Studies on the mechanism of the selective suppression of plasma levels of follicle-stimulating hormone in the female rat after administration of steroid-free bovine follicular fluid

1983 ◽  
Vol 97 (3) ◽  
pp. 327-338 ◽  
Author(s):  
W. J. de Greef ◽  
F. H. de Jong ◽  
J. de Koning ◽  
J. Steenbergen ◽  
P. D. M. van der Vaart

Steroid-free bovine follicular fluid (bFF) selectively suppresses the plasma levels of FSH in the female rat, demonstrating that bFF contains inhibin-like material. The present study was concerned with the effects of bFF on the hypothalamic release of LH releasing hormone (LH-RH) into hypophysial stalk blood and on the metabolic clearance rates of gonadotrophins. The metabolic clearance rates of FSH, LH and prolactin were determined after a single injection of and during a constant infusion with adenohypophysial extract. Similar results were obtained with both methods, and treatment with bFF did not alter the metabolic clearance rates of FSH, LH and prolactin. Anaesthesia with urethane, used for surgery involved in the collection of hypophysial stalk blood, did not interfere with the effect of bFF on plasma levels of FSH. The administration of bFF did not change the hypothalamic content of LH-RH, but caused a 30% decrease in the levels of LH-RH in hypophysial stalk plasma. However, a fraction isolated from bFF, which contained 20 times more inhibin-like activity per mg protein than bFF, did not alter the hypothalamic release of LH-RH into the hypophysial portal blood while this fraction was effective in specifically suppressing the plasma levels of FSH. It was concluded that the inhibin-like activity in bFF does not suppress the plasma levels of FSH by affecting its plasma clearance or by influencing the hypothalamic release of LH-RH, but that it has a direct effect on the adenohypophysis in inhibiting the release of FSH. Besides the inhibin-like activity, bFF also contains another factor which can decrease the levels of LH-RH in hypophysial stalk plasma.

1988 ◽  
Vol 118 (2) ◽  
pp. 254-259 ◽  
Author(s):  
Daniel Fröhli ◽  
Jürg W. Blum

Abstract. Experiments were designed to study effects of 3 days of fasting on blood plasma levels, metabolic clearance rates (MCR) and effects of norepinephrine (NE) and epinephrine (E) on levels of glucose, nonesterified fatty acids (NEFA) and immunoreactive insulin (IRI) in 12 steers. During fasting, levels of E, NE and protein did not change, whereas IRI, T3 and glucose decreased and NEFA, acetoacetate and β-hydroxybutyrate increased. Before and at the end of fasting, NE or E were iv infused for 120 min. NE and E were elevated after 15 min and to the end of the infusion. The increase in E, but not in NE, was significantly greater after 3 days of fasting than before fasting (P < 0.05). MCR for E was lower after fasting (299 ± 17 vs 204 ± 10 ml·kg−0.75·min−1; P < 0.001), whereas MCR for NE was not significantly different (455 ± 37 vs 400 ±27 ml·kg−0.75·min−1). MCR was higher for NE than for E, both before and after fasting (P < 0.05). After the infusions, E and NE decreased within minutes to pre-infusion concentrations. During E infusions, NEFA increased significantly more, whereas glucose increased less in fasted than in fed animals. During NE infusions, NEFA increased in fasted, but not in fed animals, and glucose increased less at the end than before fasting. IRI decreased during E infusions only in fed animals, and transiently increased after the infusion, except after NE infusion in fasted steers. Changes in plasma levels, clearance rates and sensitivity to effects of NE and E, together with alterations of insulin and T3 concentrations, may contribute to shifts in energy metabolism during food restriction.


Endocrinology ◽  
1970 ◽  
Vol 87 (5) ◽  
pp. 874-880 ◽  
Author(s):  
R. DE HERTOGH ◽  
E. EKKA ◽  
I. VANDERHEYDEN ◽  
J. J. HOET

1982 ◽  
Vol 94 (3) ◽  
pp. 369-379 ◽  
Author(s):  
W. J. de Greef ◽  
J. Th. J. Uilenbroek ◽  
F. H. de Jong

The present study was concerned with a possible involvement of LH in the process of functional luteolysis in the pseudopregnant rat. Daily injections with 2 μg ovine LH during pseudopregnancy reduced peripheral and ovarian levels of progesterone in intact and hysterectomized rats and in hypophysectomized rats with a pituitary transplant under the kidney capsule. However, a daily dose of 10 μg LH did not alter the levels of progesterone. A short-lasting decrease in plasma progesterone occurred when endogenous levels of LH were temporarily raised in pseudopregnant rats by a single injection of LH releasing hormone (LH-RH). Treatment with LH or LH-RH, however, did not shorten the duration of pseudopregnancy. Daily treatment of pseudopregnant rats with 5 or 20 ng oestradiol benzoate, but not with 1000 ng, decreased plasma levels of progesterone. On the other hand, daily treatment with oestradiol benzoate did not affect plasma progesterone in pseudopregnant rats which were hypophysectomized and had an ectopic pituitary gland. Plasma levels of LH were not increased in the animals receiving 5 or 20 ng oestradiol benzoate daily, suggesting that the effect of oestradiol benzoate on plasma progesterone is not through an enhanced secretion of LH. Treatment with oestradiol benzoate did not affect the duration of pseudopregnancy. In conclusion, low doses of LH can reduce peripheral levels of progesterone during pseudopregnancy, but it seems improbable that LH is involved in the process of functional luteolysis. Furthermore, low doses of oestradiol benzoate can also decrease plasma progesterone, but the mechanisms involved are still not understood.


