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PubMed1985

Pulsatile infusion of luteinizing hormone-releasing hormone induces precocious puberty (vaginal opening and first ovulation) in the immature female guinea pig.

Previously we have hypothesized that an increase in luteinizing hormone-releasing hormone (LHRH) due to hypothalamic maturation is the key factor controlling the onset of puberty. This led to the working hypothesis that precocious puberty would be induced if LHRH is administered with an appropriate protocol. Thus, effects of pulsatile infusion of LHRH on the onset of first vaginal opening and first ovulation in immature female guinea pigs were studied. Luteinizing hormone-releasing hormone in hourly pulses of either 5 ng or 50 ng was infused through a chronically implanted jugular catheter for 9-29 days starting at 20 days of age. For the control experiment saline was infused in a similar manner. Infusion of 5 ng LHRH/h resulted in significantly earlier (P less than 0.001) ages at first vaginal opening (24.7 +/- 0.9 days) and at first ovulation (28.8 +/- 0.9 days) compared to saline controls (first vaginal opening 53.3 +/- 6.8 days; first ovulation 55.2 +/- 6.5 days). Infusion with a 10-fold higher LHRH dose (50 ng/h) also advanced the age at first vaginal opening (25.3 +/- 0.7 days), but precocious ovulation was no longer induced (53.7 +/- 5.3 days). Interestingly, LHRH infusion with the high dose resulted in a prolonged period of vaginal opening and cornification without ovulation. These results indicate that 1) pulsatile infusion of a small amount of LHRH with a constant frequency induces precocious puberty in a laboratory rodent, and 2) infusion of LHRH with a dose higher than the effective dose for the induction of early puberty results in a persistent estrous anovulatory syndrome. Therefore, the present study not only supports our hypothesis that an increase in endogenous LHRH release is responsible for the onset of puberty, but also further suggests that excessive release of LHRH or abnormal patterns of LHRH release may be involved in the etiology of the anovulatory persistent estrus syndrome.

Age Factors↗
PubMed1996

Immunization against growth hormone releasing factor or chronic feed restriction initiated at 3.5 months of age reduces ovarian response to pulsatile administration of gonadotropin-releasing hormone at 6 months of age and delays onset of puberty in heifers.

A severe or moderate suppression of serum insulin-like growth factor I (IGF-I) was induced in heifers, beginning at 104 days of age, by active immunization against growth hormone-releasing factor (GRFi) or by chronic feed restriction (RES), respectively. We hypothesized that reduced serum IGF-I results in decreased serum estradiol-17 beta (E2), which in turn delays onset of puberty. The objectives of this experiment were to determine 1) whether GRFi and RES would alter follicular development and delay onset of puberty through similar mechanisms, and 2) whether GnRH would enhance follicular growth in control, GRFi, and RES heifers at 6 mo of age. Changes in IGF-I, somatotropin, LH, FSH, and E2 were evaluated. Serum IGF-I was greater in control than in RES heifers, and was greater in both these groups than in GRFi heifers by 169 days of age. Basal LH decreased in control and RES but not in GRFi heifers from 136 to 157 days of age. During the same period, a decrease in mean FSH was detected in control but not in GRFi and RES heifers. RES decreased mean serum E2 from 148 to 183 days of age. At 6 mo of age, pulsatile administration of GnRH (5 micrograms every 2 h for 42-46 h) increased serum LH and FSH similarly across treatments but had no effect on the number of follicles > or = 8 mm in GRFi and RES heifers relative to saline treatment. Serum E2 and IGF-I in follicular fluid from follicles > or = 8 mm were increased in all GnRH-treated heifers; however, concentrations of both hormones were lower in GRFi than in control or RES heifers. The main effect of treatments on serum IGF-I was reflected in follicles < or = 7 mm; follicular fluid IGF-I was greater in control than in RES heifers and was greater in both these groups than in GRFi heifers. Serum E2 was lower in RES than in control and GRFi heifers from 253 to 281 days of age. Because of an interaction, E2 was lower in GRFi-GnRH than in control-GnRH heifers but similar in GRFi-saline and control-saline heifers. By 393 days of age, 0% of RES and 32% of GRFi heifers had reached puberty compared to 71% of control heifers. These data support our hypothesis that decreased serum IGF-I results in decreased serum E2. GRFi appears to delay puberty in heifers because decreased serum IGF-I impairs the ovary's ability to synthesize preovulatory concentrations of E2, thereby delaying stimulation of an LH surge. In contrast, RES may delay puberty by delaying follicular development at two stages: a) decreased IGF-I in follicles < or = 7 mm may delay predominant follicular growth, and b) decreased LH may delay maturation of the preovulatory follicle.

