LH Secretion Research Articles

Expression of Kisspeptin, Neurokinin B, and Dynorphin During Pubertal Development in Female Sheep

Puberty onset depends upon an increase in pulsatile GnRH/LH secretion, which in sheep is the result of reduced sensitivity to estrogen negative feedback. Neurons within the arcuate nucleus of the hypothalamus (ARC) expressing kisspeptin, neurokinin B (NKB), and dynorphin (i.e. KNDy neurons) express estrogen receptors and are believed to play a key role in mediating the effects of estrogen on GnRH/LH secretion. Therefore, the purpose of this study was to assess changes in kisspeptin, NKB, and dynorphin within the ARC across pubertal development in female sheep. Blood samples were collected at 12-minute intervals for 4 hours and assessed for LH secretion in five age groups of ewes: 5 months (n=6), 6 months (n=6), 7 months (n=5), 8 months (n=5), and 10 months (n=6) of age. Following each bleed, ewes were sacrificed, hypothalamic tissue containing the ARC was collected, and then processed for use in dual immunofluorescence and RNAscope. Mean LH and LH pulse frequencies followed the expected patterns: concentrations and frequencies were low during the prepubertal ages (5-7 months of age), intermediate during the peripubertal age (8 months of age), and elevated in the postpubertal age group (10 months of age). Using immunofluorescence, kisspeptin and NKB immuno-positive cell numbers did not change significantly (P > 0.50) over time with cell numbers averaging 235.3±16.8 and 231.3±16.8, respectively. Colocalization of kisspeptin and NKB was greater than 90% for all age groups. Using RNAscope, the total number of cells expressing mRNA for kisspeptin and dynorphin did not change significantly (P > 0.05) over time with cell numbers averaging 46.7±12.0 and 28.3±10.0 cells/hemisection, respectively. Taken together, our data suggest that the increase in LH secretion that drives puberty onset is not limited by changes in kisspeptin, NKB, or dynorphin expression, but may instead depend on other factors such as changes in receptor expression or changes in KNDy neuron activity via a reduction in inhibitory and/or an increase in stimulatory afferent inputs.

Luteal phase deficiency: pathophysiology and role in reproductive disorders

It is well known that corpus luteum normal functioning is crucial for the luteal phase, which determines the embryo implantation and the progression of pregnancy. Luteal phase deficiency (LPD), associated with impaired progesterone secretion by the corpus luteum, is considered as a significant factor of infertility and early pregnancy loss, both in the natural cycle and in assisted reproductive technology (ART) programs. The LPD formation is associated with hypothalamic-pituitary-ovarian axis dysregulation, which leads to abnormal secretion of FSH, LH, ovulation and luteinization disorders, premature luteolysis. The most significant problem in the study of LPD is the lack of reliable and reproducible methods of its verification. This review summarizes the available data on the methods and issues of LPD diagnosing, including the duration of the luteal phase, the level of progesterone secretion, and endometrial biopsy. LPD is an important factor in reproductive failures during IVF, which is caused by suppression of the physiological FSH, LH secretion and requires mandatory progesterone support in the luteal phase of the cycle. It’s hard to define the contribution of LPD to miscarriage, however, empirical progestogen therapy may increase the live births rate in women with recurrent pregnancy loss. Currently, there is no evidence of the LPD role and progesterone support effectiveness in infertility management, so the diagnosis and therapy of LPD among these patients should not be considered.

RESPUESTA REPRODUCTIVA EN OVEJAS DE PELO SINCRONIZADAS CON ACETATO DE MEDROXIPROGESTERONA IMPREGNADO EN ESPONJAS INTRAVAGINALES NO COMERCIALES

