Central injection of ketone body suppresses luteinizing hormone release via the catecholaminergic pathway in female rats

Ketosis is found in various pathophysiological conditions, including diabetes and starvation, that are accompanied by suppression of gonadal activity. The aim of the present study was to determine the role of ketone body in the brain in regulating pulsatile luteinizing hormone (LH) secretion in female rats. Injection of 3-hydroxybutyrate (3HB), a ketone body, into the fourth cerebroventricle (4V) induced suppression of pulsatile LH secretion in a dose-dependent manner in ovariectomized (OVX) rats with an estradiol (E2) implant producing diestrus plasma E2 levels. Plasma glucose and corticosterone levels increased immediately after the 4V 3HB injection, suggesting that the treatment caused a hunger response. The 3HB-induced suppression of LH pulses might be mediated by noradrenergic inputs to the hypothalamic paraventricular nucleus (PVN) because a local injection of α-methyl- p-tyrosine, a catecholamine synthesis inhibitor, into the PVN blocked 3HB-induced suppression of LH pulses and PVN noradrenaline release was increased by 4V 3HB injection in E2-primed OVX rats. These results suggest that ketone body sensed by a central energy sensor in the hindbrain may suppress gonadotropin release via noradrenergic inputs to the PVN under ketosis.     

Paraventricular alpha1- and alpha2-adrenergic receptors mediate hindbrain lipoprivation-induced suppression of luteinizing hormone pulses in female rats

Acute central lipoprivation suppresses pulsatile luteinizing hormone (LH) release and increases blood glucose levels through noradrenergic input to the hypothalamic paraventricular nucleus (PVN) in female rats. The present study was conducted to identify adrenergic receptor subtypes involved in central lipoprivation-induced suppression of pulsatile LH secretion and increases in plasma glucose levels in female rats. Acute hindbrain lipoprivation was produced by injection into the fourth cerebroventricle (4V) of 2-mercaptoacetate (MA), an inhibitor of fatty acid oxidation, in estradiol-implanted ovariectomized rats. Two min before MA injection, alpha1-, alpha2- or beta-adrenergic receptor antagonist was injected into the PVN. Injection of MA into the 4V suppresses pulsatile LH release in PVN vehicle-treated rats, whereas pretreatment of animals with injection of alpha1- or alpha2-adrenergic antagonist into the PVN blocked the effect of the 4V MA injection on LH pulses. beta-Adrenergic antagonist did not affect MA-induced suppression of LH pulses. The counter-regulatory increase in plasma glucose levels after 4V MA injection was also partially blocked by pretreatment with alpha1- and alpha2-adrenergic receptor antagonists. These results suggest that alpha1- and alpha2-adrenergic receptors in the PVN mediate hindbrain lipoprivation-induced suppression of LH release and counter-regulatory increases in plasma glucose levels in female rats.     

A rat model for the energetic regulation of gonadotropin secretion: role of the glucose-sensing mechanism in the brain

Energy availability has been considered to regulate gonadal activity by modulating the release of gonadotropin-releasing hormone (GnRH)/luteinizing hormone (LH) at various reproductive phases, such as lactation and puberty in domestic as well as wild animals. Experimental models with rats and sheep have demonstrated that fasting or glucoprivation suppresses pulsatile LH release. From those experiments, the information on energy deficiency is considered to be detected by specific central sensors and conveyed to the hypothalamus to regulate LH release as well as food intake. Noradrenergic neurons, originating in the medulla oblongata and projecting to the hypothalamic paraventricular nucleus (PVN), is reported to be one of the pathways mediating the response of LH release to energy deficiency. The other component is considered to be an energy-sensing mechanism in the brain. Glucose or other oxidizable fuels may function as a metabolic signal to regulate LH release. Previous studies suggest the presence of a glucose-sensing mechanism in the rat hindbrain. From our previous results in the rat, the ependymocytes lining the wall of the cerebroventricle could possibly serve as a glucose sensor to regulate GnRH/LH release. Greater understanding of the nature of the energy-sensing mechanism in the brain will contribute to the nutritional manipulation of reproductive performance in domestic animals in various conditions.     

