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Effects of wheat bran and energy restriction on onset of puberty, cell proliferation and development of mammary tissue in female rats.

Delayed onset of puberty and mammary development is assumed to reduce the risk of mammary cancer. An animal experiment was performed to investigate the influence of dietary fiber, which is known to affect hormonal balance, on these characteristics. Forty-five immature female rats were randomized into three groups, which were fed ad libitum a low-fiber diet (less than 0.5% dietary fiber based on white wheat flour), a high-fiber diet (9.2% dietary fiber based on wheat bran), or an energy-restricted low-fiber diet providing 90% of the energy of the ad libitum low-fiber diet. Energy intake in the second and third groups was similar. Wheat bran slightly delayed onset of puberty, whereas restricted energy intake delayed onset of puberty by about six days. At 48-58 days of age, 14 rats of the low-fiber group, 10 of the high-fiber group and 7 of the restricted group were in cycle. Development of mammary tissue was rudimentary in rats of the energy-restricted low-fiber group, stronger in the high-fiber group and strongest in the ad libitum low-fiber group. Cell proliferation in mammary tissue was similar for both groups fed ad libitum, but significantly lower in the restricted group. Peroxidase activity, a biomarker for estrogenicity, was lower in the high-fiber group than in the two low-fiber groups. It is concluded that wheat bran and, even more effectively, an imposed restricted energy intake delays onset of puberty and mammary development. This shortens the time for mammary cells to be initiated to tumor cells and hence reduces the risk of mammary cancer development.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Pinealectomy delays puberty in ewe lambs.

Fifteen pinealectomized and 15 unoperated ewes were exposed to constant light for 3 weeks before and 10 weeks after lambing. Fourteen pinealectomized and 15 unoperated ewes were allowed to lamb outdoors. Five ewe lambs born in constant light to the 2 groups of dams were pinealectomized at 10 weeks of age. Ewes and lambs were then returned to the field. Puberty (determined by weekly progesterone analysis) was significantly delayed (P less than 0.05) in the pinealectomized ewe lambs. Median pubertal age in pineal-intact ewe lambs was 37 weeks compared to 49 weeks in pinealectomized lambs. Constant light during the first 10 weeks of life had no effect upon puberty onset nor did the pineal status of the dam. Control lambs entered seasonal anoestrus at the time pinealectomized ewe lambs were entering puberty. Pinealectomized lambs entered anoestrus at the same time as control lambs were beginning their second breeding season. These results confirm a key role of pineal-mediated hormonal signals in the control of puberty in the sheep.

Anestrus↗

Effect of maternal treatment with altrenogest on age at puberty, hormone concentrations, pituitary response to exogenous GnRH, oestrous cycle characteristics and fertility of fillies.

Puberty was studied using 15 fillies of Quarter Horse phenotype. Fillies were from dams treated daily from Days 20 to 325 of gestation with: (1) 2 ml neobee oil per 50 kg body weight (controls); or (2) 2 ml altrenogest (2.2 mg/ml) per 50 kg body weight. The clitoris was measured at birth and approximately every 12 weeks until 84 weeks of age. Blood samples were collected from 9 fillies (5 treated, 4 controls) every 4 days over a 28-day period at 8-week intervals from 4 to 68 weeks of age; sampling continued every 4 days after 72 weeks of age until first oestrus. Blood samples were collected daily during oestrus (greater than or equal to 35 mm follicle) and on Days 4, 6, 10, and 14 after ovulation for the first 2 oestrous cycles. GnRH challenges (5 micrograms/kg) were administered every 8 weeks from 32 to 96 weeks of age. Puberty was defined as the first oestrus with ovulation. Beginning 1 February 1987, fillies were teased daily and their ovaries were examined by ultrasonography every 3 days (daily during oestrus). Fillies were inseminated with 500 x 10(6) motile spermatozoa from one stallion. Pregnancy was diagnosed by ultrasonography on Days 11, 12, 15 and every 5 days until Day 50 after ovulation. Prenatal altrenogest treatment caused clitoral enlargement (P less than 0.05) and increased serum concentrations of LH from 1 to 7 months of age. The amount of LH released in response to exogenous GnRH was greater (P less than 0.05) in treated fillies at 32, 64, and 72 weeks of age. Treated fillies had higher serum concentrations of FSH from 1 to 4 months (P less than 0.05), but FSH was lower (P less than 0.05) in treated fillies before and during first oestrus. Serum concentrations of LH and FSH peaked transiently at 10 months and LH was depressed from 64 to 88 weeks and began to rise 14 days before first oestrus. Concentrations of FSH began to decline 14 days before first oestrus. The median age at puberty was 90 weeks. Durations of oestrus, dioestrus, and the oestrous cycle were not different between groups and were similar to those for adult mares. First cycle pregnancy rates and overall rates were 100 and 82% and 100 and 91.7% for control and treated fillies, respectively (P greater than 0.05). Maternal treatment with altrenogest did alter gonadotrophin secretion before puberty, but had no effect on functional reproductive performance in fillies.