<p><strong>Background.</strong> Intravaginal sponges impregnated with medroxyprogesterone acetate or fluorogestone acetate are routinely used in oestrus synchronization protocols in sheep, non-commercial sponges are a viable option in the reproductive control of female sheep.<strong> Objective.</strong> To evaluate the reproductive response in hair sheep synchronized with medroxyprogesterone acetate impregnated in non-commercial intravaginal sponges. <strong>Methodology.</strong> 31 adult hair sheep 5/8 Pelibuey x 2/8 Black Belly x 1/8 Dorper, average weight of 40 ± 3.2 kg and a body condition of 3-3.5 were used. They were randomly assigned to one of four treatments: T1 (n = 8 ewes), 5 mg of medroxyprogesterone acetate impregnated in non-commercial intravaginal sponges + 1 mg of estradiol cypionate + 200 IU of eCG; T2 (n = 8 ewes), synchronization similar to T1, but 500 IU of eCG were applied; T3 (n = 8 ewes), 20 mg of fluorogestone acetate impregnated in intravaginal sponges + 200 IU of eCG; T4 (n = 7 ewes), synchronization similar to T3, but 500 IU of eCG were applied. In all treatments the sponges were placed for 10 days. Blood samples were collected by jugular puncture and the concentrations of progesterone and LH were determined. <strong>Results.</strong> The sponge removal interval to estrus was different (P <0.05) between T1 and T3 (14.5 ± 5.5 and 38.8 ± 2.5 h, respectively). Estrus duration was similar (P> 0.05) between T1, T2 and T3 (54.5 ± 5.5, 46.5 ± 5.8 and 38.3 ± 2.6 h, respectively), T4 (59.3 ± 4.1 h) was similar (P> 0.05) to T1 and T2 (54.5 ± 5.5 h and 46.5 ± 5.8 h, respectively) but different (P <0.05) from T3 (38.3 ± 2.6 h). The progesterone concentration was higher than 1 ng ml<sup>-1</sup>, on days 0 to 4 (T2), 0 to 5 (T4) and 0 to 7 (T1 and T3), then it decreased to <1 ng ml<sup>-1</sup> in all the treatments. The sponge removal and oestrus onset intervals at the LH preovulatory peak were similar (P> 0.05) between treatments, however, the LH profile at T1 and T2 shows scattered elevations. 5 mg of medroxyprogesterone acetate + 1 mg of estradiol cypionate, impregnated in non-commercial sponges advance oestrus and do not adjust for the occurrence of LH preovulatory peak.<strong> Implications. </strong>The study demonstrates that it is feasible to use reduced doses of medroxyprogesterone acetate impregnated in non-commercial intravaginal sponges in estrous synchronization protocols in hair sheep, the progesterone profile confirms the inhibitory effect of the drug on GnRH / LH secretion.<strong> Conclusion. </strong>The application of 200 or 500 IU of eCG does not modify the occurrence or duration of estrus and the LH preovulatory peak. It is suggested that it is feasible to synchronize hair sheep under tropical conditions with reduced doses of medroxyprogesterone acetate impregnated in non-commercial sponges, however, dispersion of ovulation may occur, which would reduce fertility. The use of eCG and estradiol cypionate does not affect the effectiveness of synchronization.<strong></strong></p>

A Mathematical Model For Maximum Likelihood Estimation To Atrazine Inhibits Pulsatile Gonadotropin-Releasing Hormone In Animals

In this study, we present a Extreme possibility estimation to analyze examine the strong ATR doses can work hypothalamic GnRH inhabiting life unlocks patterns in a style that is exactly the same as seen in the LH secretion. In presentation, inflammatory hormone levels are likely to work in response to GnRH. Finally, we decide that a computational model is based on the submission portion and we result with the medical refort . This paper will be very useful in the future for medical field.

Efficiency of GnRH-Loaded Chitosan Nanoparticles for Inducing LH Secretion and Fertile Ovulations in Protocols for Artificial Insemination in Rabbit Does.

