Effect of Long-Acting Thyroid Stimulator on Serum Concentration of Luteinizing Hormone in the Rat

1975 ◽  
Vol 48 (3) ◽  
pp. 231-233
Author(s):  
P. Dandona ◽  
D. J. El Kabir ◽  
F. Naftolin ◽  
P. C. B. MacKinnon
Keyword(s):  
Luteinizing Hormone ◽  
Serum Concentration ◽  
Pituitary Gland ◽  
Immunoglobulin G ◽  
Adrenocorticotrophic Hormone ◽  
Serum Concentrations ◽  
Serum Luteinizing Hormone ◽  
Serum Lh ◽  
Long Acting ◽  
Dexamethasone Suppression

1. The effect of long-acting thyroid stimulator (LATS) on the serum luteinizing hormone (LH) levels of the rat in pro-oestrus has been studied. 2. The injection of three out of four LATS-containing immunoglobulin G fractions caused an increase in amounts of serum LH. 3. Adrenalectomy and dexamethasone suppression did not alter this response. 4. Injection of large doses of adrenocorticotrophic hormone did not produce any increase in serum concentrations of LH. 5. It is postulated that LATS may have a direct effect on the release of LH from the pituitary gland.

FEEDBACK CONTROL OF FSH IN THE MALE: ROLE OF OESTROGEN

1973 ◽  
Vol 74 (3) ◽  
pp. 449-460 ◽  
Author(s):  
Patrick C. Walsh ◽  
Ronald S. Swerdloff ◽  
William D. Odell
Keyword(s):  
Luteinizing Hormone ◽  
Follicle Stimulating Hormone ◽  
Oestrogen Therapy ◽  
Serum Concentrations ◽  
Elderly Men ◽  
Normal Range ◽  
Oestrogen Treatment ◽  
Serum Lh ◽  
Higher Doses

ABSTRACT Serum follicle stimulating hormone (FSH) and luteinizing hormone (LH) were measured by radioimmunoassay in a group of elderly men following castration and oestrogen therapy. Prior to orchiectomy, mean serum concentrations of LH and FSH were within the normal range. Two days following castration, serum LH concentrations increased in all eight patients; higher levels of LH were subsequently measured in all but one patient after periods of time ranging from 49 to 210 days. Serum FSH levels, measured in three patients following castration, increased in a pattern parallel to LH changes. Ethinyl oestradiol (EOe) in doses ranging from 5 to 300 μg/day was administered to ten men who had been castrated 3 to 72 months earlier. Oestrogen treatment suppressed both LH and FSH in a parellel manner in nine of ten patients. LH was first suppressed to intact levels in one of eight patients treated with 20 μg/day of EOe, in two of six patients treated with 50 μg/day, and in one patient by 80 μg/day. FSH was not suppressed to precastration levels until 50 μg/day of EOe was administered; this dose suppressed three of six patients. Higher doses of EOe (150–300 μg/day) suppressed both LH and FSH to levels below the sensitivity of the assay. These data fail to demonstrate any differential effect of oestrogen on LH and FSH release.

RESTORATION OF OESTROGEN POSITIVE FEEDBACK EFFECT ON LH RELEASE BY BROMOCRIPTINE IN HYPERPROLACTINAEMIC PATIENTS WITH GALACTORRHOEA-AMENORRHOEA

1979 ◽  
Vol 91 (3) ◽  
pp. 591-600 ◽  
Author(s):  
Toshihiro Aono ◽  
Akira Miyake ◽  
Takenori Shioji Motoi Yasuda ◽  
Koji Koike ◽  
Keiichi Kurachi
Keyword(s):  
Luteinizing Hormone ◽  
Follicle Stimulating Hormone ◽  
Serum Prolactin ◽  
Serum Luteinizing Hormone ◽  
Serum Lh ◽  
Lh Release ◽  
The Mean ◽  
Lh Rh ◽  
Lh Releasing Hormone ◽  
Positive Feedback Effect