Role of noradrenergic receptors in the bed nucleus of the stria terminalis in regulating pulsatile luteinizing hormone secretion in female rats

The bed nucleus of the stria terminalis (BNST) is one of the brain areas densely innervated by noradrenergic neurons originating in the brain stem. The present study aims to determine the role of noradrenergic receptors in the BNST in regulating pulsatile luteinizing hormone (LH) secretion in female rats. Ovariectomized (OVX) or estrogen-primed OVX (OVX+E2) rats received three 1-h-interval injections of 0.05 micromol of noradrenaline (NA), phenylephrine (alpha1-adrenergic receptor agonist), clonidine (alpha2-agonist), or isoproterenol (beta-agonist) into the BNST. Injection of NA or alpha1-adrenergic agonist into the BNST strongly suppressed pulsatile LH secretion in OVX+E2 rats with a significant (P < 0.05) decrease in the mean LH level for 3 h and LH pulse frequency, but alpha2-and beta-agonists did not affect any of the LH pulse parameters. In OVX animals, alpha1- and alpha2-adrenergic agonists caused a significant change in LH pulse frequency and amplitude, respectively, though the effect was not as apparent as the NA- or alpha1-agonist-induced changes in OVX+E2 animals. These results indicate that NA inputs to the BNST suppress pulsatile LH secretion via alpha1-adrenergic receptors and that estrogen enhances this suppression.     

Effects of dietary energy on control of luteinizing hormone secretion in cattle and sheep.

Prolonged restriction of dietary energy delays onset of puberty, disrupts cyclicity in sexually mature animals, and lengthens the postpartum anestrous period in domestic ruminants. One important mechanism by which energy restriction impairs reproductive activity seems to be suppression of the increase in LH pulse frequency that is necessary for growth of ovarian follicles to the preovulatory stage. Under-nutrition apparently inhibits pulsatile secretion of LH by reducing LHRH secretion by the hypothalamus. The ability of an animal to sustain a high-frequency mode of pulsatile LH release is related to its metabolic status. Mechanisms linking metabolic status to LHRH secretion have not been fully characterized. Changes in body fat have been associated with changes in reproductive activity, but it is unlikely that body fat per se regulates LHRH secretion. It is possible that pulsatile LHRH release is regulated by specific metabolites and(or) metabolic hormones that reflect nutritional status. Alternatively, availability of oxidizable metabolic fuels, such as glucose and nonesterified fatty acids, may influence activity of neurons that control LHRH release. Our understanding of how the central nervous system transduces information about nutritional status into neuroendocrine signals that control reproduction in cattle and sheep is limited by a lack of information concerning the nature of neurons controlling LHRH release in these species.     

Effect of dexamethasone on gonadotrophin secretion in the gonadectomized sow and boar.

Saline solution or dexamethasone (DXM, 35 micrograms/kg bodyweight) was injected intramuscularly twice daily for four days into five ovariectomized sows and five castrated boars. Blood samples from an indwelling jugular vein catheter were taken at 15 min intervals for 12 h prior to DXM injection and on the fourth day of treatment in order to compare the effect on variables describing the pulsatile secretion of luteinizing hormone (LH) and follicle stimulating hormone (FSH). Dexamethasone treatment caused a decrease (p less than 0.05) in the number of pulsatile episodes of LH secretion in both gonadectomized boars and sows resulting in a significant decrease in mean concentrations. Follicle stimulating hormone secretion parameters appeared to be unaffected by DXM injection in both groups of animals. It is concluded that previously described differences in LH suppression in boars and sows given glucocorticoids may be attributed to the influence of gonadal hormones.     

