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PubMed1978

Gonadal luteinizing hormone receptors and adenylate cyclase: transfer of functional ovarian luteinizing hormone receptors to adrenal fasciculata cells.

Luteinized rat ovaries contain a high concentration of particulate luteinizing hormone (lutropin, LH) receptors and a small quantity of lipid-associated receptors that float in the 360,000 X g supernatant fraction of ovarian homogenates. During fractionation of Lubrol-solubilized LH receptors and adenylate cyclase [ATP pyrophosphate-lyase (cyclizing), EC 4.6.1.1] from the ovary and testis, LH receptors and adenylate cyclase were coincident on gel filtration, but could be resolved during ion-exchange chromatography of soluble ovarian preparations and were completely separated by lectin-affinity chromatography on Sepharose-concanavalin A. For further analysis of receptor-adenylate cyclase coupling, the lipid-rich fraction of ovarian luteal cells was used to transfer gonadal LH receptors to isolated adrenal fasciculata cells. The lipid vesicles obtained from ovarian homogenates by flotation at 360,000 X g contained 5--10% of the ovarian LH receptors and were devoid of adenylate cyclase activity. During incubation of lipid-associated receptors with dispersed rat fasciculata cells at 16 degrees C, progressive incorporation of LH binding sites into the adrenal cells was observed. When adrenal cells bearing heterotopic LH receptors were incubated with 1 nM human choriogonadotropin, cyclic AMP production was consistently stimulated, with an accompanying increase in corticosterone production. These results indicate that LH receptors exist as separate entities from adenylate cyclase in the gonadal cell membrane and can become functionally coupled to adenylate cyclase to evoke cyclic AMP production and steroidogenesis in the host adrenal cells to which they are transferred.

Adenylyl Cyclases↗
PubMed1982

Temporal patterns of serum luteinizing hormone and testosterone and endocrine response to luteinizing hormone releasing hormone in aging male rats.

Temporal patterns of serum testosterone and luteinizing hormone (LH) concentration and responsiveness to luteinizing hormone releasing hormone (LHRH) were measured in young (2 to 3 months), middle-aged (12 to 13 months), and aged (22 to 26 months) male rats. Average testosterone and LH concentrations, as well as individual sample variations, were higher in young than in middle-aged and aged rats and higher in middle-aged than in aged groups. In addition, the young group showed a diurnal pattern of serum testosterone concentration and greater ranges of LH and testosterone concentrations in individual blood samples. Young male rats showed greater increases in serum LH and testosterone than middle-aged and aged groups after intravenous LHRH, 1 and 5 ng/g of body weight. These data indicate that LH and testosterone secretion are progressively reduced in the aged male rat and suggest alterations in neuroendocrine control of pituitary gonadotropin secretion as the most important alteration in the gonadal control system in these animals.

Aging↗
PubMed1991

Plasma luteinizing hormone bioactivity and immunoactivity in ovariectomized rats treated with a long-acting agonist of luteinizing hormone releasing hormone.

The dose response of a luteinizing hormone releasing hormone (LHRH) agonist in rats with high endogenous gonadotrophin levels was determined. Female rats were ovariectomized and injected with 0.3 microgram (group B), 3.2 micrograms (group C), 32 micrograms (group D) and 320 micrograms (group E) of a slow-releasing microcapsule preparation of the LHRH agonist D-Trp 6-LHRH. Control ovariectomized rats (group A) remained untreated. Plasma luteinizing hormone (LH) concentrations were measured by radioimmunoassay (RIA) before the LHRH agonist injection as well as 5, 15 and 30 days thereafter. Furthermore, LH bioactivity was determined by an in vitro rat LH bioassay in order to evaluate changes in bioactivity after administration of LHRH agonist. In control rats, plasma LH concentrations increased to 4.8 +/- 1.3 ng/ml on day 5, reaching peak levels of 9.9 +/- 1 ng/ml on day 30. In contrast to the control group, those rats which received 320 micrograms of LHRH agonist did not show any increase. Rats which received intermediate doses (groups C and D) tended to maintain levels of LH halfway between group A and group E during the first 15 days of treatment. Thereafter LH concentrations were similar to the untreated control group. The course of the LH concentrations during treatment measured by bioassay (BA) showed a similar pattern to the LH concentrations measured by RIA. The BA/RIA ratio was similar in all groups.