Animals↗

Seasonal inhibition of puberty in domestic gilts is overcome by melatonin administered orally, but not by implant.

The ability of exogenous melatonin, applied either orally or by implant, to overcome the seasonal inhibition of puberty in domestic gilts was tested in two experiments. In Expt 1, 24 gilts received two melatonin implants at 126 days of age and again at 161 days and 196 days, while 24 gilts acted as controls. All gilts were slaughtered at a mean age of 223 days. Blood samples were collected by venepuncture from eight gilts in each treatment at 126, 144 and 178 days of age and the plasma was assayed for melatonin concentration by direct radioimmunoassay. In Expt 2A, four gilts (125 days of age) were fed either 0, 1, 2 or 4 mg of melatonin at 14:00 h on each of four consecutive days. Blood samples for melatonin assay were collected via indwelling jugular catheters every 30 or 60 min from 12:00 to 22:00 h. In Expt 2B, 27 gilts were fed 1 mg of melatonin at 15:00 h each day from 129 days of age until slaughter at 221 days, while 25 gilts acted as controls. In both experiments, the presence of morphologically normal corpora lutea at slaughter was the criterion for puberty. In Expt 1, constant-release melatonin implants had no effect on the percentage of gilts which reached puberty. Among the 24 control gilts, two (8.3%) reached puberty compared with one of the 24 (4.2%) gilts with implants. In all the samples from control gilts, and in the samples taken from treated gilts prior to implantation at 126 days of age, mean plasma melatonin concentration was below the sensitivity of the assay (3.6 pg/ml).(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗

Changes in circulating and ovarian concentrations of bioactive tumour necrosis factor alpha during the first ovulation at puberty in rats and in gonadotrophin-treated immature rats.

