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Dietary arginine deprivation and delayed puberty in the female rat.

Dietary arginine deprivation was found to delay puberty in the female rat. Physiological pinealectomy by exposing to constant light suggests this gland is not involved in this delay. Compensatory ovarian hypertrophy (COH) was used to test the hypothalamic sensitivity to negative steroid feedback. COH occurred in hemiovariectomized immature rats ad libitum fed the control or arginine-deficient diet but failed to occur in hemiovariectomized, underfed, growth-matched control rats, which suggests that feed restriction and arginine deficiency do not exert identical effects on the hypothalamic-pituitary-gonadal axis. Puberty, as defined by vaginal opening, first ovulation and the initiation of estrous cycles, was advanced by a week in the immature female rat fed a control diet after treatment with estradiol benzoate, 0.05 microgram/(100 g body weight X day) starting at 26 days of age. The time of first estrus and the first ovulation was not advanced in arginine-deficient rats by the same dosage of estrogen when administration began at 26 days of age. Treatment at an older age (40 or 54 days) or with a higher dosage [0.25 microgram/(100 g body weight X day)] at 26 days of age did advance puberty. The failure of estrogen to induce a vaginal cyclicity suggests an insufficient amount of endogenous estrogen to trigger a gonadotropin surge to cause the onset of puberty in the rat fed an arginine-deficient diet.

Animals↗

Effect of maternal exposure to the environmental estrogen, octylphenol, during fetal and/or postnatal life on onset of puberty, endocrine status, and ovarian follicular dynamics in ewe lambs.

Octylphenol (OP) is one of a number of compounds found in the environment that has estrogen-mimicking actions in vivo. Our objective was to determine if maternal exposure to octylphenol during fetal and/or postnatal life would affect the onset of puberty, endocrine status, and subsequent ovarian follicular dynamics of ewe lambs. Lambs were born in March to ewes that received twice weekly s.c. injections of octylphenol (1000 micro g/kg/day) from Day 70 of gestation to weaning (n = 6); Day 70 of gestation to birth (n = 3); birth to weaning (n = 5; gestation = 145 days); or corn oil from Day 70 of gestation to weaning (control; n = 5). Blood samples were collected twice weekly to determine progesterone and FSH concentrations from 20 wk of age throughout the first breeding season. Onset of puberty and interestrous intervals were determined from 20 wk of age by twice daily observation for estrus in the presence of a vasectomized ram. During January the ovaries of each lamb were examined using transrectal ultrasonography from the day of estrus for 15 days. Blood samples were collected every 8 h to examine FSH concentrations and every 2 h to detect the preovulatory gonadotropin surge throughout this estrous cycle. The onset of puberty and first progesterone rise was advanced and the FSH preovulatory surge was elevated for longer in the OP-treated lambs compared with the control lambs (P < 0.05). Interestrous intervals, FSH profiles, and ovarian follicular dynamics were not affected (P > 0.05) by exposure to octylphenol. In conclusion, octylphenol exposure advanced the onset of puberty but it did not disrupt FSH concentrations or the dynamics of ovarian follicular growth.

Animals↗

Endocrine mechanisms of puberty in heifers: estradiol negative feedback regulation of luteinizing hormone secretion.

The hypothesis that luteinizing hormone (LH) secretion in prepubertal females is responsive to estradiol negative feedback and that decreased feedback occurs as puberty approaches was tested in heifers. In the first experiment, seven heifers were maintained prepubertal by dietary energy restriction until 508 days of age (Day 0). All heifers were placed on a high-energy diet on Day 0 at which time they received no additional treatment (CONT), were ovariectomized (OVX) or were ovariectomized and subcutaneously implanted with estradiol-17 beta (OVX-E2). This feeding regimen was used to synchronize reproductive state in all heifers. A second experiment was performed with 16 prepubertal heifers using the same treatments at 266 days (Day 0) of age (CONT, OVX and OVX-E2) but no dietary intake manipulation. In both experiments, LH secretion increased rapidly following ovariectomy in OVX heifers. In the initial experiment, LH secretion was maintained at a low level in OVX-E2 heifers until a synchronous rapid increase was noted coincidental with puberty in the CONT heifer. In the second experiment, LH secretion increased gradually in OVX-E2 heifers and attained castrate levels coincidental with puberty in CONT heifers. A gradual increase in LH secretion occurred as puberty approached in CONT heifers. These results indicate that: a) LH secretion in prepubertal heifers is responsive to estradiol negative feedback; and b) estradiol negative feedback decreases during the prepubertal period in beef heifers.