Simple SummaryNano-drug delivery systems can be employed for improving ovulation induction prior to artificial insemination (AI) in rabbits. In this study, different routes of administration and different doses of GnRH–loaded chitosan nanoparticles (GnRH–ChNPs) were assessed for inducing ovulation in rabbits, proving their usefulness to reduce the GnRH dose and animal handling and improving AI outcomes. The use of GnRH–ChNPs allows for the reduction of the conventional intramuscular GnRH dose to half without compromising fertility. However, the addition of GnRH–ChNPs to semen extenders, although successfully inducing ovulation, has negative impacts on fertility. Thus, more studies are needed to allow further adjustments.Gonadotropin-releasing hormone (GnRH)–loaded chitosan nanoparticles (GnRH–ChNPs) were used at different doses and routes of administration to induce ovulation in rabbits as an attempt to improve artificial insemination (AI) procedures and outcomes. In this study, the characteristics (size, polydispersity, loading efficiency, and zeta-potential) of GnRH–ChNPs and the GnRH release pattern were determined in an in vitro study. A first in vivo study assessed the pituitary and ovarian response to different GnRH–ChNPs doses and routes of administration (two i.m. doses, Group HM = 0.4 µg and Group QM = 0.2 µg, and two intravaginal doses, Group HV = 4 µg and Group QV = 2 µg) against a control group (C) receiving bare GnRH (0.8 µg). The HM, QM, and HV treatments induced an earlier LH-surge (90 min) than that observed in group C (120 min), whilst the QV treatment failed to induce such LH surge. The number of ovulation points was similar among treatments, except for the QV treatment (no ovulation points). A second in vivo study was consequently developed to determine the hormonal (progesterone, P4, and estradiol, E2) profile and pregnancy outcomes of both HM and HV treatments against group C. The treatment HM, but not the treatment HV, showed adequate P4 and E2 concentrations, conception and parturition rates, litter size, litter weight, and viability rate at birth. Overall, the use of GnRH–ChNPs allows for a reduction in the conventional intramuscular GnRH dose to half without compromising fertility. However, the addition of GnRH–ChNPs to semen extenders, although successfully inducing ovulation, has negative impacts on fertility. Thus, more studies are needed to explore this point and allow further adjustments.

Influence of Insulin on LH, Testosterone and SHBG in various PCOS Categories based on the Mode of Secretion of LH in relation to FSH Levels.

Polycystic ovary syndrome (PCOS) or disease (PCOD) is one of the most common causes of female infertility. The objective of this study was to find out the influence of insulin on LH, testosterone and SHBG in diffrent PCOS categories. A total of 800 women who were subjected to infertility treatment at infertility clinics were selected. About 60 healthy females with regular menstrual cycles were considered as control. The data were collected from hospital records using subject's consent. Relationship of insulin to LH and testosterone was positive and significant (p<0.05) in the entire PCOS group and in five PCOS subcategories with increased LH rise (i.e. 1.3, 2, 3, 4 & 5 times of LH rise in relation to FSH levels in each group respectively). The correlation pattern showed an increasing trend from lower to increased rise of LH compared to FSH. The relationship between insulin and SHBG was negative and significant (p<0.05) in all PCOS subcategories, except for the group having similar LH and FSH levels and also in another group with FSH levels higher than LH levels. A strong positive correlation was established between insulin and SHBG in normal subjects. The percentage of negative correlation was strong in PCOD subcategories with elevated rises of LH. This study established the influence of insulin on other marker hormones (LH, testosterone an SHBG) in various PCOS categories in view of their percentage of relationship.

Influence of Insulin on LH, Testosterone and SHBG in Various PCOS Categories Based on the Mode of Secretion of LH in Relation to FSH Levels

Influence of Insulin on LH, Testosterone and SHBG in Various PCOS Categories Based on the Mode of Secretion of LH in Relation to FSH Levels

Multiple matings modify the estrous length, the moment of ovulation, and the estradiol and LH patterns in ewes.