Tumour necrosis factor alpha (TNF-alpha) concentrations were measured during periods of controlled and natural follicular development and ovulation in rat ovaries. Concentrations of bioactive TNF-alpha were determined in the ovaries and sera of rats during puberty (the period of vaginal opening and the first ovulation) and in immature rats after gonadotrophin treatment. Ovaries and sera were collected from 33-, 35-, 37-, 39-, 41- and 43-day-old rats (n = 6 or 7 per group); vaginal opening occurs on day 35. The presence of ovarian follicles and corpora lutea or ova in the oviducts was assessed. For gonadotrophin treatment, a single subcutaneous injection of 5 iu equine chorionic gonadotrophin (eCG) was administered at 08:00 h to 28-day-old rats to stimulate follicular development. A single subcutaneous injection of 10 iu human chorionic gonadotrophin (hCG) was administered 48 h later to induce ovulation. Ovaries and sera from three to six animals per group were collected 0, 3, 24, 48, 51, 54, 57, 60 and 72 h after injection of eCG. At puberty, ovarian concentrations of TNF-alpha were highest (approximately 1.1 fg micrograms-1 ovarian protein) before vaginal opening and the first ovulation. After vaginal opening and ovulation at day 37, ovarian concentrations of TNF-alpha were markedly reduced (0.091 fg microgram-1 ovarian protein) and remained low up to day 43. Serum concentrations of TNF-alpha remained low throughout the period of vaginal opening and the first ovulation (8-32 pg ml-1). In 43-day-old rats serum concentrations of TNF-alpha increased (105 pg ml-1). In the immature ovaries of 28-day-old rats TNF-alpha concentrations were highest before injection of eCG (approximately 1.2 fg micrograms-1 ovarian protein) and decreased to approximately 0.4 fg microgram-1 protein 3 h after injection. TNF-alpha concentrations decreased further 24 h after eCG injection (< 0.1 fg microgram-1 protein) and remained low until 48 h after eCG injection. Serum concentrations of TNF-alpha did not change during the 48 h period after injection of eCG. hCG was administered 48 h after eCG, and ovarian and serum TNF-alpha concentrations increased transiently. Serum TNF-alpha concentrations increased 3 h after hCG and remained elevated until 9 h after injection, after which concentrations decreased. Ovarian concentrations of TNF-alpha increased 6 h after hCG, peaked (approximately 0.5 fg microgram-1 protein), and then declined. These results indicate that during puberty and the first ovulation, circulating and ovarian TNF-alpha concentrations change. In addition, exogenous gonadotrophins alter circulating and ovarian TNF-alpha concentrations. These data suggest that TNF-alpha has a role in follicular development and ovulation during puberty and in immature rats treated with gonadotrophins to induce ovulation.

Aging↗

The timing of the onset of puberty, extension of the breeding season, and length of postpartum anestrus in the female mouflon (Ovis gmelini musimon).

The timing of the onset of puberty, duration of seasonal ovulatory activity, and length of postpartum anestrus were studied by means of blood plasma progesterone concentrations in a flock of European female mouflons (Ovis gmelini musimon) maintained in captivity under natural photoperiod (40 degrees 25'N). Concentrations of progesterone in the peripheral blood were determined by radioimmunoassay in samples collected from the jugular vein twice a week. First ovulations in the breeding season were highly synchronized and occurred in mid-October. In contrast, the cessation of ovulatory cycles showed significant variation among females and extended from February to May, depending on age, with 2-yr-old animals exhibiting the longest anovulatory period (P < 0.01). When lambing occurred within the breeding season (February-April), 12 out of 26 animals had their first ovulation 25 +/- 1.8 days after parturition. The 14 late-lambing females had the first postpartum ovulation delayed until the next breeding season. March/April-born mouflon lambs that reached a minimum threshold body weight (23.8 +/- 0.6 kg) in their first breeding season reached puberty at 8 mo of age. In those with slower growth rates, however, the prepubertal period was extended throughout the first breeding and nonbreeding seasons, reaching puberty during the breeding season of the following year at 19 mo of age and 27 +/- 0.3 kg body weight. Further, attainment of puberty in ewe lambs born in June/July was also delayed until the breeding season of the following year, when animals had reached a threshold body weight at 17 mo of age.

Analysis of Variance↗

Seizure-induced delay of puberty in female rats: effects of age, stress and opioid antagonists.

We have shown that pre- and post-pubertal female rats are sensitive to seizures. For example, daily convulsions commencing at 24 days of age delay puberty. Here we examine the effect of seizures at various ages. In addition, because opioid peptides are implicated in regulating the onset of puberty and are activated by convulsions, we also investigate the effect of opioid antagonists in the seizure-induced delay of puberty. A single daily electroconvulsive shock (ECS) was given for 10 days to neonatal (days 2-11), infantile (days 15-24) and juvenile (days 22-31) rats. The treatment delayed vaginal opening (VO) in juvenile rats. Neonatal and infantile rats were unaffected. VO was also delayed by daily ECS for only 5 days in the late juvenile (days 27-31) period. The opioid receptor antagonists naloxone, naltrexone and nalmefene injected before and after single daily ECS were unable to block this effect of ECS on VO. To examine whether the effect of ECS is related to stress, we examined several stressors known to induce opioid-mediated alterations in gonadotrophin secretion. Footshock, immobilization and ether stress administered in the juvenile period (days 27-31) did not affect the timing of VO. In addition, rats anaesthetized with halothane, and then given ECS, still showed a delay of VO. These data demonstrate that rats in the late juvenile stage of development are most sensitive to convulsions. We also suggest that opioids are not critical to the mechanism by which the ECS disturbs puberty, and that ECS elicits its effect seemingly independently of the convulsive stress.

