of the dw mutation and/or bromocriptine on the Leydig cells.

EFFECT OF GLUCOCORTICOIDS ON PLASMA TESTOSTERONE IN MEN

1978 ◽  
Vol 89 (1) ◽  
pp. 126-131 ◽  
Author(s):  
G. Schaison ◽  
F. Durand ◽  
I. Mowszowicz
Keyword(s):  
Chorionic Gonadotrophin ◽  
Human Chorionic Gonadotrophin ◽  
Plasma Testosterone ◽  
Acth Stimulation ◽  
Testosterone Levels ◽  
Before And After ◽  
The Mean ◽  
Normal Men ◽  
Lh Secretion ◽  
Dexamethasone Suppression

ABSTRACT ACTH decreases plasma testosterone levels in men. The aim of this study was to assess the part played by the glucocorticoids in this effect, and the mechanism of their action. Plasma androstenedione, testosterone, cortisol and LH were measured in 8 normal men, before and after the following tests: ACTH stimulation (2 mg im), metyrapone administration (500 mg/every 4 h/6 times) and dexamethasone suppression (8 mg/day/3 days). In addition, androstenedione and testosterone were evaluated under human chorionic gonadotrophin (5000 IU HCG/day/3 days) before and after dexamethasone suppression (8 mg/day/6 days). In all patients, ACTH decreased plasma testosterone from 5.87 ± 1.59 (sd) ng/ml to 3.06 ± 0.8 (sd) ng/ml (P < 0.001). In contrast, after metyrapone, the mean plasma testosterone was increased to 6.98 ± 1.75 (sd) ng/ml. This increase, though not statistically significant, was observed in all patients but one. Both tests resulted in a significant increase of plasma androstenedione (P < 0.01 and P < 0.001, respectively). Dexamethasone suppressed both testosterone and androstenedione levels. None of the three tests had a significant effect on the LH concentration. HCG injection increased the mean plasma testosterone to 11.46 ± 2.80 ng/ml. Dexamethasone significantly depressed (P < 0.01) the testosterone response to HCG. These data are consistent with the following conclusions: 1) The decrease of plasma testosterone levels, observed in men after ACTH administration, is not observed after metyrapone induced ACTH increase. This confirms that it is related to cortisol levels rather than to ACTH itself. 2) Glucocorticoids act directly on testicular biosynthesis since they do not induce any change in LH secretion and since dexamethasone reduces testosterone response to HCG.

ISOLATION OF RAT LEYDIG CELLS BY DENSITY GRADIENT CENTRIFUGATION

1982 ◽  
Vol 92 (2) ◽  
pp. 293-NP ◽  
Author(s):  
J. S. GALE ◽  
J. ST J. WAKEFIELD ◽  
H. C. FORD
Keyword(s):  
Density Gradient ◽  
Binding Sites ◽  
Leydig Cells ◽  
Interstitial Cell ◽  
Density Gradient Centrifugation ◽  
Gradient Centrifugation ◽  
Chorionic Gonadotrophin ◽  
Human Chorionic Gonadotrophin ◽  
Collagenase Treatment

A rapid method for preparing Leydig cells from rat testes is described. An interstitial cell suspension, prepared by collagenase treatment of decapsulated testes, was centrifuged for 10 min over a cushion of 60% (v/v) Percoll to remove red blood cells, and then centrifuged for 20 min in a 0–60% linear density gradient of Percoll. Seventy-four per cent of the cells present in that fraction of the gradient comprising 35–50% Percoll were Leydig cells; the yield from each testis was about 1·5 × 106 cells. The Leydig cells appeared viable, excluded Trypan blue, possessed high-affinity binding sites for human chorionic gonadotrophin (hCG) and synthesized increased quantities of testosterone in response to hCG. The cells could be stored overnight in 20% (v/v) glycerol at −20 °C, with only minimal effect on the specific activities of a number of enzymes used as markers of subcellular components. Testosterone production in vitro by the cells after storage for 20 h was greater than that of hCG-stimulated fresh cells and was not further increased by hCG.

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