Aging↗
PubMed1997

Fat accretion and the regulation of insulin-mediated glycogen synthesis after puberty in rats.

Peripheral insulin sensitivity decreases after puberty in both humans and rodents and can be explained mostly by a reduction in insulin-mediated glycogen synthesis. We tested the hypothesis that the increase in postpubertal fat mass (FM), reflecting an alternative energy store, regulates a decrease in the capacity to store muscle glycogen. We studied Sprague-Dawley rats (n = 21) before puberty (Pre) or after puberty (at 4 mo of age) in groups that were either ad libitum fed (Post) or moderately caloric restricted (CR). FM (by 3H2O isotope dilution technique) was decreased by >40% in CR compared with Post. Glucose uptake (Rd, by 18 mU x kg(-1) x min(-1) hyperinsulinemic clamp) was 63 +/- 8 mg x kg(-1) x min(-1) in Pre and decreased to 39 +/- 2 mg x kg(-1) x min(-1) in Post (P < 0.001). However, it increased in CR to 53 +/- 2 mg x kg(-1) x min(-1) (P < 0.001 vs. Post). This increase in Rd was mainly accounted for by an increase in glycogen synthesis (Rd glycolysis determined by the rate of conversion of 3H-labeled glucose to 3H2O) from 23 +/- 2 in Post to 33 +/- 2 mg x kg(-1) x min(-1) in CR (P < 0.001; 38 +/- 7 mg x kg(-1) x min(-1) in Pre). Correction of glycogen synthesis in CR to near-prepubertal levels was further supported by directly assayed muscle glycogen content after insulin stimulation that was 45% higher and by a 35% enhanced accumulation of [3H]glucose into glycogen. No changes in the enzyme kinetics of glycogen synthase or phosphorylase were observed. An additional group of 2-mo-old postpubertal ad libitum-fed rats was matched with CR for lean body mass but had more FM. This group demonstrated 25% lower rates of insulin-mediated glycogen synthesis compared with CR, further supporting the notion that a moderate reduction of FM prevents the decline in insulin responsiveness and glycogen synthesis occurring after puberty. These data suggest a cause-effect relationship between the increased deposition of fat and the reduced ability to store glucose in skeletal muscle after puberty.

Adipose Tissue↗
PubMed1983

Neuroendocrine mechanisms controlling the onset of female puberty: the rat as a model.

The advent of female puberty represents the culmination of a diversity of developmental processes which affect all components of the reproductive axis. Development of neuroendocrine reproductive functions proceeds in a harmonious and interrelated manner. No unique 'trigger' of puberty can be discerned, but rather puberty represents the climax of a cascade of events, finely interconnected throughout the continuum of sexual maturation. A resetting of the hypothalamic 'gonadostat' to steroid negative feedback appears to be a phenomenon associated with puberty, but not its cause. Although the central nervous system plays a pivotal role in the development of the ovary, it is the acquisition of ovarian ovulatory capacity which finally determines the timing of the first preovulatory surge of gonadotropins. In contrast to primates, development of the central component of estradiol positive feedback is an early event in the female rat. However, in most species--including the rat--amplification (or initiation) of a particular, synchronous pattern of LHRH release appears essential for the initiation of puberty. The mechanisms underlying this functional change of the LHRH secreting system are not clearly understood. In the rat, ovarian development proceeds under the influence of gonadotropins, and the somatomammotropins PRL and GH. More intriguingly, evidence is now emerging that the central nervous system may convey direct information to the ovary via the ovarian nerves, thus providing a hormone-independent fine tuning for its control. Upon reaching adequate development, the ovary through its secretory products, acts on an already competent hypothalamic-pituitary axis to activate the central component of estradiol positive feedback.