Aging↗

Effect of active immunization against growth hormone-releasing factor on growth and onset of puberty in beef heifers.

Angus and Charolais heifers (195 +/- 7 kg) were actively immunized against growth hormone-releasing factor (GRF) to evaluate the effect on concentrations of somatotropin (ST), insulin-like growth factor I (IGF-I), insulin (INS), growth, and onset of puberty. Primary immunizations were given at 184 +/- 7 d of age (d 0 of experiment) by injecting (s.c.) 1.5 mg of GRF-(1-29)-Gly-Gly-Cys-NH2 conjugated to 1.5 mg of human serum albumin (GRFi, n = 22) or 1.5 mg of human serum albumin (HSAi, n = 21). Booster immunizations of .5 mg of antigen were given on d 62, 92, 153, and 251. Antibody binding (percentage at 1:2,000 dilution) to [125I]GRF on d 69 was greater (P less than .01) in GRFi (53.7 +/- 4.5) than in HSAi (10.1 +/- .6) heifers. Serum concentration (ng/ml) and frequency (peaks/5 h) of ST release, respectively, on d 78 were lower (P less than .01) in GRFi than in HSAi heifers (3.3 +/- .1 vs 5.6 +/- .2 and .9 +/- .3 vs 2.3 +/- .2). Serum IGF-I (ng/ml) was lower (P less than .01) in GRFi than in HSAi heifers on d 69 (41 +/- 5 vs 112 +/- 4). Serum INS (microU/ml) on d 78 was lower (P less than .05) in GRFi (2.2 +/- .1) than in HSAi (3.8 +/- .2) heifers. Feed intake, ADG, and feed efficiency were lower (P less than .05) in GRFi than in HSAi heifers. Hip height was lower (P less than .01) and fat thickness was greater (P less than .05) in GRFi than in HSAi heifers by d 132 and 167, respectively. Percentage of heifers attaining puberty (progesterone greater than 1 ng/ml for two consecutive weeks) by d 209 and 379 (12.9 and 18.5 mo of age), respectively, was lower (P less than .05) in GRFi (40.9 and 45.5) than in HSAi (81.0 and 100). In conclusion, growing heifers were successively immunized against GRF. Active immunization against GRF resulted in decreased serum concentration of ST, IGF-I, and INS. In addition, GRF immunization led to lowered feed intake, ADG, and feed efficiency, increased fat depth, and delayed onset of puberty in heifers. We propose that ST and IGF-I are important metabolic mediators involved in the initiation of puberty in heifers.

Animals↗

Reduction in age of puberty in gilts consuming melatonin during decreasing or increasing daylength.

Two experiments were conducted to determine whether oral administration of melatonin alters the onset of puberty in gilts during naturally increasing or decreasing daylength. In Exp. 1, 20 crossbred prepubertal gilts weighing 77.5 +/- .5 kg at 171.8 +/- 1.0 d of age were assigned randomly to receive either a daily oral dose of 3 mg of melatonin (MEL) or ethanol vehicle (ETH) at 1530 from August 31 to December 1, 1987 (decreasing daylength). Gilts were exposed to mature boars for 20 min thrice weekly and blood samples were collected twice weekly. Serum concentrations of progesterone were used to establish age at puberty and length of estrous cycle. In Exp. 2, 20 crossbred prepubertal gilts weighing 67.7 +/- .7 kg at 143.8 +/- 1.1 d of age received either MEL or ETH treatment from February 1 to May 15, 1988 (increasing daylength). Age of puberty was less in gilts that received MEL than in gilts that received ETH in both Exp. 1 (198 +/- 3 vs 228 +/- 7 d; P less than .01) and Exp. 2 (183.8 +/- 2.7 d vs 194.3 +/- 3.3 d; P less than .05). Gilts that received MEL reached puberty at a lighter weight than gilts that received ETH in Exp. 1 (95.6 +/- 2.1 vs 112.4 +/- 3.9 kg; P less than .01) and Exp. 2 (88.1 +/- 1.5 vs 96.0 +/- 1.8 kg; P less than .01). Serum concentrations of LH and FSH, length of estrous cycles, and percentage of muscle of carcasses were similar between MEL and ETH gilts.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