Animals↗
PubMed2003

Insulin-like growth factor binding protein 4 expression parallels luteinizing hormone receptor expression and follicular luteinization in the primate ovary.

It has been suggested that locally produced insulin-like growth factor binding protein 4 (IGFBP4) inhibits ovarian follicular growth and ovulation by interfering with IGF action. According to this hypothesis, IGFBP4-expressing follicles should demonstrate atresia, whereas healthy dominant follicles should be devoid of IGFBP4. Alternatively, according to this view, there could be constitutive expression of the inhibitory IGFBP4 but selective expression of an IGFBP4 protease in dominant follicles, allowing the follicle to mature and ovulate because of degradation of the binding protein. To examine these views concerning the role of IGFBP4 in primate follicular selection, we analyzed cellular patterns of IGFs 1 and 2, IGFBP4, and the IGFBP4 protease (pregnancy-associated plasma protein A [PAPP-A]) mRNA expression in ovaries from late follicular phase rhesus monkeys using in situ hybridization. The IGF1 mRNA was not detected, but the IGF2 mRNA was abundant in theca interna and externa of all antral follicles and was present in the granulosa of large preovulatory and ovulatory follicles. The IGFBP4 mRNA was selectively expressed by LH receptor (LHR) mRNA-positive theca interna cells of healthy antral follicles (defined by aromatase and gonadotropin receptor expression) and by LHR-expressing granulosa cells found only in large preovulatory and ovulatory follicles (defined by size and aromatase expression). The PAPP-A mRNA was abundant in granulosa cells of most follicles without obvious relation to IGFBP4 expression. Ovarian IGFBP4 mRNA levels were markedly increased after treatment with the LH analog, hCG, whereas IGF2 and PAPP-A mRNAs were not significantly altered. In summary, IGFBP4 expression appears to be associated with follicular selection, not with atresia, in the monkey ovary. The IGFBP4 is consistently expressed in healthy theca interna and in luteinized granulosa cells, likely under LH regulation. The IGFBP4 protease, PAPP-A, is widely expressed without apparent selectivity for IGFBP4-expressing follicles or for dominant follicles. These observations suggest that IGFBP4 or an IGFBP4 proteolytic product may be involved with LH-induced steroidogenesis and/or luteinization rather than with inhibition of follicular growth.

Animals↗
PubMed1982

Response of luteinizing hormone and follicle-stimulating hormone to luteinizing hormone releasing hormone in the fetal pig.

The responses of anesthetised fetal pigs (n=95) and chronically catheterized fetal pigs (n=10) to luteinizing hormone releasing hormone (LHRH) administration (2 micrograms/kg estimated fetal body weight) was investigated. Fetuses were studied at 55, 70, 85, 100, 106 (chronic) and 113 days. Plasma concentrations of follicle-stimulating hormone (FSH) and luteinizing hormone (LH) were measured by radioimmunoassay. Blood samples were taken from the umbilical artery (anesthetised fetuses) or carotid artery (catheterized fetuses) every 10 min for 1 h except in the youngest age group. No significant sex difference in the LH response to LHRH treatment was observed. The LH response increased with gestational age; average pretreatment plasma concentrations were below 1.1 ng/ml. No response was observed at 55 days, and the highest response was seen at 113 days when plasma LH concentrations rose to 4.3 +/- 0.7 (mean +/- SEM) ng/ml 40 min after treatment. Pretreatment plasma FSH concentrations at 55 days were 1.6 +/- 0.1 ng/ml and gradually rose in males to 3.2 +/- 0.4 ng/ml at 113 days, which was significantly lower than in females where concentrations averaged 8.1 +/- 2.0 ng/ml. LHRH did not significantly affect FSH concentrations in males, while in females a gradually increasing response was observed; at 113 days plasma FSH was 12.5 +/- 2.9 ng/ml 40 min after treatment. The increase in response to LHRH with age of plasma LH concentrations in both sexes, and of plasma FSH concentrations in females indicates the maturation of the hypothalamo-pituitary system.

Animals↗
PubMed1983

Serum and pituitary luteinizing hormone and serum androgens during luteinizing hormone releasing hormone self-priming in immature and pubertal male rats.