Age Factors↗

Absence of an increase in gonad-independent drive to pulsatile luteinizing hormone secretion during photoperiod-induced puberty.

This study was conducted to determine if photoperiod can influence the pattern of luteinizing hormone (LH) secretion in the absence of the ovaries in the developing female sheep. Lambs were raised in a photoperiod sequence (short, long, short days) known to induce puberty between 30 and 35 wk of age, or in a photoperiod (only short days) that prevents puberty during the first year. Their ovaries were removed at 10 wk of age, and the detailed pattern of LH was assessed (samples at 12-min intervals for 4 h) each 3- to 5-wk period between 9 and 45 wk of age. Rapid LH pulses (40- to 50-min interpulse interval) were evident within a few weeks after ovariectomy in both groups of females. Those exposed to the artificial photoperiod sequence that induces normal sexual maturity did not increase their pulse frequency further during the pubertal period. Moreover, their LH pulse frequencies were not greater than those in agonadal females exposed to the photoperiod that delays puberty. These findings indicate that photoperiodic induction of puberty in the sheep does not require steroid-independent modulation of pulsatile LH secretion.

Animals↗

Changes in episodic luteinizing hormone secretion leading to puberty in the lamb.

In this study, we monitored episodic luteinizing hormone (LH) secretion throughout development in eight April-born ewe lambs to determine if a change in LH pulse patterns preceded first ovulation at puberty. LH pulses were measured in samples collected every 12 min for 6 h once in July, twice a month from 22 August to 2 October, and then weekly until puberty. Progesterone concentrations, measured in samples taken 3/wk, were used as an index of first ovulation, which occurred at 29.3 +/- 0.7 wk of age. LH pulse frequencies throughout most of this period ranged from 0 to 2 pulses/6 h, with no change over time. However, during the week prior to the first progesterone rise, there was a significant increase in pulse frequency to a level seen during the follicular phase in post-pubertal lambs. This increase in pulse frequency was evident in 7 of 8 lambs; pulses were not analyzed in the last lamb because samples were taken during the LH surge. In contrast, LH pulse amplitude did not increase prior to puberty. In fact, pulse amplitude declined linearly during the 3 wk before first ovulation and then increased during the follicular phase in post-pubertal animals. These results support the hypothesis that an increase in the frequency of episodic LH secretion is a key event leading to the onset of ovarian cycles in the lamb. Whether an increase in pulse amplitude is also necessary remains unclear. If so, it must occur just before the LH surge, since it was not detected in any samples taken before puberty in this study.

Animals↗

Serum concentrations of immunoactive and bioactive luteinizing hormone (LH) in gilts. II. Biopotency of LH increases at puberty but remains constant throughout the estrous cycle.

To determine serum concentrations of immunoactive (I) and bioactive (B) LH during the pubertal surge of LH release, two groups of twelve prepubertal gilts were relocated and exposed to boars to stimulate the onset of puberty. Puberty was defined as the first sign of behavioral estrus and occurrence of a preovulatory surge of LH. Blood samples were taken every 2 h, beginning on the third or fifth day after boar exposure; sampling was continued for 24 h after each gilt had exhibited estrus, or for 7 days, or until two-thirds of the gilts in a group attained puberty. Fifty percent of the total number of gilts exposed to boars attained puberty within 7 days of first boar exposure. Total area under the ILH curve was greater (p < 0.01) than area under the BLH curve during the ovulatory rise in LH. A second experiment was conducted to compare serum concentrations of ILH and BLH during the luteal and follicular phases of the estrous cycle. Blood samples were collected every 20 min for a 6-h period of spontaneous secretion; then GnRH was injected and blood samples were collected every 20 min for 4 h from gilts during the luteal (n = 16) and follicular (n = 15) phases, respectively. BLH baseline tended to be greater (p = 0.07) during the follicular phase than during the luteal phase. Mean peak amplitude of naturally occurring peaks of ILH and BLH was greater (p < 0.05) during the luteal phase than during the follicular phase.(ABSTRACT TRUNCATED AT 250 WORDS)

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Puberty occurring either spontaneously or induced precociously in rhesus monkey (Macaca mulatta) is associated with a marked proliferation of Sertoli cells.