In several species, mating reduces the estrous length and advances ovulation. The aim of this study was to determine if multiple matings reduces the estrous length and modifies the moment of ovulation, as well as the estradiol and LH patterns in ewes. The estrous cycle of Corriedale ewes was synchronized, and the onset of receptivity was monitored every 3 h with rams, avoiding mating. At the estrous onset, ewes were assigned to two experimental groups (n=10 each): 1) estrous was monitored every 3 h with a ram avoiding mating (group CON), and 2) a ram was allowed to mate and ejaculate once every 3 h (group MAT). The ovaries were scanned with transrectal ultrasonography and blood samples were collected for measuring 17β-estradiol and LH concentrations every 3 h until ovulation. Estrus was shorter in MAT than CON ewes (24.7 ± 1.5 h vs. 30.4 ± 1.5 h, respectively; P=0.02); the proportion of animals that ovulated before the end of estrus was greater in CON ewes: (9/10 vs. 3/10, P=0.009). The area under the LH curve (AUC) was greater in MAT than CON ewes (36.1 ± 3.5 ng.h-1.mL-1 vs 24.9 ± 3.5 ng.h-1.mL-1 P=0.03). However, MAT ewes had a lower 17β-estradiol AUC than CON ewes (41.0 ± 4.9 pg.h-1.mL-1 vs 59.4 ± 4.9 pg.h-1.mL-1 P=0.01). Mating reduced the estrous length, induced a greater secretion of LH but less total 17β-estradiol secreted and, additionally, ovulation occurred more frequently after the end of estrus in mated ewes.

Di-n-butyl phthalate diminishes testicular steroidogenesis by blocking the hypothalamic-pituitary-testicular axis: relationship with germ cell apoptosis in Japanese quail.

Although di-n-butyl phthalate (DBP) induces germ cell apoptosis, the underlying mechanism is not yet clear in quail. In this study, prepubertal quails were given a single dose of 500mg kg-1 DBP by gavage and were then killed 3, 6 and 24h after treatment. There was a significant reduction in intratesticular testosterone (ITT) concentrations and testicular steroidogenic enzyme mRNA expression and a significant increase in germ cell apoptosis in DBP-treated compared with control quails at all time points. Maximum apoptosis was detected 6h after treatment and the maximum reduction in testosterone concentrations was at 3h. To investigate whether DBP suppressed testicular steroidogenesis by affecting the hypothalamic-pituitary-testicular axis, we analysed pituitary LH subunit β (Lhb) mRNA expression and serum LH concentrations. At all time points, pituitary Lhb expression and serum LH concentrations were significantly decreased following DBP treatment. The present observations suggest the possibility that DBP blocked LH secretion from the hypothalamus and/or pituitary, thereby decreasing LH stimulation of Leydig cells and reducing ITT concentrations. DBP-induced decreases in ITT concentrations may cause changes to the physical structure of Sertoli cells, which, in turn, may induce germ cell apoptosis.

GH-induced LH hyporesponsiveness as a potential mechanism for hypogonadism in male patients with acromegaly.

Male patients with acromegaly frequently have hypogonadism. However, whether excess GH affects gonadal function remains unclear. We retrospectively compared clinical features affecting total testosterone (TT) and free testosterone (FT) levels between 112 male patients with acromegaly and 100 male patients with non-functioning pituitary adenoma (NFPA) without hyperprolactinemia. Median maximum tumor diameter (14.4 vs. 26.5 mm) and suprasellar extension rate (33 vs. 100%) were lower in acromegaly, but LH, FSH, TT, and FT were not significantly different. In acromegaly, TT was less than 300 ng/dL in 57%, and FT was below the age-specific reference range in 77%. TT and FT were negatively correlated with GH, IGF-1, and the tumor size, and positively correlated with LH. In NFPA, they were positively correlated with IGF-1, LH, FSH, ACTH, cortisol, and free T4, reflecting hypopituitarism. Multiple regression analysis showed that TT and FT had the strongest correlation with GH in acromegaly, and with LH in NFPA. Surgical remission was achieved in 87.5% of 56 follow-up patients with acromegaly. TT and FT increased in 80.4 and 87.5%, respectively, with a significant increase in LH. In acromegaly, the degree of postoperative increase in TT(FT) correlated with the fold increase of TT(FT)/LH ratio, a potential parameter of LH responsiveness, but not with fold increase of LH, whereas in NFPA it correlated with both. These results suggest that excessive GH is the most relevant factor for hypogonadism in male acromegaly, and may cause impaired LH responsiveness as well as the suppression of LH secretion.