Pubertal and young adult male rats release more luteinizing hormone (LH) in response to luteinizing hormone releasing hormone (LHRH) if they are pretreated with LHRH than if they are pretreated with saline. Immature male rats do not show this self-priming effect. To examine some of the possible causes of this difference, immature or pubertal male rats were anesthetized with ketamine HCl and received 3 i.v. injections of 10 ng/100 BW LHRH or saline at 30-min intervals (Times 0, 30 and 60 min) and they were decapitated at Times 0, 15, 30, 45, 60, 75 and 90 min. Serum and pituitary LH and serum testosterone and androstenedione were determined by radioimmunoassay. A self-priming effect was apparent in pubertal rats. LH levels in response to the third LHRH injection were significantly higher compared to the response to the first injection. No self-priming effect was evident in immature rats. No changes in pituitary LH that could account for this difference were apparent. Serum testosterone levels in response to the LHRH priming were relatively higher in immature rats than in pubertal animals at 30, 45 and 60 min. Serum androstenedione levels were relatively higher in pubertal rats at 45 min. These data indicate that LHRH self-priming effect can be demonstrated in male rats using serum collected from decapitated animals for hormone analysis. They also suggest that a different relative response of serum androgens may be one cause of the appearance of LHRH self-priming during the sexual maturation of the male rat.

Androstenedione↗
PubMed1984

Direct inhibitory effect of estradiol on pituitary luteinizing hormone responsiveness to luteinizing hormone releasing hormone is specific and of rapid onset.

We have employed a perifusion technique to explore the time course and specificity of 17 beta-estradiol (E2) effects directly upon luteinizing hormone (LH) release from the isolated rat anterior pituitary under pulsatile luteinizing hormone releasing hormone (LHRH) stimulation. We first characterized the perifusion system and fitted the data to a simple dose-response model. Multiple perifusion studies were then performed with pulses of LHRH at approximately half-maximal response concentration (10(-8) M); LH responses to an initial LHRH pulse (#1) were compared with LH responses to a second LHRH pulse (#2) given at variable times after addition of E2, antiestrogen (LY 117018), and/or 17 alpha-estradiol (17 alpha-E2). Using this approach, we found that the direct inhibitory effect of E2 upon LH responsiveness to LHRH was rapid and specific. The ratio of LH secretion in response to LHRH pulse #2 to that in response to LHRH pulse #1 (LH secretion ratio) decreased steadily during 1 h of exposure to E2. This inhibition was significant (P less than 0.01) by 36 min of E2 exposure. It represented more than the removal of a LHRH self-priming effect because the LH secretion ratios were significantly less than 1.0 [0.80 +/- 0.05 (SEM), P less than 0.01] within 36 min of E2 exposure. The inhibitory effect was not seen when LY 117018 was added with E2, nor when 17 alpha-E2 replaced E2. The specificity of this rapid E2 inhibitory effect upon pituitary LH responsiveness to LHRH strongly suggests that it is receptor mediated. The rapidity of this apparent receptor-mediated estrogen effect suggests that it is a very rapid consequence of nuclear translocation of the E2-receptor complex.

Animals↗
PubMed1986

Changes in the dynamics of luteinizing hormone-releasing hormone-stimulated secretion of luteinizing hormone during sexual maturation of female rats.

Our aim was to identify age-related changes in the dynamics of luteinizing hormone (LH) release that may contribute to the decline in pituitary sensitivity to luteinizing hormone-releasing hormone (LHRH) during sexual maturation of female rats. We studied LHRH-stimulated LH secretion curves of superfused pituitaries from rats ranging in age from 10 days to the first estrous cycle. Pituitary fragments were exposed for 10 min to medium alone or to medium plus LHRH; incubation continued in medium alone for 130 min and effluent was collected for LH analysis. Secretion curves were compared on the basis of total secretion (area under the curve), maximal change in LH secretion rate, and rates of rise and decay of the curves. The data show that total LH secretion in response to LHRH is greatest in 15-, 20-day-old and first-proestrus animals. Also, the maximal change in LH secretion rate was greater, and the increase in LH secretion rate faster in younger animals than in 30-day-old animals. Analysis of secretory granules in LH-containing gonadotropes of 15- and 30-day-old animals revealed changes in he granule population with age. We conclude that younger animals respond faster with a greater LH secretion response to LHRH than do 30-day-old or first-estrus animals, and that these age-related changes in the dynamics of LH secretion may be due in part to maturation of the LH secretory granules.