Animals↗
PubMed1987

Activation of luteinizing hormone-releasing hormone release advances the onset of female puberty.

The juvenile-peripubertal transition period in the female rat is associated with an ovarian-independent afternoon increase in the amplitude of plasma luteinizing hormone (LH) pulses. To determine if the immature pituitary could be activated to cause precocious puberty juvenile female rats were subjected for 4 days to a microprocessor-driven pulsatile intravenous administration of LH-releasing hormone (LHRH) at a dose that produced a peripubertal pattern of LH release. To determine if the LHRH neurons themselves could be prematurely activated to induce such a pattern of plasma LH, and hence lead to precocious puberty, the neuroexcitatory amino acid analog N-methyl-DL-aspartic acid (NMA) was similarly administered. The time of puberty (vaginal opening and first ovulation) was advanced by both the LHRH and NMA treatments, by 5 and 7 days, respectively. Ovarian weight and incidence of corpora lutea at first diestrus were similar in all animals regardless of treatment, but a juvenile body weight was retained by the animals that underwent precocious puberty. Therefore, just as the adenohypophysis can be driven by exogenous LHRH to initiate puberty, the LHRH neuronal system can be precociously activated by the episodic administration of an excitatory amino acid analog that is known to interact with specific brain receptors. It is likely, therefore, that sexual maturation is limited by factors that lie further upstream in the hypothalamo-pituitary axis (e.g., the neuronal circuits that impinge upon LHRH-producing neurons).

Animals↗
PubMed1993

A possible role of neuropeptide Y in the control of the onset of puberty in female rhesus monkeys.

The onset of puberty is heralded by an increase in pulsatile LHRH release. Since neuropeptide Y (NPY) has been implicated as a major regulator in the control of pulsatile LHRH release in mature monkeys, we have hypothesized that maturational changes in the NPY neuronal system play an important role in puberty. To test this hypothesis, three experiments were conducted in female rhesus monkeys using a push-pull perfusion method. In the first experiment, changes in NPY release in the stalk-median eminence (S-ME) during puberty were determined in 9 prepubertal, 7 early pubertal and 8 midpubertal monkeys. NPY and LHRH levels were measured in aliquots of the same perfusate samples obtained from the S-ME. NPY release was pulsatile in all three groups. Mean NPY release and pulse frequency increased significantly from the prepubertal through the midpubertal stage. These developmental changes in NPY release were parallel to those observed for LHRH release in the same monkeys. In order to examine whether NPY infusion into the S-ME influences LHRH release during puberty, in the second experiment, NPY (10(-6) or 10(-8) M) or vehicle was infused into the S-ME for 10 min at 90-min intervals in 5 prepubertal and 9 midpubertal monkeys. In the midpubertal stage, infusion of NPY at doses of 10(-8) and 10(-6) M resulted in significant (p < 0.01) increases in LHRH release, while vehicle administration had no effect. In contrast, in prepubertal monkeys, neither NPY nor vehicle infusion altered LHRH release. In order to test whether endogenous NPY plays a role in the maintenance of pulsatile LHRH release, in the third experiment, a specific antiserum to NPY (aNPY) was infused into the S-ME of 6 prepubertal and 8 midpubertal monkeys. Infusion of aNPY (1:100, 1:1,000 dilution) significantly suppressed LHRH release in midpubertal but not prepubertal monkeys. The results are summarized as follows. (1) In prepubertal monkeys, NPY release is low, and the presence of NPY in the S-ME does not influence LHRH release. (2) At the onset of puberty, NPY release begins to increase, and NPY probably starts to stimulate LHRH release. (3) In the midpubertal period, NPY release increases further, and NPY in the S-ME is highly stimulatory to LHRH release.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed2000

Comparative analysis of different puberty inhibiting mechanisms of two GnRH agonists and the GnRH antagonist cetrorelix using a female rat model.