The effect of lean growth rate on puberty attainment in gilts.

Two hundred sixteen prepubertal Genex Manor hybrid F1 gilts were used to determine the impact of lean growth rate on sexual development of gilts. This study was composed of two experiments (Exp. 1 and Exp. 2). In Exp. 1, at approximately 96 d of age and 54 kg weight, gilts were allocated with respect to growth rate and litter origin to one of two dietary treatments: 1) a diet formulated to maximize lean growth potential (LP; n = 84) or 2) a diet formulated to produce a lower lean growth rate (LL; n = 84). In Exp. 2, at approximately 88 d of age and 50 kg weight, gilts were allocated with respect to growth rate and litter origin to one of two dietary treatments: 1) a diet formulated to maximize lean growth potential (LP; n = 24) or 2) a diet formulated to restrict lean growth further than was achieved in LL in Exp. 1 (RL; n = 24). All gilts were fed treatment diets for ad libitum consumption and housed in groups of six. Weight, backfat depth and loin depth, and feed intake were measured weekly. Starting at 135 d of age, gilts received 20 min of direct daily exposure to a boar as a pen group for pubertal stimulation. Puberty attainment was determined as the day gilts first exhibited the standing reflex in response to contact with a boar. At pubertal estrus, body weight, backfat depth, and loin depths were recorded. Diet affected (P < or = 0.05) estimated fat-free lean gain (LP, 424 vs LL, 347 g/d, Exp. 1; LP, 397 vs RL, 376 g/d, Exp. 2) during the growth period (start to stimulation). However, age at puberty was not affected by diet (LP, 157.3 vs LL, 157.6, Exp. 1; LP, 166.7 vs RL, 167.3, Exp. 2) or overall lean growth at stimulation (P > or = 0.05 in both experiments), confirming that innate variability in sexual development of commercial genotypes, rather than growth performance, determines onset of sexual maturity. A negative correlation between age at puberty and growth rate from 50 kg until puberty (P < or = 0.05) (LP, r = -0.40, LL, r = -0.36, Exp. 1; LP, r = -0.64, RL, r = -0.48, Exp. 2) was a consequence of reduced lean tissue growth during the stimulation period in later-maturing gilts.

Adipose Tissue↗

Induction of precocious puberty in heifers III: hastened reduction of estradiol negative feedback on secretion of luteinizing hormone.

