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The effects of intra-uterine growth retardation and postnatal undernutrition on onset of puberty in male and female rats.

The nutritional status, prenatally and early postnatally, plays a critical role in postnatal growth and development. Early malnutrition may change the original programming of organs, especially those in developmental phases, which can result in long-term changes in metabolism. The association between a low birth weight and the increased risk on type 2 diabetes, hypertension and cardiovascular disease is well known. In the present study we investigated whether intrauterine malnutrition or direct postnatal food restriction affects the onset of puberty in male and female rats. Intrauterine growth retardation (IUGR) was induced by uterine artery ligation on day 17 of gestation and postnatal food restriction (FR) by litter-enlargement to 20 pups per mother from day 2 after birth until weaning (24 d). Both models of malnutrition resulted in a persistent growth failure postnatally. The parameter of the onset of puberty was balano-preputial-separation (BPS) in the male rat and vaginal opening (VO) in the female rat. In both male IUGR (n = 26) and FR (n = 20) rats, the age at BPS was significantly delayed, with 48.1 +/- 1.9 d (p < 0.0001) and 50.4 +/- 2.9 d (p < 0. 0001), respectively, compared with controls (n = 30) with 45.8 +/- 1.4 d. In female IUGR rats (n = 37) the age at VO was significantly delayed, with 37.4 +/- 2.7 d (p < 0.04) compared with 36.1 +/- 1.5 d in controls (n = 23), but not in female FR rats (n = 18) with 36.5 +/- 2.2 d. Weight at onset of puberty did not differ between male IUGR and control rats, 194.5 +/- 20.0 g and 201.7 +/- 16.8 g, respectively, but was significantly lower in male FR rats with a weight of 175.6 +/- 17.5 g (p < 0.0001). In female IUGR as well as in female FR rats, weight at onset of puberty was significantly lower compared with controls: weight in IUGR 106.1 +/- 13.1 g (p < 0.001), weight in FR 85.3 +/- 7.6 g (p < 0.0001) and weight in controls 116.9 +/- 9.3 g. We conclude that early malnutrition, during late gestation or direct postnatally, results in a delayed onset of puberty in IUGR and FR male rats and in IUGR female rats, but not in FR female rats. The onset of puberty in these growth retarded rats as well as in controls does not depend on the achievement of a certain, crucial weight. The perinatal period appears to be a "critical time period" for the maturational process of pubertal development.

Age Factors↗

Insulin-like growth factor I of peripheral origin acts centrally to accelerate the initiation of female puberty.

In several species, including humans, circulating insulin-like growth factor I (IGF-I) levels increase during the onset of puberty, suggesting that this peptide contributes to attaining sexual maturity. Because IGF-I elicits LHRH release from the median eminence (ME) of immature female rats in vitro, we hypothesized that it may represent one of the peripheral signals suspected to link somatic development to the LHRH-releasing system at puberty. We now present evidence in support of this concept. Quantitation of IGF-I messenger RNA (mRNA) levels by ribonuclease protection assay revealed that expression of the IGF-I gene did not change in the medial basal hypothalamus or preoptic area of female rats during peripubertal development. In contrast, the contents of both IGF-Ia and IGF-Ib mRNA, the two alternatively spliced forms of the IGF-I gene, increased significantly in the liver during the early proestrous phase of puberty. This change was followed by an elevation in serum IGF-I levels during the late proestrous phase of puberty along with a concomitant increase is serum gonadotropin levels. The proestrous change in serum IGF-I levels was accompanied by a selective increase in IGF-I receptor (IGF-IR) mRNA in the ME. Small doses of IGF-I (2-200 ng), administered intraventricularly, effectively induced LH release in both juvenile and peripubertal female rats, an increase prevented by prior immunoneutralization of LHRH actions. Importantly, intraventricular injections of IGF-I (20 ng), administered twice daily in the afternoon to immature animals, significantly advanced puberty. Thus, these results suggest that IGF-I of peripheral origin contributes to the initiation of female puberty by stimulating LHRH release from the hypothalamus, an effect that appears to be amplified by the increased synthesis of IGF-I receptors in the ME during first proestrus.