The pubertal ontogeny of Sertoli cell proliferation in primates is controversial. In the study of the rhesus monkey presented here, we investigated this issue during normal sexual maturation and during precocious puberty induced experimentally with pulsatile GnRH treatment. Cell number was calculated by standard stereological methods employing volume fraction of either seminiferous tubule or, whenever possible, cell nuclei. In the first experiment, testes were collected from normal monkeys at three developmental phases: neonates (7-18 days old, n = 5); juveniles (approximately 17 mo old, n = 4); and adults (5 yr and older, n = 4). In the second experiment, tissue was obtained from an additional three untreated juvenile monkeys and from six other juveniles of comparable age that had been subjected to premature activation of the pituitary-testicular axis for 5 or 10 wk with pulsatile GnRH (1 microgram/min for 3 min every 3 h). The number of Sertoli cells in adults was 6-fold greater than that in neonatal and juvenile animals. A similar increase in number of this somatic cell type was also observed during experimentally induced puberty. A less dramatic proliferation of Sertoli cells occurred during the neonatal-juvenile transition. Although the increase in Sertoli cell number between the juvenile and adult stages of development was paralleled by a comparable change in Ad and Ap spermatogonia, proliferation of these stem spermatogonia during premature activation of the pituitary-testicular axis was less striking. These results lead to the suggestion that, in primates, the onset of puberty is associated with a rapid and substantial proliferation of Sertoli cells, which is subsequently followed by amplification of stem spermatogonia. They also indicate that while Sertoli cells and stem spermatogonia proliferate during infancy and juvenile development, these earlier changes appear to be more insidious than those at puberty.

Animals↗

Estradiol regulation of luteinizing hormone secretion in heifers of two breed types that reach puberty at different ages.

The working hypothesis was that 17 beta-estradiol (E(2)) negative feedback on the hypothalamic-pituitary axis in regulation of LH secretion decreases during peripuberty in heifers of 2 different genotypes. We investigated whether Bos indicus heifers had a period postpuberty, as compared with prepuberty, of greater E(2) inhibition of LH secretion at a time when heifers of this genotype have been reported to have a period of anestrus. Prepubertal heifers 9 mo of age of 2 genotypes (B. indicus and B. taurus) were assigned to 3 groups (6 animals/group) to either remain intact (control), be ovariectomized, or be ovariectomized and implanted with E(2). Variables evaluated from 10 to 28 mo of age were circulating concentrations of progesterone (P(4)), presence of corpora lutea, and pulsatile pattern of LH release. Results confirmed that B. taurus heifers attained puberty at younger ages (P < 0.001) and at lower live weights (P = 0.015) than did B. indicus heifers (507 +/- 37 days of age vs. 678 +/- 7 days of age; 259 +/- 14 kg vs. 312 +/- 11 kg; respectively). There was cessation of E(2) inhibition of LH pulses coincident with the onset of puberty in heifers of both breed types but at a much younger age in B. taurus heifers. There was no evidence of enhanced negative feedback of E(2) on LH secretion subsequent to puberty in B. indicus heifers nor was there cessation of estrous cycles in control heifers of either breed type after puberty.

Aging↗

A study on puberty and oestrus in gilts.