Energy balance and pulsatile LH secretion in early postpartum dairy cattle

The relationships between energy balance (EB), pulsatile LH secretion and circulating levels of insulin and various energy metabolites were assessed in ten lactating Holstein cows. Cows were blood sampled every 12 min via indwelling jugular catheters for 8 hr twice weekly beginning in the first week postpartum (PP) through first ovulation (1stOV). Days to negative EB nadir and days to 1stOV were highly correlated (P less than .02). LH pulse frequency (P less than .01), LH baseline (P less than .05) and mean LH (P less than .1) increased, while LH pulse amplitude tended to decrease when comparing the frequent sampling series immediately before and after the negative EB nadir. Plasma levels of non-esterified fatty acids (NEFA, r = -.40, P less than .01), insulin (r = .38, P less than .01), glucose (r = .31, P less than .01) and beta-hydroxybutyrate (r = .19, P less than .06) were correlated with EB. For within animal comparisons, NEFA was significantly correlated (r = -.44 to -.89, P less than .05) with EB in 8 of 10 cows, but no other correlations were significant. Additionally, none of the metabolites nor insulin were significant in multiple regression models for 1stOV. Therefore, it appears that pulsatile LH secretion is suppressed until the negative EB nadir is reached, at which time LH pulse frequency increases stimulating 1stOV. Since NEFA and EB are directly related, NEFA may serve as a peripheral signal of EB to the central nervous system.     

Endogenous opiates and the hypothalamic-pituitary-gonadal axis in male sheep

The effects of morphine and the opiate receptor antagonist, naloxone, on the secretory pattern of luteinizing hormone (LH) were assessed in male sheep. Morphine infusion (250 mg/hr) abruptly stopped LH pulsatile secretion in castrates (wethers) and decreased mean serum LH concentrations by nearly 70 percent. Response of the pituitary to exogenous LH releasing hormone was not affected by morphine suggesting that the effects of morphine on LH secretion were mediated through the hypothalamus. Estradiol-implanted wethers, characterized by a nonpulsatile LH secretory pattern, responded to intravenous injection of naloxone (20, 50 and 200 mg Lv.) with an immediate release (pulse) of L.H. Similarly, LH release was significantly increased following naloxone infusion (200 mg/hr for four hours) in intact rams and wethers implanted with testosterone or estradiol. In contrast, naloxone infusion altered the pattern of LH secretion in wethers but without affecting mean serum LH concentrations. These results support the notion that LH secretion in male-sheep is tonically regulated by endogenous opiates and further suggests that opioid modulation of the hypothalamic-pituitary-LH axis in sheep involves an interaction with the steroid negative feedback system.     

Analysis of pulsatile and surge-like luteinizing hormone secretion with frequent blood sampling in female mice

Mice have become more important as genetically-modified model animals for analysis of physiological functions. The establishment of a frequent blood sampling system in conscious mice would provide a powerful tool for a better and more detailed understanding of the physiological status of circulating hormonal changes, such as pulse or surge modes of luteinizing hormone (LH) secretion. Frequent blood sampling, however, is considered problematic in mice because of the limited blood volume for their small body size. The present study, therefore, aims to establish a blood sampling protocol to determine the pulse and surge modes of LH secretion using intra-atrial cannulation and frequent blood sampling in free-moving conscious mice. Ovariectomized mice were bled every 3 min for 1.5 h to detect LH pulses. Blood glucose levels, an indicator of stress, were kept constant throughout the 1.5-h sampling period, suggesting that sampling can be performed under stress-free conditions. Obvious LH pulses were observed in ad lib-fed ovariectomized mice, whereas they were significantly suppressed after a 24-h fast. This indicates that the present sampling protocol is suitable for detecting physiological changes in pulsatile LH secretion. In addition, 1-h-interval blood collections in proestrous mice between 1300 and 2200 h revealed that individual preovulatory LH surges occur in the evening of proestrous days. Thus, the present study has developed a blood sampling protocol to detect individual profiles of pulse and surge modes of LH secretion in mice.     

Luteinizing hormone and growth hormone secretion in ewes infused intracerebroventricularly with neuropeptide Y