GnRH agonists are the established treatment of precocious puberty caused by premature stimulation of gonadotropin secretion. It has been reported that after an initial stimulation ("flare-up") they reduce LH secretion by desensitization of pituitary GnRH receptors. Little has been published about the use of GnRH antagonists such as cetrorelix to control the onset of puberty and whether they are potentially advantageous compared with GnRH agonists. We conducted two multigroup experiments (12 and 10 d, respectively) treating prepubertal/peripubertal female rats with either the GnRH agonist triptorelin or buserelin and compared them with rats treated with the GnRH antagonist cetrorelix and controls to assess the effects on pubertal progress and serum hormones. In the second experiment, the effects of buserelin and cetrorelix on gene expression of the GnRH receptor, LH-beta, FSH-beta, and the alpha subunit genes in the pituitary were also investigated. Cetrorelix, triptorelin, and buserelin retarded the onset of puberty as determined by delayed vaginal opening, lower ovarian weights, and lower serum estradiol levels. However, although LH and FSH levels were stimulated by both agonists, they were inhibited by cetrorelix. In the cetrorelix versus buserelin experiment, pituitary gene expression of the GnRH receptor and LH-beta subunit were significantly lower in cetrorelix treated rats compared with controls whereas buserelin had little effect. Expression of FSH-beta and alpha subunit were stimulated by buserelin but not by cetrorelix. Even though all three of these GnRH analogues inhibited gonadal development and delayed the onset of puberty, the GnRH agonists had stimulating and inhibiting effects on the pituitary-gonadal axis whereas cetrorelix exerted only inhibiting effects. We conclude from this female rat model that cetrorelix may offer advantages for a more controlled medical treatment of precocious puberty compared with GnRH agonist treatment.

Animals↗
PubMed2005

Effects of chronic hyperghrelinemia on puberty onset and pregnancy outcome in the rat.

Ghrelin, the endogenous ligand of the GH secretagogue receptor, has been recently involved in a wide array of biological functions, including signaling of energy insufficiency and energy homeostasis. On the basis of the proven reproductive effects of other regulators of energy balance, such as the adipocyte-derived hormone leptin, we hypothesized that systemic ghrelin may participate in the control of key aspects of reproductive function. To test this hypothesis, the effects of daily treatment with ghrelin were assessed in rats, pair-fed with control animals, in two relevant reproductive states, puberty and gestation, which are highly dependent on proper energy stores. Daily sc injection of ghrelin (0.5 nmol/12 h; between postnatal d 33 and 43) significantly decreased serum LH and testosterone levels and partially prevented balano-preputial separation (as an external index of puberty onset) in pubertal male rats. On the contrary, chronic administration of ghrelin to prepubertal females, between postnatal d 23 and 33, failed to induce major changes in serum levels of gonadotropins and estradiol, nor did it modify the timing of puberty, as estimated by the ages at vaginal opening and first estrus. Moreover, females treated with ghrelin at puberty subsequently displayed normal estrous cyclicity and were fertile. Conversely, ghrelin administration (0.5 nmol/12 h) during the first half of pregnancy (d 1-11) resulted in a significant decrease in pregnancy outcome, as estimated by the number of pups born per litter, without changes in the number of successful pregnancies at term or gestational length. Overall, our data indicate that persistently elevated ghrelin levels, as a putative signal for energy insufficiency, may operate as a negative modifier of key reproductive states, such as pregnancy and (male) puberty onset.