The main purpose of this study was to investigate the oestrous symptoms at puberty and during the two subsequent oestrous periods in the gilt. The investigation comprised a total of 369 purebred Swedish Yorkshire gilts. The gilts were carefully checked for oestrous symptoms twice daily, from 160 to 260 days of age, and blood samples for progesterone determination were drawn from 170 days until puberty. The duration of prooestrus was longer (p less than or equal to 0.001) at the at the first oestrous period than at the two subsequent oestrous periods and decreased (p less than or equal to 0.05) with an increase in age at puberty. Most of the oestrous symptoms were significantly correlated within the first and between the first three oestrous periods. Twenty percent of the gilts did not show standing reflex and anovulatory oestrus was found in 2% of the gilts at puberty, as demonstrated by progesterone determinations. The frequency of gilts not showing standing reflex at the second and third oestrus was approximately the same as at the first oestrous period. The first oestrous cycle was longer (p less than or equal to 0.001) than the second cycle. Approximately 95% of the gilts had a cycle length within 18 to 24 days at the first and second oestrous cycle.

Animals↗

Night-time melatonin secretion and seasonally delayed puberty in gilts.

This study was conducted to determine whether the seasonal delay in puberty in autumn is driven by individual differences in night-time melatonin secretion in domestic gilts at the attainment of puberty. A group of spring-born gilts (n = 30) were expected to reach puberty in autumn by the age of 7 months. Eighteen of these gilts were selected in pairs on the basis of matched days of birth. By the expected time, half of the animals showed oestrous symptoms (group CYCLING, n = 9) with the rest remaining silent (group SILENT, n = 9). Afterwards, all gilts were fitted with indwelling jugular catheters for frequent blood sampling. Blood samples were collected from all animals three times during the day followed by three times in the night at 2-h intervals for 48 h. The samples were analysed by a commercial radioimmunoassay (RIA). The results show a consistent 25-fold rise (on average) in night-time melatonin concentration in every animal sampled with group averages ranging from 0.28 +/- 0.04 to 0.37 +/- 0.06 pg/ml at day and from 10.20 +/- 2.16 to 10.67 +/- 0.05 pg/ml at night. Night-time group mean values between CYCLING and SILENT gilts did not differ significantly (10.26 +/- 0.67 and 10.38 +/- 0.94 for the CYCLING; 10.67 +/- 0.05 and 10.20 +/- 2.16 for the SILENT). When 10 pg/ml was used as a threshold value, six individuals did not reach it during the night (low responders). Two of these gilts were CYCLING and four were SILENT. In conclusion, the results presented imply no involvement of the level of night-time melatonin concentration in the seasonal delay of puberty in gilts.

Animals↗

Acceleration of puberty onset in female mice by male urinary proteins.

1. Puberty onset in female mice is accelerated by exposure to conspecific adult male urine, which acts through the vomeronasal organ and the accessory olfactory system. A distinctive component of adult male mouse urine is the major urinary protein complex (MUP), which is a lipocalin; it has a hydrophobic pocket that binds small endogenous volatile molecules. The MUP gene family also codes for a hexapeptide, which has four residues in common with the N-terminal region of MUP. 2. MUP, the volatiles bound to MUP and the MUP-related hexapeptide have been tested for the induction of puberty acceleration by measuring the increase in uterus weight related to the first pro-oestrus phase. MUP, together with its bound volatiles, induces puberty acceleration. Its activity is retained even when the volatiles have been removed either by organic extraction or competition displacement with a high-affinity ligand. 3. MUP-related hexapeptide also induces puberty acceleration in female mice. In contrast, the odorants bound to MUP do not exert this effect. 4. It is proposed that the vomeronasal organ contains receptors that recognize the short N-terminal consensus sequence, N-Glu-Glu-Ala-X-Ser (where X is a polar residue), common to both MUP and the hexapeptide.

Animals↗

Puberty delay by a urinary cue from female house mice in feral populations.

Urine produced by wild female house mice, living in high- and low-density populations and confined to areas within a highway cloverleaf, was tested for its ability to delay puberty in juvenile female mice. Only urine collected from females in the dense population at its maximum density delayed puberty in test females. Urine collected when the population was less dense, or from a population that remained sparse, failed to delay puberty. These results suggest that a urinary factor present at high densities may delay puberty and thus help to slow further population growth.

Animals↗

Regulation of gonadal and somatotropic axis by chronic intraventricular infusion of insulin-like growth factor 1 antibody at the initiation of puberty in male rats.