Neuropeptide Y (NPY) provides an important hypothalamic link between nutritional status and neuroendocrine mechanisms regulating growth and reproduction. The objective of the following series of experiments was to determine the effects of single or continuous administration of NPY on secretion of luteinizing hormone (LH) and (or) growth hormone (GH). In experiment 1, four ovariectomized (OVX) ewes and four OVX + estrogen-treated ewes each received, in a 4 x 4 Latin Square arrangement of treatments, a single injection of 0, 0.5, 5, or 50 microg NPY via an intracerebroventricular (i.c.v.) cannulae to determine the effects on secretion of GH. NPY significantly elevated serum GH at the 50 microg dose regardless of estrogen exposure (P = 0.003). In experiment 2, eight OVX ewes were infused i.c.v. with NPY or saline (n = 4/trmt) continuously for 20 h in a linearly increasing dose, ending at 50 microg/h NPY. Blood samples were collected via jugular cannulae every 10 min during hour -4-0 (interval 1, pre-treatment), hour 6-10 (interval 2) and hour 16-20 (interval 3) relative to the initiation of infusion (0 h). Mean LH and LH pulse frequency were lower in NPY- versus saline-infused ewes during intervals 2 and 3 (P < 0.01), but NPY had no discernable effect on serum GH (P > 0.10). In experiment 3, four OVX ewes were continuously infused with NPY as in experiment 2, except that the maximum 50 microg/h dose was achieved after only 10 h of infusion. Blood samples were collected every 10 min, beginning 4 h before and continuing until 4h after the NPY infusion. Mean serum LH changed significantly over time (P = 0.0001), decreasing below pre-treatment levels by hour 3 of NPY infusion (P < 0.01), and returning to pre-treatment concentrations following the end of infusion (P > 0.15). Serum GH also changed significantly over time (P < 0.001). Mean GH levels tended to be greater than pre-treatment levels by hour 2 of infusion (P < 0.08), but thereafter returned to basal levels. Serum GH also increased following the end of NPY infusion (P < 0.03). From these data we conclude that NPY exerts a persistent inhibitory effect on secretion of LH, and may stimulate the secretion of GH during the initiation and cessation of infusion of NPY. These observations support a role for NPY in mediating the effects of undernutrition on both LH and GH, and also provide evidence for potential mechanisms by which leptin, acting through NPY, may stimulate the secretion of GH.     

Dynorphin-Kappa Opioid Receptor Signaling Partly Mediates Estrogen Negative Feedback Effect on LH Pulses in Female Rats

Accumulating evidence suggests that the arcuate nucleus (ARC) kisspeptin/neurokinin B (NKB)/dynorphin (KNDy) neurons play a role in estrogen negative feedback action on pulsatile gonadotropin-releasing hormone (GnRH)/luteinizing hormone (LH) release. The present study aimed to determine if dynorphin (Dyn) is involved in estrogen negative feedback on pulsatile GnRH/LH release. The effect of the injection of nor-binaltorphimine (nor-BNI), a kappa-opioid receptor (KOR) antagonist, into the third cerebroventricle (3V) on LH pulses was determined in ovariectomized (OVX) adult female rats with/without replacement of negative feedback levels of estradiol (low E₂). The mean LH concentrations and baseline levels of LH secretion in nor-BNI-injected, low E₂-treated rats were significantly higher compared with vehicle-treated controls. On the other hand, the nor-BNI treatment failed to affect any LH pulse parameters in OVX rats without low E₂ treatment. These results suggest that Dyn is involved in the estrogen negative feedback regulation of pulsatile GnRH/LH release. The low E₂ treatment had no significant effect on the numbers of ARC Pdyn (Dyn gene)-,Kiss1- and Tac2 (NKB gene)-expressing cells. The treatment also did not affect mRNA levels of Pdyn and Oprk1 (KOR gene) in the ARC-median eminence region, but significantly increased the ARC kisspeptin immunoreactivity. These findings suggest that the negative feedback level of estrogen suppresses kisspeptin release from the ARC KNDy neurons through an unknown mechanism without affecting the Dyn and KOR expressions in the ARC. Taken together, the present result suggests that Dyn-KOR signaling is a part of estrogen negative feedback action on GnRH/LH pulses by reducing the kisspeptin release in female rats.     