ABSTRACT Five mg of bromocriptine was administered for 3 weeks to 8 hyperprolactinaemic women with galactorrhoea-amernorrhoea, in whom the response of serum luteinizing hormone (LH) and follicle-stimulating hormone (FSH) to 100 μg of iv LH-releasing hormone (LH-RH) had been evaluated. Twenty mg of conjugated oestrogen (Premarin®) was injected iv any day between the 10th and 12th day from the initiation of the treatment, and serum LH levels were serially determined for 120 h. Hyperresponse of LH with normal FSH response to LH-RH was observed in most patients. Bromocriptine treatment for 10 to 12 days significantly suppressed mean (± se) serum prolactin (PRL) levels from 65.1 ± 23.0 to 10.4 ± 2.0 ng/ml, while LH (12.6 ± 2.1 to 24.8 ± 5.9 mIU/ml) and oestradiol (40.1 ± 7.6 to 111.4 ± 20.8 pg/ml) levels increased significantly. Patients on bromocriptine treatment showed LH release with a peak at 48 h after the injection of Premarin. The mean per cent increases in LH were significantly higher than those in untreated patients with galactorrhoea-amenorrhoea between 32 and 96 h after the injection. The present results seem to suggest that the restoration of LH-releasing response to oestrogen following suppression of PRL by bromocriptine may play an important role in induction of ovulation in hyperprolactinaemic patients with galactorrhoea-amenorrhoea.

SERUM LUTEINIZING HORMONE AND FOLLICLE-STIMULATING HORMONE CONCENTRATIONS IN IMMATURE FEMALE RATS TREATED WITH MULTIPLE INJECTIONS AND VARIOUS AMOUNTS OF LUTEINIZING HORMONE RELEASING HORMONE

1975 ◽  
Vol 66 (1) ◽  
pp. 13-20 ◽  
Author(s):  
D. C. JOHNSON ◽  
R. S. MALLAMPATI
Keyword(s):  
Luteinizing Hormone ◽  
Constant Stimulus ◽  
Female Rats ◽  
Intact Female ◽  
Immature Female ◽  
Luteinizing Hormone Releasing Hormone ◽  
Releasing Hormone ◽  
Serum Luteinizing Hormone ◽  
Serum Lh ◽  
Lh Rh

SUMMARY Release of immunoreactive LH and FSH was induced in immature intact female rats by repeated injections of synthetic luteinizing hormone releasing hormone (LH-RH). Altering the dose of LH-RH (5, 10, 20, 50 ng) and the frequency of administration (every 10, 20, 30 or 60 min) over a period of 2 h produced a variety of serum LH and FSH concentrations and ratios. When the dose was a constant 20 ng but the frequency of injections was either 20 or 30 min, a steady state in serum gonadotrophin concentrations was reached within 1 h and the level remained the same during the second hour. When given every 10 min, 20 ng LH-RH produced a much higher concentration of both LH and FSH during the second hour of stimulation. Examination of the gonadotrophin levels after each injection of LH-RH showed that the pituitary response was variable in spite of a constant stimulus.

LUTEINIZING HORMONE RELEASING HORMONE-INDUCED RELEASE OF LUTEINIZING HORMONE FROM PITUITARY EXPLANTS OF COWS KILLED BEFORE OR AFTER OESTRADIOL TREATMENT

1981 ◽  
Vol 88 (1) ◽  
pp. 17-25 ◽  
Author(s):  
E. M. CONVEY ◽  
J. S. KESNER ◽  
V. PADMANABHAN ◽  
T. D. CARRUTHERS ◽  
T. W. BECK
Keyword(s):  
Luteinizing Hormone ◽  
Pituitary Gland ◽  
Lh Surge ◽  
Releasing Hormone ◽  
Oestradiol Treatment ◽  
Readily Releasable Pool ◽  
Serum Lh ◽  
Pituitary Glands ◽  
Lh Rh ◽  
Lh Releasing Hormone