Age Factors↗
PubMed1986

Catecholamine stimulation of androgen production by rat Leydig cells. Interactions with luteinizing hormone and luteinizing hormone-releasing hormone.

The mechanism(s) of the development of response to catecholamines (CA) by Leydig cells in culture was investigated with the use of primary culture of purified Leydig cells of adult rats. The interactions of a CA agonist, isoproterenol (ISOP), with luteinizing hormone (LH) and a luteinizing hormone-releasing hormone agonist analog (LHRHa) on production of androgen by the Leydig cells were also studied. Cells incubated with ISOP for 3 h increased release of cyclic adenosine 3',5'-monophosphate (cAMP) to similar extents at 0, 3, and 24 h of culture. The beta-agonist did not increase androgen release at 0 h but had a concentration-dependent effect at 3, 24, and 48 h of culture, with maximal effects at 24 h. LH stimulated high increases in production of cAMP and androgen by the cells at 0-24 h of culture. Leydig cell beta-receptors decreased with culture time. Low concentrations but not high levels of LH had additive effects with ISOP on androgen release. ISOP showed a complex interaction with LHRHa on androgen release. Chronic exposure of Leydig cells to LHRHa reduced basal androgen release as well as release of androgen stimulated by ISOP, forskolin, and LH. These studies suggest that the development of response to CA by rat Leydig cells is a postreceptor, postcAMP event and showed that CA can interact with LH or LHRH to regulate Leydig cell function.

1-Methyl-3-isobutylxanthine↗
PubMed1987

Enhanced luteinizing hormone release by luteinizing hormone-releasing hormone in incubating female turkeys (Meleagris gallopavo).

To determine what role pituitary responsiveness plays in the suppression of gonadotropin level during incubation in the turkey, the ability of the pituitary to release luteinizing hormone (LH) in response to luteinizing hormone-releasing hormone (LHRH) was compared in incubating, laying, and photorefractory birds. In all three groups, the i.m. injection of LHRH (4 micrograms/kg) increased serum LH levels; however, the LH response was markedly enhanced in the incubating turkeys as compared with the laying (6.6-fold increase over preinjection levels vs. 1.9-fold; p less than 0.05) or the photorefractory birds (9.7-fold vs. 3.1-fold; p less than 0.05). The LHRH-induced LH release was also determined in turkeys as they shifted from the laying to the incubating phase of the reproductive cycle. This response increased (p less than 0.05) in magnitude as the birds started to incubate. The high prolactin level of incubating turkeys does not have a depressing effect on LHRH-stimulated LH release; thus, impaired LH response to LHRH is not a mechanism involved in the diminished gonadotropin secretion of incubating turkeys.

Animals↗
PubMed1988

Modulation of luteinizing hormone pulse amplitude by the frequency of luteinizing hormone-releasing hormone stimulation and by testosterone in castrated, hypothalamic-lesioned male rats.

The frequency of spontaneous luteinizing hormone (LH) pulses is thought to be a direct result of the frequency of luteinizing hormone-releasing hormone (LHRH) pulses from the hypothalamus. By contrast, the amplitude of spontaneous LH pulses may be controlled by several factors other than the amplitude of LHRH pulses. We tested two hypotheses: 1) that LH pulse amplitude is determined in part by the frequency of LHRH pulses of constant magnitude, and 2) that testosterone (T) exerts a direct feedback effect on the pituitary gland to regulate LH pulse amplitude. Gonadal feedback was eliminated by castrating adult male rats (n = 20). Endogenous LHRH secretion was eliminated by lesioning the medial basal hypothalamus. Serum LH levels (0.19 +/- 0.04 ng/ml RP-2, mean +/- SEM) and T levels (0.15 +/- 0.02 ng/ml), measured several weeks after hypothalamic lesioning, confirmed the hypogonadotropic hypogonadal state of the animals. During a 8-h period, unanesthetized, unrestrained animals were injected with 40-ng pulses of LHRH via catheters into the jugular vein, and blood samples for LH measurement were drawn at 10-min intervals. The LHRH pulse interval was 20 min during the first 4 h in all animals. The pulse interval was doubled to 40 min in half of the animals (n = 10) during the next 4 hours; in the other 10 animals, the pulse interval was maintained constant at 20 min throughout the study. Within both of these groups, one-half of the animals (n = 5) were infused with T to achieve a physiological level of T in serum (2.46 +/- 0.36 ng/ml at 4 h), while the other half received vehicle.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

A new male hypogonadism mutant rat (hgn/hgn): concentrations of testosterone (T), luteinizing hormone (LH), and follicle-stimulating hormone (FSH) in the serum and the responsiveness of accessory sex organs to exogenous T, FSH, human chorionic gonadotropin, and luteinizing hormone-releasing hormone.