链脲佐菌素和四氧嘧啶联合注射建立犬I型糖尿病模型

旨在探索链脲佐菌素和四氧嘧啶联合注射建立犬I型糖尿病模型的最佳剂量。本试验选取18只9~12月龄、平均体重为（5.09±0.30）kg的健康中华田园犬，随机分为6组（每组3个重复，每个重复1只）。按链脲佐菌素和四氧嘧啶不同剂量混合分组，其中Ⅰ组（20 mg·kg^-1/40 mg·kg^-1）、Ⅱ组（30 mg·kg^-1/50 mg· kg^-1）和Ⅲ组（40 mg·kg^-1/60 mg·kg^-1）进行单次静脉注射；Ⅳ组（10 mg·kg^-1/20 mg·kg^-1）、Ⅴ组（15 mg·kg^-1/25 mg·kg^-1）和Ⅵ组（20 mg·kg^-1/30 mg·kg^-1）进行两次静脉注射，两次注射间隔为24 h。通过注射后血糖、葡萄糖耐量、血液生理生化和胰腺组织形态学变化来评价各组建模效果。结果显示：1）Ⅰ组和Ⅳ组的空腹血糖始终处于正常水平，Ⅱ组和Ⅲ组连续7 d超过15 mmol·L^-1，Ⅴ组和Ⅵ组虽有上升，但试验期间均未超过10 mmol·L^-1；2）葡萄糖耐量试验显示，各组血糖均在15 min升高至峰值，之后Ⅰ组和Ⅳ组逐渐下降到注射前水平，Ⅴ组血糖虽下降但未达到注射前水平，Ⅱ组、Ⅲ组和Ⅵ组持续保持高血糖水平；3）各组血常规指标均在正常生理范围内，Ⅲ组的丙氨酸氨基转移酶（ALT）、天冬氨酸氨基转移酶（AST）、碱性磷酸酶（ALP）、尿素（UREA）和肌酐（CREA）均超过正常生理范围；4）胰腺组织形态学显示，Ⅱ组和Ⅲ组的胰岛结构被明显破坏。综上所述，对犬使用30 mg·kg^-1+50 mg·kg^-1的链脲佐菌素和四氧嘧啶联合单次静脉注射，血糖值连续7 d大于15 mmol·L^-1且未造成严重的肝肾毒性，可有效建立I型糖尿病模型。     

Acute lipoprivation suppresses pulsatile luteinizing hormone secretion without affecting food intake in female rats

The present study examined the effect of acute lipoprivation on pulsatile luteinizing hormone (LH) secretion in both normal-fat diet, ad libitum-fed and fasted female rats. To produce an acute lipoprivic condition, mercaptoacetate (MA), an inhibitor of fatty acid oxidation, was administered intraperitoneally to ad libitum-fed or 24-h fasted ovariectomized (OVX) rats with or without an estradiol (E2) implant, that produces a negative feedback effect on LH pulses. The steroid treatment was performed to determine the effect of estrogen on lipoprivic changes in LH release, because estrogen enhances fasting- or glucoprivation-induced suppression of LH pulses. Pulsatile LH secretion was suppressed by MA administration in a dose-dependent manner in the ad libitum-fed OVX and OVX+E2 rats. LH pulses were more severely suppressed in the 24-h-fasted OVX and OVX+E2 rats compared to the ad libitum-fed rats. Estrogen slightly enhanced lipoprivic suppression but the effect was not significant. In the present study, increased plasma glucose and free-fatty acid concentrations may indicate a blockade of fatty acid metabolism by the MA treatment, but food intake was not affected by any of the MA doses. Acute vagotomy did not block lipoprivic suppression of LH pulses. Thus, the present study indicates that lipid metabolism is important for maintenance of normal reproductive function even in rats fed a normal-fat diet and lipoprivation may be more critical in fasted animals that probably rely more heavily on fatty acid oxidation to maintain appropriate metabolic fuel levels. In addition, failure of blockade of lipoprivic LH inhibition by vagotomy suggests that lipoprivic information resulting in LH suppression is not transmitted to the brain via the vagus nerve.     

Involvement of neurokinin receptors in the control of pulsatile luteinizing hormone secretion in rats

It has recently been shown that neurokinin B, a tachykinin, is associated with GnRH pulse generation in sheep and goats. The aim of the present study was to clarify the role of tachykinin receptors in the control of LH secretion in rats. To this end, we evaluated the effect of CS-003, an antagonist for all three neurokinin receptors (NK1, NK2 and NK3 receptors), on pulsatile LH secretion in both sexes of rats with different routes of administration. Both oral and third ventricular administration of CS-003 suppressed LH secretion in both sexes of gonadectomized animals. Furthermore, intact male rats with oral administration of CS-003 showed decreased serum testosterone levels, which might be due to suppressed LH secretion. None of the three subtype-specific neurokinin receptor antagonists showed a significant effect on LH secretion in ovariectomized rats when each antagonist was singly administered. The present results suggest that neurokinins play a role in the control of pulsatile GnRH/LH secretion via multiple neurokinin receptors in both male and female rats.     