In ovariectomized heifers, oestradiol decreases concentrations of LH in serum for approximately 12 h after which LH is released in a surge comparable in size and duration to the preovulatory surge. Using this model, we measured LH release induced by LH releasing hormone (LH-RH) from pituitary explants taken from ovariectomized heifers before or after an oestradiol-induced LH surge. These changes were related to changes in LH concentrations in serum and pituitary glands and hypothalamic LH-RH content. Twenty Holstein heifers were randomly assigned to one of four treatment groups to be killed 0, 6, 12, or 24 h after the injection of 500 μg oestradiol-17β. Jugular blood was collected at −2, −1 and 0 h then at intervals of 2 h until slaughter. Pituitary glands were collected and ≃2 mm3 explants were exposed to 4 ng LH-RH/ml medium for 30 min (superfusion) or 4 ng LH-RH/ml medium for 2 h in Erlenmeyer flasks. Levels of LH were measured in the medium. Hypothalami, collected at autopsy, were assayed for LH-RH content. To determine pituitary LH content, an additional 15 ovariectomized heifers were killed, five each at 0, 12 and 24 h after the injection of 500 μg oestradiol. In both groups of heifers, oestradiol reduced serum LH concentrations to ≃ 1 ng/ml, a level which persisted for 12 h, when LH was released in a surge. Pituitary sensitivity to LH-RH was increased at 6 and 12 h after the injection of oestradiol, but was markedly decreased at 24 h, i.e. after the LH surge. Despite this twofold increase in capacity of the pituitary gland to release LH in response to LH-RH, pituitary LH content did not change during 12 h after oestradiol treatment. However, LH content decreased after the LH surge and this decrease was associated with a decrease in pituitary responsiveness to LH-RH. Hypothalamic LH-RH content was not altered by these treatments. We have interpreted our results as evidence that oestradiol exerts a positive feedback effect on the pituitary gland of ovariectomized heifers such that pituitary sensitivity to LH-RH is increased twofold by the time the LH surge is initiated. In addition, oestradiol causes a transitory inhibition of LH-RH release as shown by the fact that serum LH concentrations remained low during the interval from injection of oestradiol until the beginning of the LH surge despite the fact that pituitary sensitivity to LH-RH is increased at this time. Depletion of a readily releasable pool of pituitary LH may be the mechanism by which the LH surge is terminated.

A note on the effects of previous photoperiod exposure and gradual transitions of light intensity at dawn and dusk on growth in Holstein heifers

1988 ◽  
Vol 46 (2) ◽  
pp. 300-303 ◽  
Author(s):  
S. A. Zinn ◽  
L. T. Chapin ◽  
H. A. Tucker
Keyword(s):  
Luteinizing Hormone ◽  
Light Intensity ◽  
Growth Response ◽  
Live Weight ◽  
Long Day ◽  
Serum Luteinizing Hormone ◽  
Serum Lh ◽  
Proportional Increase ◽  
Short Days

Long-day photoperiods of 16 h light (L) and 8 h dark (D) stimulate a proportional increase in live-weight (LW) gain of peripubertal Holstein heifers of 0·08 to 0·17 compared with heifers exposed to short days of less than 12 h L per day (Peters, Chapin, Leining and Tucker, 1978; Peters, Chapin, Emery and Tucker, 1980; Petitclerc, Chapin, Emery and Tucker, 1983; Zinn, Chapin and Tucker, 1986). One factor that could account for some of this variation in the magnitude of the growth response to long days is that the previous photoperiod exposure may influence the response to a subsequent different photoperiod (Moore-Ede, Sulzman and Fuller, 1982). For example, exposure to 13L: 11D induced pulsatile activity of serum luteinizing hormone (LH) in ewes previously exposed to 16L: 8D, but reduced serum LH to undetectable levels in sheep previously exposed to 8L: 16D (Robinson and Karsch, 1987). Thus, sheep exposed to identical photoperiods exhibited different responses depending on previous photoperiod exposure.

scholarly journals Erythropoietin-producing hepatocellular receptor A7 restrains estrogen negative feedback of luteinizing hormone via ephrin A5 in the hypothalamus of female rats

2020 ◽  
Vol 319 (1) ◽  
pp. E81-E90 ◽  
Author(s):  
Shang Li ◽  
Junyu Zhai ◽  
Bing Xu ◽  
Jiansheng Liu ◽  
Weiwei Chu ◽  
...  
Keyword(s):  
Luteinizing Hormone ◽  
Negative Feedback ◽  
Female Rats ◽  
Female Rat ◽  
Female Reproduction ◽  
Systemic Injection ◽  
Serum Luteinizing Hormone ◽  
Serum Lh ◽  
17Β Estradiol ◽  
Lh Secretion