To determine the etiology of male hypogonadism in a newly found mutant rat (hgn/hgn, with a single autosomal recessive trait), concentrations of testosterone, luteinizing hormone (LH), and follicle-stimulating hormone (FSH) were measured, and the responsiveness of the urogenital organs, hypothalamus, and pituitary gland to testosterone (1 mg/kg s.c. for 7 days), FSH (0.3 AU/kg s.c. for 7 days), human chorionic gonadotropin (hCG) (40 IU/kg s.c. for 7 days), and luteinizing hormone-releasing hormone (LHRH) (0.5 or 5.0 micrograms/kg s.c. for 7 days) were tested. Treatment with testosterone only increased the weights of all of the accessory sex organs, whereas treatment with FSH, hCG, or LHRH did not. Levels of serum FSH and LH were extremely higher and testosterone was lower in hgn/hgn males than in normal males. Serum FSH and LH decreased to levels found in intact animals after treatment with testosterone, suggesting that hypothalamic responsiveness to exogenous testosterone is present in the hgn/hgn males. Thus, the status of the hgn/hgn males was indicated to be due to primary Leydig cell dysfunction.

Animals↗
PubMed1989

Thermal stress reduces serum luteinizing hormone and bioassayable hypothalamic content of luteinizing hormone-releasing hormone in hens.

Studies were conducted to evaluate the effects of acute (24 h) thermal stress on anterior pituitary function in hens. Circulating levels of luteinizing hormone (LH) were measured and the ability of the pituitary to respond to luteinizing hormone-releasing hormone (LHRH) challenge was determined. Moreover, bioassayable hypothalamic LHRH content was assessed by using dispersed anterior pituitary cells. In two separate experiments, circulating levels of LH were reduced in hens exposed to acute thermal stress (35 degrees C). Injection of LHRH did not result in significant differences in release of LH between normothermic and hyperthermic hens. However, the hypothalamic content of bioassayable hypothalamic releasing activity from hyperthermic hens were significantly reduced compared with normothermic hens. Taken together, these data suggest that the reproductive decline in the acutely heat-stressed hen is mediated by reduced LH releasing ability of the hypothalamus.

Animals↗
PubMed1976

Luteinizing hormone and follicle stimulating hormone and the response to luteinizing hormone releasing hormone in relation to sex and age.

Serum follicle stimulating hormone (FSH) and luteinizing hormone (LH) before and after intravenous injection of luteinizing hormone releasing hormone (LHRH) were studied in 71 male and female subjects of various ages. Mean basal FSH and LH levels were not significantly different in the male groups, except that FSH was significantly higher in the very old subjects. Postmenopausal female subjects had much higher concentrations of both hormones than had premenopausal women. LH was higher in female subjects shortly after the menopause than in very old female subjects. The serum concentrations of both FSH and LH 30 min. after intravenous injection of 200 mug LHRH were not different from the 60 min. values. There was no significant difference in the response of LH in the male groups. The peak FSH concentration was higher in the very old male subjects. Postmenopausal women had a much higher peak concentration of both FSH and LH than had younger subjects. The increment of LH, but not of FSH, was larger in female subjects shortly after the menopause than in very old female subjects. In both sexes there was a significant correlation between the basal FSH/LH ratio and age. In younger male subjects there was a close positive correlation between basal LH and serum testosterone, in older male subjects this correlation was negative and significant.

Adult↗
PubMed1984

The actions of prostaglandin E2, naloxone and testosterone on starvation-induced suppression of luteinizing hormone-releasing hormone and luteinizing-hormone secretion. In vitro and in vivo studies.