Idiopathic central precocious puberty in a Klinefelter patient: highlights on gonadotropin levels and pathophysiology

BackgroundIdiopathic central precocious puberty (ICPP) is supposed to be non-existent in a context of testicular destruction that is typically present in Klinefelter syndrome (KS). Herein, we describe a rare case of ICPP in a Klinefelter patient (47,XXY) with 2 maternal X chromosomes. Moreover, we highlight the differences in gonadotropin levels in comparison to males with ICPP and a normal karyotype.Case presentationAn 8 years old boy with a history of cryptorchidism was evaluated for precocious puberty (Tanner staging: P2/G3). Both testes measured 25x35mm. His hormonal profile confirmed a central origin of precocious puberty with high serum testosterone (4.3 ng/ml), luteinizing hormone [LH (3.5 UI/l)] and follicle stimulating hormone [FSH (7.7 UI/l)] levels. Luteinizing hormone-releasing hormone (LHRH) test amplified LH and FSH secretion to 24 and 14 UI/l respectively. Brain magnetic resonance imaging (MRI) was normal. No MKRN3 mutation was detected. He was treated for ICPP for two years. During puberty, he suffered from hypergonadotropic hypogonadism leading to the diagnosis of KS (47,XXY karyotype). Chromosomal analysis by fluorescent multiplex polymerase chain reaction (PCR) using X chromosome microsatellite markers identified 2 maternal X chromosomes.Analysing 8 cases of KS developing ICPP (our reported case and 7 other published cases) revealed that these KS patients with ICPP have higher LH and FSH levels during ICPP episode than in ICPP patients with a normal karyotype (ICPP with KS vs ICPP with a normal karyotype: LH levels 9.4 ± 12 vs 1.1 ± 0.6 UI/l; FSH levels 23.1 ± 38.5 vs 2.7 ± 1.5 UI/l). Furthermore, their response to gonadotropin-releasing hormone (GnRH) stimulation is characterized by excessive LH and FSH secretion (LH levels post-GnRH: 58 ± 48 vs 15.5 ± 0.8 UI/l; FSH levels post-GnRH: 49.1 ± 62.1 vs 5.7 ± 3.9 UI/l).ConclusionsICPP in boys is extremely rare. The pathophysiology of ICPP in KS is unknown. However, maternal X supplementary chromosome and early testicular destruction may play a significant role in the initiation of ICPP, in part explaining the relative “overrepresentation of ICPP in KS. Thus, karyotype analysis could be considered for boys suffering from ICPP, especially if testicular size is smaller or gonadotropins are significantly elevated.

Phoenixin: More than Reproductive Peptide.

Phoenixin (PNX) neuropeptide is a cleaved product of the Smim20 protein. Its most common isoforms are the 14- and 20-amino acid peptides. The biological functions of PNX are mediated via the activation of the GPR173 receptor. PNX plays an important role in the central nervous system (CNS) and in the female reproductive system where it potentiates LH secretion and controls the estrus cycle. Moreover, it stimulates oocyte maturation and increases the number of ovulated oocytes. Nevertheless, PNX not only regulates the reproduction system but also exerts anxiolytic, anti-inflammatory, and cell-protective effects. Furthermore, it is involved in behavior, food intake, sensory perception, memory, and energy metabolism. Outside the CNS, PNX exerts its effects on the heart, ovaries, adipose tissue, and pancreatic islets. This review presents all the currently available studies demonstrating the pleiotropic effects of PNX.