Precocious puberty (<300 d of age) can be induced in beef heifers by early weaning and feeding a high-concentrate diet. The objective of this experiment was to determine whether precocious puberty occurs as a result of a hastened reduction of estradiol negative feedback on secretion of LH. Thirty crossbred Angus and Simmental heifers were weaned at 83 +/- 2 d of age and 114 +/- 3 kg of BW, blocked by BW, and randomly assigned to receive a high-concentrate (60% corn; H) or control (30% corn; C) diet and to receive ovariectomy (OVX), OVX plus an estradiol implant (OVXE), or to remain intact (INT). Residual ovarian tissue after OVX necessitated withdrawal of 6 heifers during the course of the experiment, resulting in the following treatment groups: OVX-C, n = 3; OVX-H, n = 5; OVXE-C, n = 4; OVXE-H, n = 2; INT-C, n = 5; INT-H, n = 5. To determine concentrations of progesterone and estradiol, blood samples were collected weekly beginning at a mean age of 160 d. To characterize LH concentrations, serial blood samples were collected at 12-min intervals for 12 h at mean ages of 119, 149, 188, 217, 246, 281, 323, 365, 407, and 449 d. By a mean age of 202 d, heifers fed the H diet were heavier (P < 0.05) than those fed the C diet. Heifers in the INT-H treatment attained puberty earlier (P < 0.05) than in the INT-C treatment (275 +/- 30 vs. 385 +/- 14 d of age, respectively). Overall mean concentrations of estradiol did not differ between OVXE-H and OVXE-C, between INT-H and INT-C, or between OVXE and INT treatments. The OVX treatments exhibited greater LH pulse frequency than the OVXE and INT treatments by the first serial blood collection (treatment x age, P < 0.05). The frequency of LH pulses was greater (P < 0.05) in the INT-H than the INT-C treatment by a mean age of 246 d and was greater (P < 0.05) in the OVXE-H than the OVXE-C treatment by a mean age of 281 d. In the OVXE-H treatment, LH secretion increased and subsequently "escaped" from estradiol negative feedback (detection of > or = 1 LH pulse/h) earlier (P < 0.05) than in the OVXE-C treatment (307 +/- 30 and 420 +/- 21 d of age, respectively). It is concluded that advancing the reduction of estradiol negative feedback on secretion of LH is the mechanism by which early weaning and feeding a high-concentrate diet results in precocious puberty in heifers.

Aging↗

Serum luteinizing hormone and estrogen profiles before puberty in the gilt.

The hypothesis that an increase in serum luteinizing hormone (LH) concentration occurs before the onset of puberty in the gilt was tested. Blood samples were collected from 14 gilts, 166 d of age and 72.6 +/- 1.8 kg body weight, every 15 min for 8 h 1 d after jugular cannulation. Gilts were checked daily for estrus with a boar. The sampling procedure was repeated 21 and 33 d later, by which time three gilts had attained puberty (first estrus with continued regular estrous cycles), and then every 7 d thereafter until an additional five gilts attained puberty. Serum LH and estrogen (E) concentrations were quantitated by radioimmunoassay. Bleeding periods were grouped into seven common physiological ages before puberty; age 1 greater than or equal to 57 d (n = 4), age 2 = 43 to 50 d (n = 5), age 3 = 31 to 38 d (n = 4), age 4 = 22 to 26 d (n = 5), age 5 = 17 to 19 d (n = 4), age 6 = 10 to 12 d (n = 5) and age 7 = 3 to 5 d (n = 5). Mean serum LH concentration (ng/ml, mean +/- SE) at age 7 (1.0 +/- .1) was greater (P less than .01) than at ages 2, 3, 4 and 5 (6 +/- .1) but not ages 1 and 6 (.8 +/- .1).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Serum profiles of progesterone, LH, FSH and prolactin immediately preceding induced puberty in gilts.

Two experiments were conducted to determine if the secretory patterns of luteinizing hormone (LH), follicle stimulating hormone (FSH) and prolactin (PRL) and serum concentrations of progesterone change immediately preceding induced puberty in gilts. To help predict when prepubertal gilts would attain puberty, gilts were induced into puberty by relocation from confinement housing to an outdoor lot and exposure to mature boars. In Exp. 1, 17 prepubertal gilts were bled on two successive days from 0800 to 1200 h before relocation and boar exposure and until the second day of estrus or for 8 d in gilts that failed to exhibit estrus. Blood samples were collected from indwelling cannulas at 20-min intervals for 4 h. In Exp. 2, blood samples were collected from 20 prepubertal gilts at 20-min intervals from 0800 to 1200 h and from 2000 to 2400 h until the second day of estrus or for 6 d if the gilt failed to exhibit estrus. In each experiment, 11 gilts exhibited pubertal estrus 3 to 6 d after relocation and boar exposure. When the frequency of LH spikes in each gilt was normalized to the day of her preovulatory surge of LH (d 0), a decline in the frequency of LH secretory spikes was observed as gilts approached puberty. However, neither the average magnitude of LH spikes nor mean LH concentrations were different among these days. Mean serum concentrations, frequency of spikes or average magnitude of secretory spikes of FSH or PRL did not change on the days preceding the preovulatory peak of LH.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Effect of unilateral hysterectomy and ovariectomy on puberty, uterine size and embryo development in swine.