Animals↗
PubMed1991

Metabolic interfaces between growth and reproduction. IV. Chronic pulsatile administration of growth hormone and the timing of puberty in the female sheep.

Puberty in the female lamb is accompanied by an increased frequency of LH pulses, and during normal development this is preceded by a decline in GH. Conversely, in the growth-retarded lamb, when LH levels are depressed by low nutrition, GH secretion is elevated. Based upon this inverse relationship, we tested the hypothesis that GH may act as a metabolic signal from the brain to inhibit the secretion of LH, and that the decline in GH times puberty. Our approach was to extend high circulating GH levels far beyond the early postnatal period, in a physiological pattern and level, in an attempt to block the pubertal LH rise. To evaluate the pattern of LH as a continuous variable under conditions of constant estradiol negative feedback, the gonadotropin was measured in blood samples collected by jugular venipuncture twice weekly; the lambs were ovariectomized and treated chronically with estradiol (Silastic capsule) beginning at 3 weeks of age. Nine lambs served as untreated controls, and 7 were infused iv with pituitary-derived bovine GH (bGH) between 5 and 28 weeks of age. A programmable backpack infusion pump delivered bGH as hourly pulses, with a total dose of 18 micrograms/kg.24 h, to maintain a physiological pattern and level of GH. At various ages, blood samples were collected at 12-min intervals for 6 h to monitor patterns and levels of peripheral LH and GH. Circulating GH in untreated and treated lambs averaged 7.7 +/- 1.5 ng/ml over a 6-h period at 4 weeks of age and declined to 1.1 +/- 0.2 ng/ml by 19 weeks in the untreated lambs; in contrast, bGH-infused lambs averaged 10.4 +/- 0.9 ng/ml at 19 weeks. Although body weights did not differ, back fat depth and quantity of perirenal fat were reduced in bGH-treated females compared to that in controls. Moreover, insulin-like growth factor-I levels were higher in bGH-treated compared with control lambs, and the bGH-treated lambs exhibited glucose intolerance, thus confirming that infused bGH was biologically active. Neuroendocrine sexual maturity, however, was not different in bGH-treated and control lambs, and it occurred at 21-22 weeks of age. The results do not support our hypothesis that decreasing GH secretion is a requirement for puberty in the sheep. Moreover, unlike in children with delayed puberty, exogenous bGH did not advance normal puberty in the lamb.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1992

Effects of rat alpha-fetoprotein administration on estradiol free fraction, the onset of puberty, and neural and uterine nuclear estrogen receptors.

The cause of the onset of puberty in the rat or any other mammalian species is unknown. According to one theory, puberty is initiated through switching of the brain "gonadostat." It is hypothesized here that puberty in the rat is the consequence of the appearance of free, and therefore physiologically active, estrogen in the circulation. To test this, the unbound fraction of estradiol in serum of immature female rats was measured in relation to the nuclear receptor occupancy of estradiol in the hypothalamus, preoptic area, and uterus at various times after birth. In addition, an attempt was made to alter the free fraction of estradiol by injection of the estradiol-binding protein alpha-fetoprotein (AFP) into immature female rats. The free fraction of estradiol was low (less than 1%), but began rising at about 20 days of age, and a significant increase in nuclear bound estradiol was observed in 23-day-old rats (P less than 0.001). By day 30, unbound levels attained adult values (3.99 +/- 0.15%). At this time, nuclear bound estradiol in all tissues examined fell (P less than 0.01), but by day 40, these were greatly increased in rats in estrus (P less than 0.001), being trebled in the preoptic areas and doubled in the hypothalamus. Injection of AFP into immature female rats extended the period of low free estradiol (1.22 +/- 0.08%), while in albumin-injected rats, the free fraction was 4.44 +/- 0.1%. Injection of AFP resulted in levels of nuclear-bound estradiol that were less than half those measured in nuclei from AFP-injected animals (P less than 0.001), and AFP delayed puberty. The affinity of the reaction between estradiol and nuclear receptors in brains of immature and mature rats was not significantly different; the Kd fell within the range of 0.05-0.08 nM. It is suggested that in the rat, puberty is the result of the appearance in the circulation of physiologically active estradiol after day 20.