Animals↗

A role of gamma-amino butyric acid (GABA) and glutamate in control of puberty in female rhesus monkeys: effect of an antisense oligodeoxynucleotide for GAD67 messenger ribonucleic acid and MK801 on luteinizing hormone-releasing hormone release.

Previously we have shown that gamma-aminobutyric acid (GABA) is an inhibitory neurotransmitter restricting the pubertal increase in LHRH release in juvenile monkeys, and that interfering with GABA synthesis with an antisense oligodeoxynucleotide (AS) for glutamic acid decarboxylase (GAD67) mRNA results in an increase in LHRH release in prepubertal monkeys. GAD67 is a catalytic enzyme that synthesizes GABA from glutamate. To further clarify the role of GABA in puberty, we examined whether the inhibition of LHRH release by GABA continues after the onset of puberty and whether input from glutamatergic neurons plays any role in the onset of puberty when GABA inhibition declines, using a push-pull perfusion method. In Study I, the effects of the AS GAD67 mRNA on LHRH release in pubertal monkeys (34.3 +/- 1.5 months of age, n = 8) were examined, and the results were compared with those in prepubertal monkeys (18.5 +/- 0.4 months, n = 12). Direct infusion of AS GAD67 (1 microM) into the stalk-median eminence (S-ME) for 5 h stimulated LHRH release in both prepubertal and pubertal monkeys. However, the increase in LHRH release in pubertal monkeys was significantly (P < 0.01) smaller than that in prepubertal monkeys. Infusion of a scrambled oligo as a control was without effect in either group. In Study II, to examine the possibility that an increase in glutamate tone after the reduction of an inhibitory GABA tone contributes to the AS GAD67-induced LHRH increase, the effects of the NMDA receptor blocker MK801 (5 microM) on LHRH release were tested in monkeys treated with AS GAD67. MK801 infusion into the S-ME during the treatment of AS GAD67 (1 microM) suppressed the AS GAD67-induced LHRH release in both age groups. MK801 alone did not cause any significant effect in either group. The data are interpreted to mean that GABA continues to suppress LHRH release after the onset of puberty, although the degree of suppression is weakened considerably after the onset of puberty, and that the increased LHRH release after AS GAD67 treatment may be partly due to an increase in glutamate tone mediated by NMDA receptors, as well as due to the decrease in GABA release following the decrease in GAD synthesis. Taken together, the present results suggest that GAD may play an important role in the onset and progress of puberty in nonhuman primates.

Animals↗

Impact of androgens, growth hormone, and IGF-I on bone and muscle in male mice during puberty.

UNLABELLED: The interaction between androgens and GH/IGF-I was studied in male GHR gene disrupted or GHRKO and WT mice during puberty. Androgens stimulate trabecular and cortical bone modeling and increase muscle mass even in the absence of a functional GHR. GHR activation seems to be the main determinant of radial bone expansion, although GH and androgens are both necessary for optimal stimulation of periosteal growth during puberty. INTRODUCTION: Growth hormone (GH) is considered to be a major regulator of postnatal skeletal growth, whereas androgens are considered to be a key regulator of male periosteal bone expansion. Moreover, both androgens and GH are essential for the increase in muscle mass during male puberty. Deficiency or resistance to either GH or androgens impairs bone modeling and decreases muscle mass. The aim of the study was to investigate androgen action on bone and muscle during puberty in the presence and absence of a functional GH/insulin-like growth factor (IGF)-I axis. MATERIALS AND METHODS: Dihydrotestosterone (DHT) or testosterone (T) were administered to orchidectomized (ORX) male GH receptor gene knockout (GHRKO) and corresponding wildtype (WT) mice during late puberty (6-10 weeks of age). Trabecular and cortical bone modeling, cortical strength, body composition, IGF-I in serum, and its expression in liver, muscle, and bone were studied by histomorphometry, pQCT, DXA, radioimmunoassay and RT-PCR, respectively. RESULTS: GH receptor (GHR) inactivation and low serum IGF-I did not affect trabecular bone modeling, because trabecular BMD, bone volume, number, width, and bone turnover were similar in GHRKO and WT mice. The normal trabecular phenotype in GHRKO mice was paralleled by a normal expression of skeletal IGF-I mRNA. ORX decreased trabecular bone volume significantly and to a similar extent in GHRKO and WT mice, whereas DHT and T administration fully prevented trabecular bone loss. Moreover, DHT and T stimulated periosteal bone formation, not only in WT (+100% and +100%, respectively, versus ORX + vehicle [V]; p < 0.05), but also in GHRKO mice (+58% and +89%, respectively, versus ORX + V; p < 0.05), initially characterized by very low periosteal growth. This stimulatory action on periosteal bone resulted in an increase in cortical thickness and occurred without any treatment effect on serum IGF-I or skeletal IGF-I expression. GHRKO mice also had reduced lean body mass and quadriceps muscle weight, along with significantly decreased IGF-I mRNA expression in quadriceps muscle. DHT and T equally stimulated muscle mass in GHRKO and WT mice, without any effect on muscle IGF-I expression. CONCLUSIONS: Androgens stimulate trabecular and cortical bone modeling and increase muscle weight independently from either systemic or local IGF-I production. GHR activation seems to be the main determinant of radial bone expansion, although GHR signaling and androgens are both necessary for optimal stimulation of periosteal growth during puberty.