There has been increasing experimental evidence to suggest that insulin-like growth factor 1 (IGF-I) may be one of the essential regulators in the reproductive system of the rat. IGF-I is synthesized in the hypothalamus and IGF-I immunoreactivity increases during puberty. Consequently we hypothesized that centrally located IGF-I might contribute to the initiation of puberty. Centrally located IGF-I was immunoneutralized to assess this hypothesis. Male Wistar rats, 28 days old, were infused intracerebroventricularly with specific purified IgGs from rabbit IGF-I antiserum (IGF-I-Ab). The intracerebroventricular administration of IGF-I-Ab resulted in a reduction in testicular weight and consequently in delayed pubertal development. There was also a reduction in serum testosterone, pituitary immunoreactive (IR) luteinizing hormone (LH) and serum IR follicle-stimulating hormone (FSH). The accumulation of betaLH mRNA was not modified, whereas betaFSH mRNA was increased. An increment in the serum growth hormone (GH) levels was also observed. There were no significant alterations in hypothalamic IR growth hormone releasing factor content, although IR somatostatin (SRIH) content was increased by IGF-I-Ab. The body weight gain remained unaltered. As a whole, our study suggests that centrally located IGF-I influences pubertal development, production and release of gonadotropins and supports the finding that endogenous centrally located IGF-I plays a role at the initiation of puberty in the male rat. It also gives support to the physiological role of centrally located IGF-I in the release of GH mediated by hypothalamic SRIH at the initiation of puberty.

Animals↗

A reassessment of leptin's role in triggering the onset of puberty in the rat and mouse.

Leptin is an adipocyte-derived hormone that has been implicated to serve as a metabolic signal to the reproductive axis. The role of leptin in pubertal maturation, however, has been a much-debated topic. We have previously reported that leptin serves as a permissive signal to the onset of puberty in the female rat. In an attempt to further understand the mechanics of leptin during pubertal maturation in rodent species, we had three experimental objectives: first, to describe the temporal relationship of leptin with development in the male and female rat; second, to seek evidence for an increase in responsiveness of the neuroendocrine axis to leptin by assessing for possible changes in leptin receptor expression during pubertal developmental in the female rat; and, third, to reevaluate the possible role of leptin as a permissive signal to the onset of puberty in the mouse. We found that serum leptin levels remain relatively constant during the prepubertal and postpubertal stages of both sexes. In addition, we could not detect any significant developmental changes in leptin receptor gene expression in the hypothalamus of the female rat. Lastly, we corroborated our findings in the female rat that leptin reversed the delay in pubertal maturation secondary to food restriction but did not advance the onset of puberty in female mice. Together, these results suggest that leptin is not a metabolic trigger for the onset of puberty in the rodent; instead, leptin is one of several permissive factors, whose presence may be necessary but alone is not sufficient to initiate sexual maturation in these species.

Animals↗

Effects of ethanol during the onset of female puberty.

To assess more closely the physiological mechanism(s) by which ethanol (ETOH) delays the onset of female puberty, we have evaluated its effects on body weight, the vaginal opening (VO)-first diestrus (D1) interval and the serum concentrations of growth hormone (GH), luteinizing hormone (LH) and follicle-stimulating hormone (FSH) throughout the peripubertal period in the rat. Using a specific intragastric feeding regimen, 29-day-old rats began receiving either a liquid diet containing ETOH or an isocaloric control liquid diet. Additional controls consisted of animals maintained on laboratory chow and water provided ad libitum. Animals were either killed between 32 and 37 days of age, categorized with regard to their phase of puberty and their serum hormones measured; or, in some animals, the ETOH liquid diet was administered through day 41 and at that time replaced by the control liquid diet in order to determine if recovery would occur. Our results indicate that ETOH-treated animals showed significantly lower body weights and a significantly longer mean VO-D1 interval than the control animals. Also, serum GH and LH levels were significantly lower in the ETOH-treated animals; however, FSH levels were not affected. Administration of the ETOH liquid diet through day 41 produced varying detrimental effects on the onset of puberty and subsequent removal of ETOH from the diet resulted in rapid growth of the animals, followed by the onset of puberty.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Feed restriction in prepubertal lambs: effect on puberty onset and on in vivo release of luteinizing-hormone-releasing hormone, neuropeptide Y and beta-endorphin from the posterior-lateral median eminence.