Eighty crossbred gilts were assigned randomly to treatments: 1) removal of an ovary and ipsilateral uterine horn (UHO) at 130 d of age and removal of the remaining ovary and uterine horn 12 d post-puberty; 2) UHO at 130 d of age, mated and reproductive tracts recovered when slaughtered at 30 d of gestation; 3) UHO 12 d post-puberty, mated and slaughtered at 30 d of gestation and 4) unoperated controls that were mated and slaughtered at 30 d of gestation. Age of puberty was not affected by treatments. Gilts in treatment 1 had a mean ovulation rate at the pubertal estrus comparable to gilts in treatment 3. But, gilts in treatments 2 and 3 had 16% fewer (P less than .01) corpora lutea at 30 d of gestation than control gilts. Length and weight of the remaining uterine horn at 12 d post-puberty for gilts treated at 130 d of age were similar to the averages of gilts left intact. Gilts with one uterine horn had 2.2 fewer live embryos at 30 d of gestation than control gilts (P less than .01). But, the proportion of corpora lutea represented by live embryos did not differ significantly among treatments. Gilts with one uterine horn had 1.1 fewer live embryos (P less than .15) after adjustment for number of corpora lutea, less uterine space occupied by each embryo (P less than .01) and less total placental membrane per embryo (P less than .05) than control gilts.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Effect of nursing management and skeletal size at weaning on puberty, skeletal growth rate, and milk production during first lactation of dairy heifers.

Forty Israeli-Holstein 5-d-old calves were used to determine the effect of increasing calf body weight (BW) and skeletal size during the nursing period on age and skeletal size at puberty and on skeletal size and performance during first lactation. The calves were randomly allotted to 2 experimental groups as follows: milk replacer (MR) [calves were given 0.450 kg/d dry matter of milk replacer for the first 50 d of life] and milk-fed (MF) [calves had free access to milk in two 30-min meals/d]. From weaning to 180 d of age, all calves were fed the same diet. At 180 d of age, the MR and MF calves were each divided into 2 equal subgroups: one subgroup from each treatment was given only growing ration, and the other was given the same ration supplemented with fish meal to supply 2% crude protein (CP) (treatments MR + CP and MF + CP, respectively). Finally, at 270 d of age, all calves were housed together and fed a growing heifer's ration until first calving. During the entire nursing period, the MF calves consumed 9.8% more DM, 39.7% more CP, and 52.4% more metabolizable energy than the MR calves. At 60 d of age, BW and all skeletal parameters were higher in the MF calves than in the MR calves. During the entire rearing period (60 to 550 d), the average BW of the MF calves was greater by 16 kg than the BW of the MR calves. Nursing management did not affect differences in skeletal parameters at calving. Average age at puberty onset was 272 +/- 26.8 d; MF calves reached puberty 23 d earlier than MR calves. Yields of milk (kg/305 d) and fat-corrected milk (FCM, kg/d) were greater for the MF + CP heifers than for the MR heifers. It was concluded that nursing by ad libitum milk, as compared with milk replacer, affected BW but not skeletal size of the adult animal, decreased age of puberty onset, and increased FCM yield at first lactation. Supplementing the diet with 2% CP during the prepubertal period increased BW but not skeletal size of the adult animal and 305-d milk and FCM yields during first lactation.

Animal Feed↗

Alpha-difluoromethylornithine modifies FSH secretion and puberty onset in the female rat.