1980 ◽  
Vol 87 (1) ◽  
pp. 141-146 ◽  
Author(s):  
MARIKO SHIROTA ◽  
SHUJI SASAMOTO

Maximal levels of progesterone in the plasma after premature ovulation induced by either the administration of human chorionic gonadotrophin (HCG) or LH-releasing hormone (LH-RH) to dioestrous (day 0) rats were observed from 33 to 45 h but decreased 3 h earlier than after spontaneous ovulation. This suggested an earlier decline in the secretory activity of corpora lutea formed from premature ovulations than that of corpora lutea formed during a normal oestrous cycle. The next spontaneous ovulation occurred 4 days (day 5) after premature ovulation induced by LH-RH on day 0. A single s.c. injection of 2·5 μg oestradiol-17β (OE2) at 10.00 h on day 2 to these animals advanced the next spontaneous ovulation by 1 day. A normal number of oocytes was shed, indicating that earlier secretion of oestrogen on day 2 had advanced the next spontaneous ovulation. A single injection of 2·5 μg OE2 to normal 4-day cyclic rats at metoestrus failed to advance the next ovulation. An earlier decline of progesterone levels in the plasma of rats after premature ovulation as compared with spontaneous ovulation may explain the greater effectiveness of oestrogen in the former group. The progesterone surge was observed during the period of premature ovulation in both HCG- and LH-RH-treated groups. This progesterone release in the periovulatory period may be responsible for the inhibition of gonadotrophin surges on the expected day of prooestrus (day 1).


2004 ◽  
Vol 287 (3) ◽  
pp. E431-E438 ◽  
Author(s):  
Ramona Trebbien ◽  
Letty Klarskov ◽  
Mette Olesen ◽  
Jens J. Holst ◽  
Richard D. Carr ◽  
...  

Glucagon has a short plasma t1/2in vivo, with renal extraction playing a major role in its elimination. Glucagon is degraded by neutral endopeptidase (NEP) 24.11 in vitro, but the physiological relevance of NEP 24.11 in glucagon metabolism is unknown. Therefore, the influence of candoxatril, a selective NEP inhibitor, on plasma levels of endogenous and exogenous glucagon was examined in anesthetized pigs. Candoxatril increased endogenous glucagon concentrations, from 6.3 ± 2.5 to 20.7 ± 6.3 pmol/l [COOH-terminal (C)-RIA, P < 0.05]. During glucagon infusion, candoxatril increased the t1/2determined by C-RIA (from 3.0 ± 0.5 to 17.0 ± 2.5 min, P < 0.005) and midregion (M)-RIA (2.8 ± 0.5 to 17.0 ± 3.0 min, P < 0.01) and reduced metabolic clearance rates (MCR; 19.1 ± 3.2 to 9.4 ± 2.0 ml·kg−1·min−1, P < 0.02, C-RIA; 19.2 ± 4.8 to 9.0 ± 2.3 ml·kg−1·min−1, P < 0.05, M-RIA). However, neither t1/2nor MCR determined by NH2-terminal (N)-RIA were significantly affected ( t1/2, 2.7 ± 0.4 to 4.5 ± 1.6 min; MCR, 30.3 ± 6.4 to 28.5 ± 9.0 ml·kg−1·min−1), suggesting that candoxatril had no effect on NH2-terminal degradation but leads to the accumulation of NH2-terminally truncated forms of glucagon. Determination of arteriovenous glucagon concentration differences revealed that renal glucagon extraction was reduced (but not eliminated) by candoxatril (from 40.4 ± 3.8 to 18.6 ± 4.1%, P < 0.02, C-RIA; 29.2 ± 3.1 to 14.7 ± 2.2%, P < 0.02, M-RIA; 26.5 ± 4.0 to 19.7 ± 3.5%, P < 0.06, N-RIA). Femoral extraction was reduced by candoxatril when determined by C-RIA (from 22.7 ± 2.4 to 8.0 ± 5.1%, P < 0.05) but was not changed significantly when determined using M- or N-RIAs (10.0 ± 2.8 to 4.7 ± 3.7%, M-RIA; 10.5 ± 2.5 to 7.8 ± 4.2%, N-RIA). This study provides evidence that NEP 24.11 is an important mediator of the degradation of both endogenous and exogenous glucagon in vivo.


1986 ◽  
Vol 111 (3) ◽  
pp. 449-NP ◽  
Author(s):  
M. J. P. G. van Kroonenburgh ◽  
J. L. Beck ◽  
H. M. Vemer ◽  
R. Rolland ◽  
C. M. G. Thomas ◽  
...  

ABSTRACT Adult male Wistar rats were treated with a single injection (500 μg s.c.) of a new biodegradable depot formulation of the LH-releasing hormone (LHRH) analogue [d-Ser(But)6]AzGly10-LH-RH (Zoladex; ICI 118 630) to evaluate its potential for inhibiting spermatogenesis. The drug produced a marked (P≤0·05) decrease in serum concentrations of FSH, LH and testosterone with a maximum effect 14 days after treatment. Since striking focal histological changes were seen in the testis after only 1 week, at a time when changes in serum gonadotrophins were minimal, there may be a direct effect of the LHRH analogue on spermatogenesis. Degenerative changes in germ cells as well as Sertoli cells could be observed. Flow-cytometric analysis of testicular cell suspensions showed a significant decline in the absolute numbers of haploid cells (spermatids), tetraploid cells (mainly pachytene spermatocytes) and of the numbers of cells in the S-phase of the cell cycle. This suggests that the drug also inhibits proliferation of spermatogonia and/or primary spermatocytes. Testis weight, serum hormone concentrations, and histological and cytological parameters returned to essentially normal values 52 days after the injection. It is concluded that this new method of administration may have practical and pharmacokinetic advantages for the purpose of reversible inhibition of spermatogenesis. J. Endocr. (1986) 111, 449–454


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