Developmental programming: gestational testosterone excess disrupts LH secretion in the female sheep fetus

BackgroundPrenatal testosterone (T) excess results in reproductive and metabolic perturbations in female sheep that closely recapitulate those seen in women with polycystic ovary syndrome (PCOS). At the neuroendocrine level, prenatal T-treated sheep manifest increased pituitary sensitivity to GnRH and subsequent LH hypersecretion. In this study, we investigated the early effects of gestational T-treatment on LH secretion and pituitary function in the female sheep fetus. Additionally, because prenatal T effects can be mediated via the androgen receptor or due to changes in insulin homeostasis, prenatal co-treatment with an androgen antagonist (flutamide) or an insulin sensitizer (rosiglitazone) were tested.MethodsPregnant sheep were treated from gestational day (GD) 30 to 90 with either: 1) vehicle (control); 2) T-propionate (~ 1.2 mg/kg); 3) T-propionate and flutamide (15 mg/kg/day); and 4) T-propionate and rosiglitazone (8 mg/day). At GD 90, LH concentrations were determined in the uterine artery (maternal) and umbilical artery (fetal), and female fetuses were euthanized. Pituitary glands were collected, weighed, and protein level of several key regulators of LH secretion was determined.ResultsFetal pituitary weight was significantly reduced by prenatal T-treatment. Flutamide completely prevented the reduction in pituitary weight, while rosiglitazone only partially prevented this reduction. Prenatal T markedly reduced fetal LH concentrations and flutamide co-treatment partially restored LH to control levels. Prenatal T resulted in a marked reduction in LH-β protein level, which was associated with a reduction in GnRH receptor and estrogen receptor-α levels and an increase in androgen receptor. With the exception of androgen receptor, flutamide co-treatment completely prevented these alterations in the fetal pituitary, while rosiglitazone largely failed to prevent these changes. Prenatal T-treatment did not alter the protein levels of insulin receptor-β and activation (phosphorylation) of the insulin signaling pathways.ConclusionsThese findings demonstrate that prenatal T-treatment results in reduced fetal LH secretion, reduced fetal pituitary weight, and altered protein levels of several regulators of gonadotropin secretion. The observations that flutamide co-treatment prevented these changes suggest that programming during fetal development likely occurs via direct androgen actions.

Molecular and hormonal changes caused by long-term use of high dose pregabalin on testicular tissue: the role of p38 MAPK, oxidative stress and apoptosis.

In 1990, pregabalin was introduced as a novel antiepileptic drug that acts by binding selectively to the alpha-2-delta subunits of voltage-gated calcium channels resulting in increasing neuronal GABA levels and inhibiting the release of exciting neurotransmitters. The aim of our study is to assess the hazardous effects of prolonged high-dose pregabalin (like that abused by addicts) on testes and to clarify the potential causative mechanisms. The current study was conducted on 70 adult male Wistar albino rats which were divided into 7 groups. In our study we evaluated the effect of pregabalin, at concentrations 150 and 300mg/kg/day for 90 days, on hormones; FSH, LH, testosterone and prolactin secretion. Our study also evaluated the expression of apoptosis-related genes BAX and BCL2 in testicular tissue in addition to the western blotted analysis of p38 Mitogen activated protein kinases (p38 MAPK). The levels of reduced glutathione, malondialdehyde and superoxide dismutase were also measured. Pregabalin decreased testosterone level while FSH, LH and prolactin showed a significant increase. It also produced genotoxicity through reversal of the BAX/BCL2 ratio; increased p38 MAPK level and induction of oxidative stress markers. The concomitant administration of vitamin E significantly reduced all the previously mentioned biochemical and hormonal adverse effects caused by pregabalin. Pregabalin can adversely affect male fertility particularly in addicts and patients who are being treated with it for long periods as those suffering from neuropathies and seizures. Antioxidants like vitamin E could have a role in amelioration.