Animals↗
PubMed1999

The Oct-2 POU domain gene in the neuroendocrine brain: a transcriptional regulator of mammalian puberty.

POU homeodomain genes are transcriptional regulators that control development of the mammalian forebrain. Although they are mostly active during embryonic life, some of them remain expressed in the postnatal hypothalamus, suggesting their involvement in regulating differentiated functions of the neuroendocrine brain. We show here that Oct-2, a POU domain gene originally described in cells of the immune system, is one of the controlling components of the cell-cell signaling process underlying the hypothalamic regulation of female puberty. Lesions of the anterior hypothalamus cause sexual precocity and recapitulate some of the events leading to the normal initiation of puberty. Prominent among these events is an increased astrocytic expression of the gene encoding transforming growth factor-alpha (TGF alpha), a tropic polypeptide involved in the stimulatory control of LHRH secretion. The present study shows that such lesions result in the rapid and selective increase in Oct-2 transcripts in TGF alpha-containing astrocytes surrounding the lesion site. In both lesion-induced and normal puberty, there is a preferential increase in hypothalamic expression of the Oct-2a and Oct-2c alternatively spliced messenger RNA forms of the Oct-2 gene, with an increase in 2a messenger RNA levels preceding that in 2c and antedating the peripubertal activation of gonadal steroid secretion. Both Oct-2a and 2c trans-activate the TGF alpha gene via recognition motifs contained in the TGF alpha gene promoter. Inhibition of Oct-2 synthesis reduces TGF alpha expression in astroglial cells and delays the initiation of puberty. These results suggest that the Oct-2 gene is one of the upstream components of the glia to neuron signaling process that controls the onset of female puberty in mammals.

Alternative Splicing↗
PubMed2001

Puberty in female mice is not associated with increases in either body fat or leptin.

It has been hypothesized that puberty is triggered when body fat and hence circulating levels of leptin exceed critical thresholds. Four kinds of experiments tested that hypothesis in female mice. When age was the independent variable, body fat and circulating levels of leptin decreased rather than increased before the onset of puberty. When stage of reproductive development was the independent variable, neither body fat nor circulating levels of leptin correlated with the onset of puberty. In sharp contrast, reproductive development was well correlated with body weight. A significant nocturnal peak in circulating levels of leptin was seen before and at all stages of reproductive development, but the highest levels were seen after rather than before the first estrous cycle was initiated. Neither acceleration nor deceleration of puberty by varying the female's social environment had any effect on either body fat or leptin. There is no support in any of these experiments for the hypothesis that an increase in body fat and thus an increase in circulating levels of leptin triggers puberty in female mice.

Adipose Tissue↗
PubMed1989

The production of and sensitivity to cues that delay puberty and prolong subsequent oestrous cycles in female mice are influenced by prior intrauterine position.

Four experiments were conducted with CF-1 house mice (Mus domesticus) to examine the relationship between a female's prior intrauterine position (2M = between 2 male fetuses, 1M = next to one male fetus, 0M = not next to a male fetus) and the timing of puberty and length of subsequent oestrous cycles under a variety of housing conditions. The results of Exp. 1 confirmed that the presence of males was required for females to enter puberty and exhibit regular oestrous cycles, regardless of prior intrauterine position. When housed individually after weaning either with a male in the cage or separated by a wire mesh partition, 0M-females ovulated and mated at a younger age and had shorter post-pubertal oestrous cycles than did 2M-females (1M-females were intermediate between 0M- and 2M-females). Other females were also housed after weaning with a male or separated by a wire mesh partition from a male in a variety of social environments (4 0M-females and 1 2M-female, 4 2M-females and 1 0M-female, 5 1M-females, 3 0M-females and 3 2M-females). The objective of these different housing conditions was to determine whether prior intrauterine position influenced the transmission of and/or sensitivity to cues that delay puberty and prolong subsequent oestrous cycles. Relative to 2M-females, 0M-females both produced more potent cues and were more sensitive to the cues (again, 1M-females were intermediate between 0M- and 2M-females). Specifically, in the presence of other females, puberty was delayed and post-pubertal oestrous cycles were prolonged to the greatest extent in 0M-females. Prior intrauterine position is therefore a source of individual variation in the production of and sensitivity to cues that modulate the timing of puberty and the length of subsequent oestrous cycles in female mice. The findings suggest that prenatally-androgenized 2M-females may have a reproductive advantage over other females at high population densities.