Pituitary-testicular responses of estradiol-17 beta-implanted bull calves to continuous versus pulsatile infusion of luteinizing hormone releasing hormone

The luteinizing hormone (LH), follicle-stimulating hormone (FSH) and testosterone response of bull calves implanted with estradiol-17 beta to continuous and pulsatile infusion of luteinizing hormone releasing hormone (LHRH) has been examined. Estradiol-17 beta reduced serum LH and FSH concentrations and suppressed testosterone secretion and testicular growth when compared with sham-implanted bulls. Pulsatile iv infusion of LHRH [500 ng every 2 h (6 micrograms/d)] for a 4-wk period to estradiol-17 beta-implanted bulls resulted in elevated mean serum LH and testosterone concentrations that were characterized by discrete secretory episodes. Mean serum FSH was also increased by LHRH pulse infusion, but LHRH-coupled secretory episodes were not apparent. Continuous infusion of LHRH (6 micrograms/d) did not increase the low serum gonadotropin levels observed in estradiol-17 beta-implanted calves. Testicular growth was normal in LHRH pulse-infused calves, but was markedly curtailed in continuously infused calves. These results suggest that estradiol-17 beta inhibits testicular development by blocking gonadotropin release at the level of the hypothalamus because pulsatile administration of LHRH can override the inhibitory effect by increasing LH and FSH secretion.     

Bovine C-terminal octapeptide of RFamide-related peptide-3 suppresses luteinizing hormone (LH) secretion from the pituitary as well as pulsatile LH secretion in bovines

Gonadotropin-inhibiting hormone (GnIH), observed in quail as a member of the RFamide neuropeptide family, suppresses luteinizing hormone (LH) secretion from the avian pituitary. Rats and cattle have an active gene of another member of the RFamide neuropeptide family, termed RFamide-related peptide-3 (RFRP-3), although bovine RFRP-3 is different from that of rats in both length and amino-acid sequence. A single injection of GnIH or RFRP-3 inhibited LH secretion in rodents, which continued for various periods. This study was conducted to evaluate the effects of bovine C-terminal octapeptide of RFRP-3 (RFRP-3-8) on LH secretion from cultured anterior pituitary (AP) cells of cattle, and the effects of RFRP-3-8 injections on pulsatile LH secretion in castrated male calves. The suppressive effect of RFRP-3-8 on LH secretion from AP cells was observed in the presence of gonadotropin-releasing hormone (GnRH), but not in the absence of GnRH in culture media. In another experiment collecting blood samples serially from castrated male calves with repeated intravenous injections of RFRP-3-8 (n = 6) or saline (n = 6), the RFRP-3-8 group showed suppressed LH pulse frequency during the injection period (P < 0.05); however, the RFRP-3-8 group showed no difference from the saline group in all measures of LH secretion in the postinjection period. In conclusion, our results suggested that RFRP-3-8 suppresses LH secretion from cultured AP cells, as well as LH pulse frequency in cattle.     

LHRH antagonist decreases LH and progesterone secretion but does not alter length of estrous cycle in heifers.