We have previously shown that systemic injection of erythropoietin-producing hepatocellular receptor A7 (EPHA7)-Fc raises serum luteinizing hormone (LH) levels before ovulation in female rats, indicating the induction of EPHA7 in ovulation. In this study, we aimed to identify the mechanism and hypothalamus-pituitary-ovary (HPO) axis level underlying the promotion of LH secretion by EPHA7. Using an ovariectomized (OVX) rat model, in conjunction with low-dose 17β-estradiol (E2) treatment, we investigated the association between EPHA7-ephrin (EFN)A5 signaling and E2 negative feedback. Various rat models (OVX, E2-treated OVX, and abarelix treated) were injected with the recombinant EPHA7-Fc protein through the caudal vein to investigate the molecular mechanism underlying the promotion of LH secretion by EPHA7. Efna5 was observed strongly expressed in the arcuate nucleus of the female rat by using RNAscope in situ hybridization. Our results indicated that E2, combined with estrogen receptor (ER)α, but not ERβ, inhibited Efna5 and gonadotropin-releasing hormone 1 ( Gnrh1) expressions in the hypothalamus. In addition, the systemic administration of EPHA7-Fc restrained the inhibition of Efna5 and Gnrh1 by E2, resulting in increased Efna5 and Gnrh1 expressions in the hypothalamus as well as increased serum LH levels. Collectively, our findings demonstrated the involvement of EPHA7-EFNA5 signaling in the regulation of LH and the E2 negative feedback pathway in the hypothalamus, highlighting the functional role of EPHA7 in female reproduction.

Decrease of LRH receptors in the pituitary gland in streptozotocin-induced diabetic rats

1985 ◽  
Vol 110 (1) ◽  
pp. 46-49 ◽  
Author(s):  
Keiichi Tasaka ◽  
Naoki Terakawa ◽  
Ikuya Shimizu ◽  
Shirou Ohtsuka ◽  
Akira Miyake ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Body Weight ◽  
Serum Concentration ◽  
Pituitary Gland ◽  
Diabetic Rats ◽  
Oestrous Cycle ◽  
Female Rats ◽  
Normal Female ◽  
Medial Basal Hypothalamus ◽  
Serum Lh

Abstract. In studies into the mechanism of anovulation in the diabetic condition, the LRH receptor content of the pituitary gland of rats with diabetes mellitus was determined. Normal female rats weighing 180–200 g were injected iv with either streptozotocin (6 mg/100 g body weight) or vehicle in dioestrus of the oestrous cycle. The rats were sacrificed by decapitation 9 days after treatment, and serum LH concentrations and the LRH content of the medial basal hypothalamus (MBH) were measured by radioimmunoassay (RIA), and the LRH receptor content of the pituitary gland was determined. The serum concentration of LH and the LRH content of the MBH in diabetic rats were 34.4 ± 4.8 ng/ml (mean ± sem) and 2.05 ± 0.04 ng/MBH, respectively, which were similar to the respective values of normal rats in dioestrus. However, the LRH receptor content of diabetic rats (13.2 ± 3.9 fmol/pituitary) was significantly (P < 0.05) lower than that of normal rats in dioestrus (68.0 ± 7.1 fmol/pituitary) and pro-oestrus (59.4 ± 13.6 fmol/pituitary). These results suggest that anovulation in diabetic rats is at least partly attributable to a low content of LRH receptors in the pituitary gland.

Specific FSH suppression in male rat by porcine follicular fluid

1981 ◽  
Vol 240 (2) ◽  
pp. E209-E215
Author(s):  
J. R. Lorenzen ◽  
G. H. Dworkin ◽  
N. B. Schwartz
Keyword(s):  
Luteinizing Hormone ◽  
Total Dose ◽  
Follicular Fluid ◽  
Follicle Stimulating Hormone ◽  
Test Subject ◽  
Male Rats ◽  
Male Rat ◽  
Rat Serum ◽  
Serum Luteinizing Hormone ◽  
Serum Lh