Role of neuropeptides and amino acids in controlling secretion of hormones from the anterior pituitary gland in pigs

All reproductive processes involve one or more of the protein hormones secreted from the anterior pituitary gland: LH, FSH, prolactin, growth hormone, ACTH and thyroidstimulating hormone (TSH). Primary hormones of reproduction, such as LH and FSH, directly regulate a reproductive activity. For example, LH and FSH stimulate follicular growth and the associated secretion of oestradiol in sows. In contrast, secondary hormones of reproduction such as TSH are permissive and regulate other physiological systems that indirectly, but profoundly, influence reproduction. Reproduction in pigs can be enhanced by developing strategies to alter and control secretion of hormones from the anterior pituitary gland. However, the successful manipulation of adenohypophysial hormone secretion will require a sound understanding of the mechanisms controlling the function of the hypothalamic—pituitary axis. Hypothalamic hormones including GrtRH, dopamine, growth hormone-releasing hormone (GHRH), somatostatin, corticotrophin-releasing hormone (CRI4) and thyrotrophin-releasing hormone (TRI-I) are synthesized in perikarya that possess axons that terminate at the median eminence. These hormones are released into the hypothalamo—hypophysial portal vasculature, travel to the anterior pituitary gland and stimulate or inhibit secretion of adenohypophysial hormones. Secretion of hypothalamic hormones is ultimately controlled by a variety of neurotransmitters and neuropeptides, the most studied in swine being the endogenous opioid peptides (EOP) and more recently, the excitatory amino acids (ExAA). In general, EOP inhibit GrtRH and hence LH secretion, and this effect involves the central catecholaminergic system. A definitive role for EOP in the modulation of FSH release remains to be determined. EOP stimulate secretion of GHRH and thus growth hormone release, and depending on the animal model studied, EOP exert either stimulatory or inhibitory influences on prolactin secretion. ExAA, working via N-methyl-o-aspartate (NINIDA) receptors at the central nervous system, stimulate secretion of LH, FSH, growth hormone and prolactin in appropriate animal models. However, in certain situations, an inhibitory effect of ExAA on LH secretion has been demonstrated. The modulation of growth hormone and prolactin secretion by ExAA involves LOP. Research investigating the function of ExAA and EOP in the physiological control of swine reproduction warrants further scrutiny.

Control of follicular development during and after lactation in sows

Summary. Follicular development during early lactation in the sow is characterized by a large population of small-sized follicles and a small population of medium-sized follicles. As lactation progresses there is a gradual shift in number of follicles into medium- or large-sized categories and the percentage of follicles classified as atretic declines. Weaning at birth often leads to aberrant follicular development, apparently because the positive feedback response of LH to oestradiol does not occur during the first week post partum. Secretion of LH during lactation is primarily controlled by suckling intensity of the litter while FSH is controlled by a nonsteroidal ovarian factor, presumably inhibin. Suckling apparently limits secretion of GnRH and weaning leads to an increase of GnRH within the hypothalamus coincident with an increase of LH in the anterior pituitary and plasma and increased follicular growth. Follicular development during both lactation and post-weaning anoestrus can be stimulated by exogenous gonadotrophins and pulsatile administration of GnRH. Factors such as nutrition, season, boar exposure, litter size and split weaning affect follicular development during lactation and after weaning, probably because they affect secretion of LH.

Nutritional regulators of the hypothalamic–pituitary axis in pigs

Nutritional signals are detected by the central nervous system (CNS) and translated by the neuroendocrine system into signals that alter secretion of LH and growth hormone (GH). Furthermore, these signals directly affect the activity of the pituitary gland independently of CNS input. Insulin-like growth factor I (IGF-I), insulin, leptin and specific metabolites, such as glucose and free fatty acids (FFA)', are potential signals of the metabolic status to the brain-pituitary axis. Intravenous injection of a lipid emulsion or glucose suppressed the GH and LH response to GH releasing hormone (GHRH) and GnRH, respectively. Insulin and IGF-I regulation of LH and GH secretion occur at the pituitary gland. Feed deprivation for 24 h suppressed leptin secretion without affecting LH or GH secretion, whereas central administration of leptin resulted in a decrease in feed intake and an increase in GH secretion. Oestrogen-induced leptin gene expression in adipose tissue increased with age and adiposity in pigs. Leptin stimulated GnRH release from hypothalamic tissue in vitro. These results identify putative signals that link metabolic status and neuroendocrine control of growth and reproduction by altering endocrine function during periods of fasting, feed restriction and lactation.