Androgens↗
PubMed1994

Factors affecting the age at onset of puberty, ovulation rate and time of ovulation in Chinese Meishan gilts.

Experiments were carried out to study: the effects of season on age at puberty, the influence of reproductive age on ovulation rate, and the time interval from the onset of oestrus to ovulation in Chinese Meishan gilts. Gilts approaching puberty either in the spring (n = 88) or in the autumn (n = 40) were housed indoors under natural daylight conditions and observed daily for oestrous behaviour. Gilts approaching puberty in the spring were younger (P < 0.001) and more likely to reach puberty by 100 days of age (P < 0.01) than were those approaching puberty in the autumn. Ovulation rate was estimated in gilts at second (n = 22), third (n = 24), fourth (n = 18), fifth to ninth (n = 9) and tenth to twenty-first (n = 17) oestrous cycle and in primiparous Meishan sows (n = 12) by counting the number of corpora lutea or corpora albicantia at laparoscopy, laparotomy or at ovarian recovery following slaughter. Ovulation rate increased (P < 0.001) with reproductive age and approached that of primiparous sows only when gilts had experienced > or = 10 oestrous cycles (19.2 versus 21.0). The time interval between the onset of oestrus and ovulation was studied in six naturally cyclic Meishan gilts and nine Meishan gilts administered hCG at the onset of oestrus. All glits were observed six times a day for the commencement of oestrous behaviour and were subsequently examined by laparoscopy at 32 h following onset of oestrous and every 8 h till ovulation, which was a maximum of 56 h.(ABSTRACT TRUNCATED AT 250 WORDS)

Aging↗
PubMed1996

Dissociation of increases in plasma insulin-like growth factor I and testosterone during the onset of puberty in bulls.

The present study was conducted to examine the relationship between plasma concentrations of testosterone, insulin-like growth factor I (IGF-I) and IGF-binding proteins (IGFBPs) during puberty, in male calves treated with GnRH or testosterone propionate. Twelve male Holstein calves (10 weeks old) were assigned to the control group (n = 6), the GnRH-treated group (n = 3) or the testosterone-treated group (n = 3). For 8 weeks, the GnRH-treated group received a single i.v. injection of GnRH (0.5 microgram kg-1 body mass) each day while the testosterone-treated group received an i.m. injection of testosterone propionate (0.5 mg kg-1 body mass) twice a day. The calves were studied until they were 200 days old. Hormone treatments were stopped one month after puberty was reached in the control group. Blood samples were collected every 30 min for 8 h every third day. Hormone concentrations were determined by radioimmunoassay. Western ligand blotting and immunoblotting, using monoclonal antibodies against IGFBP-2 and IGFBP-3, were used to characterize the IGF-binding proteins. In the control group, puberty occurred at about 120 days of age and was associated with an increase in concentrations of testosterone, IGF-I and IGFBP-3 and a decrease in concentration of IGFBP-2. In the GnRH-treated group, plasma testosterone remained low until 8 weeks after establishment of puberty in the control group (4 weeks after the end of treatment). In the testosterone-treated group, testosterone was high during the treatment period and then decreased to prepubertal values when treatment was stopped. Testosterone values increased again to reach postpubertal values 5 weeks after the end of hormone treatment. Nevertheless, independent of testosterone status, the profile of IGF-I and the IGFBPs in the GnRH- and testosterone-treated groups were parallel to that reported for the control group with the transition from prepubertal to adult values at about 120 days of age. In conclusion, concentrations of testosterone, IGF-I and IGFBP-3 increase together, but probably independently, during the onset of puberty in male calves.