Androgens↗

Leptin and thyroxine during sexual development in male monkeys: effect of neonatal gonadotropin-releasing hormone antagonist treatment and delayed puberty on the developmental pattern of leptin and thyroxine secretion.

OBJECTIVE: Neonatal treatment of male monkeys with a gonadotropin-releasing hormone antagonist (Ant) increased the incidence of delayed puberty. Using blood samples that had been collected from monkeys with normal or delayed puberty, we assessed the potential involvement of leptin and thyroxine (T4) in sexual development. DESIGN AND METHODS: Monkeys were treated from birth until 4 months of age with vehicle, Ant or Ant/androgen and blood samples were drawn from 10 to 62 months of age. RESULTS: Serum leptin and total T4 concentrations declined in parallel throughout adolescence in all treatment groups. There was no transient rise in leptin before or in association with the onset of puberty. Also, leptin did not differ during the peripubertal period between animals experiencing puberty at that time versus those in which puberty was being delayed. Neonates treated with Ant either alone or with androgen replacement had higher leptin levels than controls throughout development. While leptin exhibited no significant changes during the peripubertal period, T4 values increased and declined in parallel with the peripubertal changes in hypothalamic-pituitary-testicular activity. CONCLUSIONS: These data do not support the concept that a transient rise in leptin triggers the onset of puberty in male monkeys. However, the disruption of neonatal activity of the pituitary-testicular axis alters the developmental pattern of leptin. The changes in T4 levels during the peripubertal period suggest that thyroid status may be a significant contributor to the process of sexual development in the male monkey and that peripubertal changes in secretion of this hormone may serve as an effective physiological response during a critical period of elevated energy expenditure.

Aging↗

A study of seasonally delayed puberty in the male hare, Lepus Europaeus.

The brown hare, Lepus europaeus, has a mating season which extends from January to September. Adult males exhibit pronounced seasonal changes in the reproductive tract which are associated with changes in LH secretion. Maximum plasma levels of immunoreactive LH occur between March and June and minimal levels in the autumn non-mating period from September to December; this seasonal cycle in gonadotrophin output is reflected by the appropriate changes in the secretion of testosterone from the testes and in the activity of the accessory sex glands. Juvenile animals reach puberty only during the adult mating season, and the age of puberty thus varies with the date of birth. Males born before May reach puberty and become fertile at 3 months of age, while those born from May to July grow to a mature body size during the autumn non-mating season but puberty is delayed for several months. Since some animals experiencing delayed puberty were found to have elevated plasma levels of LH and testosterone, it is concluded that puberty is not completely suppresed by the environmental effects of the autumn, but that the developmental process is prolonged, resulting in the juveniles being synchronized with the adults in their reproductive activity.

Age Factors↗

Effects of oestradiol, zeranol or trenbolone acetate implants on puberty, reproduction and fertility in heifers.