The objective of this study was to evaluate the suppressive effect of an LHRH antagonist, Cetrorelix SB-75 (SB-75), on secretion of LH, FSH and ovarian function in beef heifers. In Exp. 1, heifers were treated with a single dose of 10 microg/kg body weight intramuscularly on d 3 of the estrous cycle. In Exp. 2, heifers received either a single injection (100 microg/kg) of SB-75 on d 3 of the estrous cycle or multiple injections of 20 microg/kg on d 3, 4, 5, 6, and 7. Serum LH, but not FSH, was suppressed from one to several days. However, neither FSH nor progesterone was significantly altered. In Exp. 3, heifers received an injection vehicle (5% mannitol) or 100 microg/kg BW of SB-75 on d 1 of the estrous cycle (30 h after first observed standing estrus). Injection of SB-75 suppressed LH pulse frequency on d 3, 5, and 7 (P < 0.001). The mean LH concentrations in the SB-75 treatment groups were lower on d 3 (P < 0.01) and 5 (P < 0.05). There were no differences (P > 0.1) between the two groups in the mean concentrations of LH on d 1, 7, or 14. Treatment did not affect the secretion pattern or concentration of FSH. Injection of SB-75 did not alter estradiol-173 concentrations (P > 0.1). Treatment reduced corpus luteum (CL) function as indicated by lower progesterone production. However, the length of the estrous cycle was not shortened. These data show that the CL can form and survive in the face of depressed LH concentrations during the early stages of the estrous cycle.     

Ovarian inhibition of pulsatile luteinizing hormone secretion in prepuberal holstein heifers

Fifteen prepuberal Holstein heifers were utilized to examine pulsatile luteinizing hormone (LH) secretion before and after ovariectomy. Heifers were ovariectornized at 3, 6 or 9 months of age (n=5/group) and scheduled for blood sampling at 1 week before, 1 week after and 4 weeks following ovariectomy. During each 8 hr sampling period (0600–1400 hr), blood samples (10 ml) were collected via indwelling jugular canulae at 10 min intervals. Prior to ovariectomy, mean plasma LH concentration and both number and amplitude of LH pulses per 8 hr sampling period were similar (P>.05) among age groups, and the absence of a pulsatile LH secretion profile was accompanied by a low mean LH concentration. Within 1 week after ovariectomy, both number of LH pulses and mean LH concentrations increased (P<.O1) in all age groups. Between 1 and 4 weeks after ovariectomy, both amplitude of LH pulses and mean LH concentrations increased (P<.O1) when the data from the three age groups were combined. We conclude that ovarian inhibition of pulsatile LH secretion is established by 3 months of age and is maintained through 9 months of age. In addition, the initial elevation mean plasma LH concentration is due to greater pulse frequency, while the subsequent rise in mean LH concentration reflects increased amplitude of LH pulses.     

Effect of short-term feed restriction and refeeding on serum concentrations of leptin, luteinizing hormone and insulin in ovariectomized gilts

Ovariectomized gilts were either placed on full feed (FF) or restricted to one-third of the full feed amount (RST) for 7 days. Blood samples were taken through jugular catheters every 15 min for 4 h at the end of the 7-day period. Then dietary treatments were reversed and 7 days later samples were taken as before. Serum concentrations of leptin, insulin and luteinizing hormone (LH) were determined by radioimmunoassay. LH pulse frequency and mean serum leptin and insulin concentrations were lower (P < 0.01) in RST than FF gilts. Reversal of treatment reversed the patterns of hormone secretion. These results confirm previous observations that feed restriction can inhibit pulsatile LH secretion and also decrease leptin and insulin secretion.     

Effects of pulsatile injection of GnRH into 6- to 14-wk-old Holstein bulls

With the goal of hastening puberty, we evaluated the effects of dose of gonadotropin releasing hormone (GnRH) during pulsatile injection on luteinizing hormone (LH) secretion in bulls 6, 10 or 14 wk old, and of pulsatile administration of GnRH every 2 h to bulls from 6 to 12 wk of age on reproductive development. Based on response to the last three of 12 bihourly injections of 20, 200 or 2,000 ng GnRH/kg, only the two higher doses of GnRH induced secretion of LH at 6 wk. At all ages, 200 ng GnRH/kg induced maximal discharges of LH. Based on comparisons between seven treated bulls and their identical twins, bihourly injections of GnRH starting on d 42 elicited discharge of LH for less than or equal to 4 d in progeny of one sire and greater than 28 d but less than 42 d in progeny of another sire. After 14 d of treatment, both elicited and spontaneous discharges of LH were smaller in all treated bulls. Within 2 d after cessation of GnRH injections on d 84, LH discharges were similar in frequency and amplitude in treated and control twins. Testicular and body growth were similar in treated and control bulls, but puberty was delayed (P less than .05) in bulls in which exogenous GnRH suppressed endogenous discharges of LH.