Nutritional and lactational effects on follicular development in the pig

In sows, follicular development is inhibited during lactation, and weaning the piglets allows recruitment and selection of follicles that will undergo preovulatory maturation and ovulate. Lactation inhibits GnRH secretion, and in turn LH secretion, through neuroendocrine stimuli induced by suckling. Pituitary response to GnRH and the sensitivity of the hypothalamo-pituitary unit to oestradiol positive feedback are also reduced. The impact of lactation on the reproductive axis is further complicated by the physiological and metabolic adaptations that are developed for milk production and that depend on nutrient intake, nutrient needs and body reserves. A strongly catabolic state during lactation amplifies the inhibition of LH secretion, thereby inducing a delay of oestrus and ovulation after weaning. Nevertheless, post-weaning ovulation is less delayed nowadays than in the 1970's or 80's. Nutritional deficiency has also deleterious effects on embryo survival, which are likely related to alterations in follicular growth and maturation. The physiological mechanisms by which information on the metabolic changes is transmitted to the hypothalamuspituitary- ovary axis are not fully understood in the sow. Glucose, insulin and leptin are the most likely signals informing the hypothalamus of the metabolic state, yet their roles have not been definitely established. At the ovarian level, folliculogenesis is likely to be altered by the reduction in insulin and IGF-I concentrations induced by nutritional deficiency. More knowledge is needed at the intrafollicular level to better understand nutritional effects on follicular development, and also on occyte quality and embryo development.

Endocrineand follicular studies in Meishan pig

The enhanced early embryonic survival in Chinese Meishan compared with Large- White gilts may be due, in part, to differences in ovarian and endocrine function, particularly during the periovulatory period. The overall patterns of oestradiol, LH and FSH secretion were not different between Meishan and Large-White hybrid controls during this period, although circulating inhibin concentrations were higher in Meishan gilts. Thus, there appeared to be a decreased sensitivity to inhibin feedback on FSH secretion in Meishan gilts. Behavioural oestrus was exhibited earlier relative to the LH surge in Meishan gilts than in Large-White hybrid gilts, but the time interval from the oestradiol peak until the LH surge was similar in both breeds. This finding suggests that Meishan gilts are more sensitive in terms of initiating a behavioural response, but not in terms of positive feedback. Although preovulatory follicular characteristics were as variable in Meishan as in Large-White hybrid gilts, follicles from Meishan gilts were smaller, but contained a higher concentration of oestradiol in the follicular fluid. This was probably due to increased aromatase activity in both granulosa and theca cells of Meishan follicles. The enhanced maturation of the intrafollicular environment in Meishan gilts was reflected in the oocyte population which was at a more advanced stage of development in the period preceding ovulation. In addition to decreasing the time between onset of oestrus and ovulation, advancing the LH surge to coincide with onset of oestrus (via hCG administration) decreased embryo survival at day 30 of gestation. It is concluded that both endocrine and follicular mechanisms have a role in ensuring the prolificacy in the Meishan breed.

Maturation of ovarian follicles in the prepubertalgilt

Summary. The processes of follicle development and puberty are closely related, and both are associated with maturation of the hypothalamic—pituitary—ovarian axis. Prenatal development of the ovary is independent of gonadotrophic stimulation. Beyond 60 days of age (postnatally), tertiary follicles develop and gonadotrophins begin to influence ovarian follicular development. Negative feedback regulation of pituitary gonadotrophins by ovarian secretions develops between 60 and 100 days of age. In the prepubertal gilt, no consistent changes in peripheral FSH, oestrogen or progesterone concentrations have been identified which are associated with recruitment of the first set or preovulatory follicles. Whether LH secretion increases before this recruitment remains equivocal. Few details are available on how gonadotrophic hormones stimulate ovarian function in the prepubertal gilt. On the basis of a follicular maturation model that has been described for the rat, the actions of FSH, LH and oestrogens on follicular cell receptors and the regulation of aromatase activity seem paramount. Aromatization of androgens to oestrogens has been proposed as a central regulator for follicular maturation.