The exact nature of the interaction between energy balance and reproduction is still elusive. Theoretically, nutrition-related variables must reach the hypothalamic luteinizing-hormone-releasing hormone (LHRH) network and/or its neuronal inputs, to alter plasma luteinizing hormone (LH) and therefore reproductive activity. In an attempt to assess the potential mechanism of such interaction at the median eminence (ME) level, the area of hypophysiotropic LHRH neuronal terminals and release, we used a decreased caloric intake lamb model which delays the onset of puberty. Thus, we determined the in vivo release of neuropeptides, by push-pull cannula (PPC) sampling from the posterior-lateral ME, in feed-restricted (FR) ewe lambs and in full-fed (FF), age-matched, contemporary control animals. Specifically, we assessed: (1) serum LH and ME in vivo release of LHRH, beta-endorphin (beta-END) and neuropeptide Y (NPY); beta-END and NPY are two putative neuronal inputs to LHRH neuronal terminals at the ME, reported to be involved in the control of both reproduction and feed intake; (2) the effect that exogenous infusion of beta-END through the PPC might have on the release of ME LHRH and NPY, and on plasma LH. In contrast to other works, the present results were obtained in lambs with intact ovaries. Furthermore, FR lambs were always compared statistically with FF contemporary paired controls that had attained puberty. Feed restriction decreased ME LHRH release, lowered plasma LH and prevented the onset of puberty. The changes induced by feed restriction in both LHRH and LH release were associated predominantly with decreases in pulse amplitude, rather than alterations in pulse frequency. The decreased LHRH and LH release occurred in the presence of a decreased beta-END but unchanged NPY release from the ME. Exogenous infusion of beta-END into the posterior-lateral ME decreased both LHRH and NPY release from this site and decreased plasma LH. In conclusion, decreased caloric intake lowers LH release and prevents puberty onset by decreasing the amplitude of the LHRH output from the hypothalamic hypophysiotropic network. A compensatory but unsuccessful mechanism for the FR status might be a lower beta-END-inhibitory tone on ME LHRH neuronal terminals. The unchanged release of NPY at this site supports the specificity of the changes induced by feed restriction on LHRH and beta-END in vivo release.

Animals↗

Development of puberty in Large White boars in a humid tropical environment.

The development of puberty in Large White boars raised and maintained in a humid tropical environment was studied histologically and by a preputial smear technique. The growth curves for the testes, epididymides and body weight were similar and exhibited a spurt between the ages of 150 and 180 days. The accessory sex glands increased slowly but steadily until the animals were about 180 days old at which time a marked increase in their growth rate was noted. Thus from morphological and histological assessment, puberty in these animals was placed between 150 and 180 days. The preputial smear technique was successfully applied in the boar. By this method, the animals were found to be 165.74 days old at puberty and to weigh 51.65 kg. These results further indicate that the development of puberty is genetically controlled and also imply that this could be slightly modified by the environment.

Age Factors↗

Induction of precocious puberty in newborn female guinea pigs by a positive feedback action of estrogens.

The existence of a positive feedback of estrogen on the gonadotrophin-releasing mechanism at birth, was tested in the female guinea pig. Estradiol benzoate (100 ng during the first 5 days of life) or HCG (100 RU during the first 5 days of life) induced a true precocious puberty, with similar characteristics to the control animals (60% of the animals ovulated at puberty age: corpora lutea present at the ovaries). The uterus was larger in ovulating than in nonovulating animals. Reserpine (2.5 mg/kg) on 15, 17 and 19 days of age did not modify the precocious puberty induced by estradiol at birth. It is concluded that exogenous or endogenous estrogen (induced by exogenous gonadotrophin administration) have a positive feedback action on the newborn female guinea pig to release gonadotrophin and develop puberty. These results are very different than those observed in the rat and differences can be related to the stage of somatic and nervous maturation attained by the animals at birth.

Animals↗