FSH secretion is high in immature female rats from Postnatal Day 5 to 18 and decreases thereafter. This is a relatively steroid-independent event of cerebral origin and of importance for puberty onset. Polyamines, a group of ubiquitous amines, play an essential role in tissue growth and differentiation, body weight increment, brain organization, and molecular mechanisms of hormonal action. Polyamine levels as well as the activity of ornithine decarboxylase, the limiting enzyme in polyamines biosynthesis, are highest during development. Inhibition of their synthesis during this period by alpha- difluoromethylornithine (DFMO), a specific and irreversible inhibitor of ornithine decarboxylase, impairs normal brain development. The present study tested the hypothesis that polyamines play a role during brain organization of reproduction. DFMO was administered following different schedules in female newborn rats, and the effect on pituitary secretion, puberty onset, and fertility was evaluated. In three groups (daily injections from Day 1 to 9, or from Day 1 to 6, or injections on alternative days from Day 1 to 9), a delay in vaginal opening and first estrous was observed. When vaginal opening was plotted against body weight, it was evident that in groups daily injected with DFMO vaginal opening occurred at a lower body weight. In the group treated on alternate days, a delay occurred but at a higher body weight than in controls. In this group, serum FSH levels on Day 10 and 20, but not on Day 30, were higher in DFMO rats. In the group treated from Day 1 to 6 daily, DFMO increased serum FSH on Postnatal Day 20. After vaginal opening, estrous cyclicity in control and DFMO injected rats was similar. There was no significant effect of treatment on fertility and litter weight or number of offspring at birth. It is concluded that DFMO, an inhibitor of ornithine decarboxylase, administered during the first week of life in female rats is followed by prolonged high FSH serum levels and delayed puberty, but once puberty occurs, fertility is normal.

Animals↗

Postweaning exposure to gossypol results in epididymis-specific effects throughout puberty and adulthood in rats.

Gossypol, a yellow pigment found in cottonseeds, well known for its antifertility properties in animals, has been used as a contraceptive by men. The aims of this work were to evaluate the effects of gossypol throughout sexual development of male rats and to provide additional data to clarify the target site or sites of this compound in the male reproductive system. Gossypol (15 mg/kg per day) was given to animals from weaning through prepuberty (41 days), early puberty (51 days), puberty (61 days), and sexual maturity (91 days). Ventral prostate weight and fructose levels were similar in control and treated rats, suggesting that androgen levels were normal. No histological effects on the testis were detected, but there was a significant decrease in the sperm concentration in the cauda epididymidis of gossypol-treated animals killed at 61 and 91 days, as well as a significant increase in abnormal sperm in the vas deferens of treated animals. Moreover, the histology of the cauda epididymidis of the rats treated throughout puberty (ie, until days 51 and 61) showed a great number of round bodies in the lumen of the epididymis. These structures stained for the epididymis-specific protein E. Collectively, the data demonstrate that the epididymis is a target of gossypol when postweaning exposure extends throughout pubertal development, and that whereas more subtle histological effects commence around puberty, indicators reproductive competence are compromised in adulthood.

Aging↗

[Effect of restored 5alpha-androgens on puberty in female rats].

The female rats at a prepubertal period were introduced to the restored 5 alpha-androgens, namely: 5 alpha-dihydrotestosterone (DHT), 5 alpha-androstane-3 alpha, 17 beta-diol (3 alpha-diol) or 5 alpha-androstane-3 beta, 17 beta-diol (3 beta-diol) in the dose of 5 mg/100 g. Both DHT and 3 alpha-diol have been determined to induce the vaginal opening as the initial stage of puberty. Stimulation of the puberty in those rats was followed with an activation of both endocrine and generative functions of the ovaries. DHT inhibited the gonadotrophic activity of the hypophysis that delayed the ovulation as the final stage of puberty. The DHT metabolite 3 alpha-diol hastened the first ovulation, while 3 beta-diol did not influence the pace of the puberty. The stimulating effect of DHT at the initial stage of the pubescence in the female rats has been suggested to be due to its conversion into 3 alpha-diol which is likely to be one of the key factors in the pubescence control in rats.

Androstane-3,17-diol↗