In man and other mammals, starvation is accompanied by a severe suppression of luteinizing hormone-releasing hormone (LHRH) and luteinizing-hormone (LH) secretion, which is caused by unknown alterations in hypothalamic functions. Prostaglandin E2 (PGE2), endorphins and testosterone (T) are know to be strongly involved in the regulation of LHRH release. The present study examined whether the influence of these substances on LHRH and LH secretion was affected by starvation. In vitro experiments checked the release of PGE2 and LHRH from median eminences (ME) of fed male rats and ones starved for 5 days. Stimulation with potassium (80 mM) induced an equally strong release of PGE2 and LHRH from the MEs of both fed and starved rats. When PGE2 (10(4) M) was added to the superfusion medium, the potassium-stimulated release of LHRH was significantly enhanced in both groups of animals. The results clearly showed that in the terminal region of the hypothalamic LHRH system the release of this hormone and the action of PGE2 were not altered by starvation. In vivo experiments tested whether the effects of LHRH, PGE2, naloxone (NAL), or T on LH secretion were different in intact or castrated male rats fed or starved for 3 and 5 days. LHRH (250 ng/kg) stimulated the same amount of LH secretion in fed and starved rats. The starvation-induced LH suppression was not due to a dysfunction at the pituitary level. The stimulatory action of PGE2 (1 mg/kg) on LH was gradually reduced throughout the starvation period. NAL (5 mg/kg) had little, respectively, no effect on LH release on the 3rd or 5th day of starvation.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1971

Dose-response relationship of luteinizing hormone to luteinizing hormone--releasing hormone in man.

In previous clinical studies with highly purified porcine luteinizing hormone-releasing hormone (LH-RH), administration of the somewhat arbitrarily chosen doses of 700-1500 mug resulted in increased serum levels of luteinizing hormone (LH) and follicle-stimulating hormone (FSH). The present study determined the minimum effective dose as well as the relationship of the response of serum LH and FSH to the dose of LH-RH administered. Three normal men received i.v. injections of 1.1-810 mug of LH-RH. A dose of 10 mug of LH-RH caused a statistically significant elevation in serum LH. 30 mug of LH-RH significantly increased serum FSH levels. A highly significant linear trend was observed in the log dose-response curve. The results indicate that both LH and FSH release occurs in man with doses of LH-RH much lower than previously used and that a linear log dose-response relationship can be obtained.

Adult↗
PubMed1984

A luteinizing hormone-releasing hormone agonist decreases biological activity and modifies chromatographic behavior of luteinizing hormone in man.

The effect of the luteinizing hormone-releasing hormone (LHRH) agonist, [D-Trp6,Pro9-NEth]LHRH (LHRHA), on luteinizing hormone (LH) bioactivity was assessed with a rat interstitial cell assay in four men during a 14-d treatment period. Biologic/immunologic (B/I) ratios were unchanged initially with treatment but by day 12 had fallen to levels lower than basal values. Frequent sampling on day 12 revealed blunted gonadotropin responsiveness to LHRHA and absence of spontaneous LH pulsations. Despite continued administration of LHRHA, human chorionic gonadotropin administration resulted in elevated B/I ratios and testosterone levels. Further characterization of the serum immunoreactive LH by Sephadex chromatography revealed a later elution profile during treatment with LHRHA. Thus, LHRHA appears to act, in part, by modification of the bioactivity of LH in man.

Adult↗
PubMed2005

Fertility in luteinizing hormone receptor-knockout mice after wild-type ovary transplantation demonstrates redundancy of extragonadal luteinizing hormone action.

The luteinizing hormone receptor (LHR), mainly expressed in gonads, is essential for normal reproduction. However, numerous recent studies have also demonstrated LHR expression in multiple extragonadal reproductive and nonreproductive tissues. Although some effects of luteinizing hormone (LH) or its agonist, human chorionic gonadotropin, have been shown in extragonadal sites, their physiological significance remains open. In the present study, we have addressed the function of the extragonadal LHR using LHR-KO mice (LuRKO mice), in which the ovaries of prepubertal mice were orthotopically replaced with pieces of WT ovary using similarly transplanted WT mice as controls. Most ovarian transplants attained normal endocrine function in both groups of mice, as demonstrated by normal age at vaginal opening, estrous cycles, and sexual behavior. Both the LuRKO and WT mice repeatedly became pregnant (9/16 vs. 16/20 after first mating; difference not significant) and delivered similarly sized litters, which grew normally after birth, indicating normal lactation. In conclusion, fertility is restored in LuRKO mice by transplantation of WT ovarian tissue. This is achieved in the absence of extragonadal LHR expression, which indicates physiological redundancy for such receptor sites.

Animals↗