FEEDBACK CONTROL OF LH-SECRETION IN THE CASTRATED ADULT MALE MINIATURE PIG

1975 ◽  
Vol 80 (1_Suppla) ◽  
pp. S76
Author(s):  
N. Parvizi ◽  
F. Elsaesser ◽  
D. Smidt ◽  
F. Ellendorff
2000 ◽  
Vol 278 (4) ◽  
pp. E744-E751 ◽  
Author(s):  
Hisashi Kishi ◽  
Mariko Itoh ◽  
Sachiko Wada ◽  
Yoko Yukinari ◽  
Yumiko Tanaka ◽  
...  

We investigated the importance of inhibin and testosterone in the regulation of gonadotropin secretion in adult male golden hamsters ( Mesocricetus auratus). After castration, plasma concentrations of inhibin and testosterone were reduced to undetectable, whereas plasma follicle-stimulating hormone (FSH) and luteinizing hormone (LH) were increased. After hemicastration, plasma FSH and LH increased moderately and plasma inhibin decreased to one-half its initial level. Plasma testosterone levels in hemicastrated animals decreased 3 h after hemicastration but returned to those in sham-operated animals at 6 h. Plasma LH in the castrated hamster declined comparably to intact animals with testosterone treatment; plasma FSH also decreased but still remained at levels higher than those in intact animals. After treatment with inhibin in long-term-castrated animals, plasma FSH decreased, whereas plasma LH was not altered. Intact males treated with flutamide, an anti-androgen, showed a significant increase in plasma LH but not in FSH. On the other hand, treatment with anti-inhibin serum induced a significant elevation in plasma FSH, but not in LH. Using immunohistochemistry, we showed that the inhibin α-subunit was localized to both Sertoli and Leydig cells. The present study in adult male hamsters indicates that FSH secretion is regulated mainly by inhibin, presumably from Sertoli and Leydig cells, and that LH secretion is controlled primarily by androgens produced from the Leydig cells. This situation is more similar to that of primates than of rats.


1984 ◽  
Vol 100 (1) ◽  
pp. 107-112 ◽  
Author(s):  
T. W. Gettys ◽  
M. J. D'Occhio ◽  
D. M. Henricks ◽  
B. D. Schanbacher

ABSTRACT Twenty acutely castrated bulls were used to investigate the role of androgenic and oestrogenic steroids in the feedback control of LH secretion. The effects of 5α-dihydrotestosterone (DHT) or the growth stimulants trenbolone acetate (TBA) or oestradiol-17β (OE2) on serum LH secretory profiles were measured. In addition, pituitary LH responses to exogenous LH releasing hormone (LHRH) were determined to differentiate between hypothalamic and pituitary sites of steroid action. At the time of castration, two groups of animals were given implants of either 45 mg OE2 or 200 mg TBA. Another group received equivalent to 30 mg daily injections of DHT. Control steers showed an increase in LH from 2·4 ± 0·5 (s.e.m.) μg/l to 7·0 ± 0·5 μg/l during the week after castration. Treatment with DHT and TBA prevented the post-castration rise in serum LH. In contrast, steers given implants of OE2 showed a significantly greater increase in LH than controls 1 day after castration, but by day 5 LH declined in the OE2-treated group to precastration values. Five weeks after castration control steers secreted LH in pulses at intervals of 40–50 min and with an amplitude of 4·2± 0·4 μg/l. Pulses were not detected in the LH profiles of the steroid-treated steers. Dihydrotestosterone and TBA significantly reduced pituitary LH responses to exogenous LHRH, whereas steers receiving OE2 showed LH responses to LHRH which were similar to those observed in castrated controls. These results support the hypothesis that androgenic and oestrogenic components participate separately in the feedback control of LH secretion in the bull. A similar LH response to exogenous LHRH in control and OE2-treated animals suggests that the primary site of oestrogen feedback is at the level of the hypothalamus. Conversely, the small LH response to LHRH in androgen-treated animals suggests that androgen feedback is, in part, imposed at the level of the pituitary gland. Interestingly, LH secretion is regulated by dosages of androgenic and oestrogenic steroids which are available commercially as growth stimulants for cattle. J. Endocr. (1984) 100, 107–112


1975 ◽  
Vol 53 (5) ◽  
pp. 237-239 ◽  
Author(s):  
G. B�rsch ◽  
J. Mauss ◽  
E. Richter ◽  
K. Bormacher ◽  
G. Leyendecker ◽  
...  

1978 ◽  
Vol 89 (4) ◽  
pp. 789-795 ◽  
Author(s):  
Karl M. Pirke ◽  
Michael Geiss ◽  
Rainer Sintermann

ABSTRACT The hypothalamic-pituitary gonadal axis was studied in young adult (3 month old) and old (24 to 27 month old) male Wistar rats. Plasma testosterone decreased significantly in old animals (x̄: 262 ng/100 ml (n = 35); versus x̄: 110 ng/100 ml (n = 30)). The fall in LH was less pronounced but still significant (54.5 ng LH-RP-1/ml in young versus 39.5 ng/ml in old rats). Groups of 6 to 8 animals of both ages were castrated and implanted with silastic capsules continuously releasing testosterone. The length of the capsules was directly proportional to the plasma testosterone levels achieved (range between 63 and 350 ng/100 ml). After one week young castrated rats not substituted with testosterone showed LH values three times higher (x̄: 351 ng/ml) than old rats treated in the same way (x̄ = 126 ng/ml). LH values in the animals substituted with testosterone indicate that the sensitivity of the negative testosterone-LH feedback is greatly increased in old rats. Testosterone can be depressed to 60 ng/100 ml before an increase in LH occurs. In young rats no increase in LH was observed when testosterone values were higher than 170 ng/100 ml. In the range between 170 and 100 ng/100 ml about half of the young animals reacted with increased LH secretion, while an increase was observed in all young animals when testosterone dropped below 100 ng/100 ml.


Endocrinology ◽  
1972 ◽  
Vol 90 (3) ◽  
pp. 771-777 ◽  
Author(s):  
T. YAMAJI ◽  
D.J. DIERSCHKE ◽  
A.N. BHATTACHARYA ◽  
E. KNOBIL

1981 ◽  
Vol 241 (3) ◽  
pp. E246-E250
Author(s):  
T. J. Worgul ◽  
R. J. Santen ◽  
E. Samojlik ◽  
G. Irwin ◽  
R. E. Falvo

A variety of data suggest an independent role for androgens and estrogens in the regulation of luteinizing hormone (LH) secretion in the male. Estrogens, in the male are primarily derived from testicular androgens that are aromatized both in peripheral tissues and in the CNS. Our prior data suggested a pharmacologic regimen that blocked CNS aromatization without lowering peripheral estrogen or testosterone levels. Such experimental conditions would permit assessment of the relative roles of CNS versus peripheral aromatization in the regulation of LH secretion. We utilized this regimen (aminoglutethimide, a potent aromatase inhibitor, and hydrocortisone) in seven adult male dogs for 14 days. Plasma LH rose to castrate levels, 450% above control values on days 7 and 14. These LH increments stimulated similar rises in androstenedione, testosterone, and dihydrotestosterone. In contrast, plasma estrone and estradiol concentrations remained constant. The induction of castrate LH levels without a concomitant fall in peripheral androgens or estrogens is best explained by a block of central aromatization and thus a reduction in local hypothalamic concentrations. We conclude that aromatization in the CNS rather than peripheral tissues is the more important site with respect to LH negative feedback in the male dog.


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