Animals↗
PubMed1985

Social factors and puberty in female rats.

The effects of postweaning social conditions on the age of puberty were studied in female rats from an early- and a late-maturing strain. The postweaning living conditions consisted of the presence or absence of an adult rat (intact or gonadectomized male, or intact female), or of bedding soiled by adult males. The infantile females exposed to these conditions were caged either singly or with three peers. Puberty was studied in terms of first ovulation, verified always by ovarian histology. Females of the late-maturing strain living without peers reached puberty about 2 days earlier than females that grew up in groups of four, irrespective of the presence or absence of an adult animal. In neither strain was puberty accelerated by the presence of intact males or the soiled bedding of such males. These results do not support the view that in the rat pheromones from adult males enhance puberty in females, contrary to what is known to happen in the mouse.

Animals↗
PubMed1991

Influence of growth rate and exposure to bulls on age at puberty in beef heifers.

Two experiments were conducted to test the following hypotheses: 1) exposure of beef heifers to sterile bulls increases the proportion of heifers attaining puberty by 14 mo of age and 2) rate of growth interacts with bull exposure to influence age at puberty in beef heifers. In Exp. I, heifers were assigned to one of two treatments: 1) heifers were exposed to bulls (BE; approximately 70-d period of exposure) or 2) heifers were isolated from bulls (NE) and served as controls. In Exp. II, heifers were assigned to either BE or NE treatments (175-d period of exposure to bulls) and were fed to gain at a moderate (MG; .6 kg/d) or high (HG; .8 kg/d) growth rate. Blood samples were collected twice weekly to determine concentrations of progesterone indicative of onset of corpus luteum function and puberty. In Exp. I a greater (P less than .05) proportion of heifers receiving the BE treatment than of heifers receiving the NE treatment initiated corpus luteum function by 14 mo of age. In Exp. II, there was a bull exposure x growth rate interaction (P less than .05). The effect of bull exposure was greater within the HG groups than within the MG groups. However, heifers fed to attain a moderate or high growth rate and exposed to bulls attained puberty at younger ages than heifers not exposed to bulls and fed to attain a moderate or high growth rate. Mean ages at puberty were 375, 422, 428, and 449 (pooled SEM = 8.6) d for heifers in the BE-HG, BE-MG, NE-HG, and NE-MG groups, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Genetic effects on beef heifer puberty and subsequent reproduction.

Significant genetic variation exists within and between breeds of beef cattle for age at puberty (AP). In general, faster-gaining breed groups of larger mature size reach puberty at a later age than do slower-gaining breed groups of smaller mature size; breeds selected for milk production reach puberty at younger ages than do those breeds not selected for milk production. Heterosis, independent of heterosis effects on weight, influences most measures of puberty in females and scrotal circumference (SC) in males. Crossbred heifers reach puberty at younger ages and heavier weights than their straightbred counterparts. Scrotal circumference has been shown to be an excellent indicator of AP in yearling bulls. Furthermore, a favorable genetic relationship exists between SC in bulls and AP of female offspring. Beef cattle breeders may take a direct approach to breeding for AP and subsequent reproduction by directly selecting for measures of fertility such as SC. However, an indirect approach, involving selection for an array of traits that provide an appropriate "genetic environment" for the expression of fertility (i.e., size, milk production, calving ease) may be preferred. Although seedstock producers are limited to making change through within-breed selection, commercial producers can take advantage of both within- and between-breed selection as well as crossbreeding to achieve the same goal.

Age Factors↗