A variety of protocols using intact, castrated, and sham-castrated adult male rats was used to test the ability of porcine follicular fluid to selectively suppress serum follicle-stimulating hormone (FSH). A total dose of 500 microliters follicular fluid injected intraperitoneally will suppress FSH in the rat with testes within 5 h of injection. This is more than is necessary to suppress FSH in the intact or ovariectomized female. A total dose of 1 ml of follicular fluid is needed to suppress FSH reliably in the castrated male rat. Serum FSH is suppressed significantly beginning between 4 and 5.5 h after intraperitoneal injection of 1 ml of follicular fluid and 3 h after intravenous injection. The suppression continues until 10 h postinjection and is abated by 26 h postinjection. Serum luteinizing hormone (LH) is unaffected by follicular fluid in any protocol tested. It is concluded that 1) follicular fluid can suppress serum FSH in the male if large enough doses are given, 2) follicular fluid has no effect on serum LH, and 3) follicular fluid suppresses serum FSH levels in the male as well as previously tried testicular sources. These results suggest that the delay in demonstrating the existence of inhibin may be due to the use of males as both source and test subject.

INFLUENCE OF AGE ON THE RELEASE OF LUTEINIZING HORMONE INDUCED BY OESTROGEN AND PROGESTERONE IN IMMATURE RATS

1972 ◽  
Vol 55 (1) ◽  
pp. 97-103 ◽  
Author(s):  
L. CALIGARIS ◽  
J. J. ASTRADA ◽  
S. TALEISNIK
Keyword(s):  
Luteinizing Hormone ◽  
Single Injection ◽  
Significant Rise ◽  
Female Rats ◽  
Serum Luteinizing Hormone ◽  
Serum Lh ◽  
Oestradiol Benzoate ◽  
Old Rats ◽  
Lh Secretion ◽  
Phasic Release

SUMMARY In immature female rats serum luteinizing hormone (LH) concentration, as measured by radioimmunoassay, was found to be higher at 10 or 15 days of age than thereafter. Animals ovariectomized soon after birth or at 5 days of age showed a significant rise in serum LH levels 10 days later. A positive feedback effect on LH secretion was observed on the day following a single injection of oestradiol benzoate (OB) in 28-day-old rats but not in younger animals. However, in animals primed with OB a second dose of OB 2 days later resulted in a significant rise in serum LH levels even in rats of 22 days of age. Progesterone (1 mg) injected 3 days after the injection of a single dose of OB induced, a few hours later, a significant rise in serum LH concentration. This effect was observed from the 22nd day of age but not in younger animals. The magnitude of the response to progesterone, as revealed by the serum LH levels, sharply decreased at the time of puberty. It is concluded that the mechanisms responsible for the tonic release of LH are ready to function at the time of birth or shortly thereafter, while those involved in the phasic release mature around 22 days of age.

SITE OF ORIGIN OF THE PULSATILE SECRETION OF LUTEINIZING HORMONE IN LONG-TERM OVARIECTOMIZED RATS

1976 ◽  
Vol 70 (1) ◽  
pp. 97-104 ◽  
Author(s):  
G. A. SCHUILING ◽  
H. P. GNODDE
Keyword(s):  
Luteinizing Hormone ◽  
Pituitary Gland ◽  
Ovariectomized Rats ◽  
Constant Infusion ◽  
Pulsatile Secretion ◽  
Releasing Hormone ◽  
Long Acting ◽  
Lh Rh

SUMMARY If long-term ovariectomized rats are treated with the long-acting barbiturate, sodium phenobarbitone, the well-known pulsatile secretion of LH is depressed, resulting in a constant, still raised, plasma LH level. This indicates that in all probability ovariectomized rats secrete LH in both a tonic and a pulsatile way, only the latter being sensitive to phenobarbitone treatment. Constant infusions of synthetic LH-RH into phenobarbitone-treated ovariectomized rats induced a steadily increasing plasma LH concentration without pulsations, whereas pulsatile infusions of the releasing hormone, following a constant infusion, resulted in a pulsatile secretion of LH. This indicates that the pulsatile secretion of LH in ovariectomized rats is the result of a pulsatile secretion of the hypothalamic releasing hormone; the pituitary gland itself is not the site of origin of the phenomenon.

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