The effects of anabolic agents on reproduction in beef heifers were determined by using 300 mg trenbolone acetate (TBA), 36 mg zeranol and 19 mg oestradiol-17 beta in a biodegradable pellet (1E: American Cyanamid, USA), or two such pellets (2E). On Day 1 of experiment, 81 Hereford x Friesian heifers (mean age = 84 +/- 1.2 days) were allocated at random to the following treatments: (1) controls (N = 15); (2) TBA (N = 15); (3) 1E (N = 12); (4) 2E (N = 15); (5) zeranol (N = 13); (6) TBA + 2E (N = 11). The 1 (1E), or 2 (2E) oestradiol implants were administered on Day 1 of the experiment only. Heifers assigned to receive TBA and zeranol were implanted on Days 1, 84, 168 and 252. Blood progesterone concentrations and oestrous activity were monitored from Days 137 and 200 respectively. Mean age (days) and weight (kg) at puberty (first ovulation), for heifers that reached puberty in Groups 1-6 respectively were 352 and 308, 419 and 356, 373 and 325, 381 and 331, 400 and 353, 423 and 383 [residual standard deviation (r.s.d.) = 43.8 and 39.4 for age and weight respectively]. Heifers in Group 4 were older (P less than 0.05), but not heavier (P greater than 0.05), while those in Groups 2 and 5 were both older (P less than 0.005) and heavier (P less than 0.005) than the controls at puberty. Age and weight at puberty were not different in heifers assigned to Groups 3 and 4, or to Groups 2 and 6. The proportion of heifers showing oestrus before puberty (prepubertal oestrus) were 3/15, 12/15, 6/12, 7/15, 10/13 and 11/11 in Groups 1-6 respectively. Heifers in Groups 2 and 5 had higher incidences of prepubertal oestrus than controls, while those in other treatment groups were not different. There was no treatment effect on the incidence of silent ovulations, but the incidence of non-ovulatory oestrus, after puberty, was increased from 4/48 in Group 1 to 26/40 (P less than 0.001), 15/56 (P less than 0.05) and 34/57 (P less than 0.001) in Groups 2, 4 and 5, respectively. Heifers in Group 6 had a higher incidence of non-ovulatory oestrus (P less than 0.05), but not of prepubertal oestrus, than did those in Group 2.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

Management considerations in heifer development and puberty.

Management of replacement beef heifers should focus on factors that enhance physiological processes that promote puberty. Age at puberty is important as a production trait when heifers are bred to calve as 2-yr-olds and in systems that impose restricted breeding periods. Calving by 24 mo of age is necessary to obtain maximum lifetime productivity. Because the reproductive system is the last major organ system to mature, factors that influence puberty are critical. The influence of environment on the sequence of events leading to puberty in the heifer is dictated largely by the nutritional status of the animal and related effects on growth rate and development. Management strategies have been designed to ensure that heifers reach a prebreeding target weight that supports optimum reproductive performance, and consequences of inadequate or excessive development have been evaluated. Those strategies are based on evidence linking postweaning nutritional development with key reproductive events that include age at puberty and first breeding, conception, pregnancy loss, incidence and severity of dystocia, and postpartum interval to estrus. Management alternatives that ultimately affect lifetime productivity and reproductive performance of heifers begin at birth and include decisions that involve growth-promoting implants, creep-feeding, breed type and(or) species, birth date and weaning weight, social interaction, sire selection, and exogenous hormonal treatments to synchronize or induce estrus. Basic and applied future research efforts should converge to match in a realistic manner the production potential of the animal with available resources. Strategies that incorporate consideration of nutrition, genetics, and emerging management techniques will need to be tested to enable producers to make decisions that result in profit. This review evaluates the current status of knowledge relating to management of the replacement beef heifer and serves to stimulate research needed to enhance management techniques to ensure puberty at an optimal age.

Animal Feed↗

The effects of ruminally undegradable protein, propionic acid, and monensin on puberty and pregnancy in beef heifers.

Two hundred ten spring-born English crossbred beef heifers were used in two experiments in consecutive years using a randomized complete block design. The objectives were to determine the effects of increasing dietary intake of ruminally undegradable protein or propionic acid on the occurrence of puberty and to elucidate the mechanism by which monensin decreases age of puberty in beef heifers. Diets were fed for 120 d beginning in mid-November and consisted of mature grass hay and barley straw with .45 kg.animal-1 x d-1 supplement (CON) formulated to obtain .4 kg.animal-1 x d-1 of BW gain; .5 kg of supplement similar to CON and containing an additional 250 g of ruminally undegradable intake protein supplied from blood and corn gluten meal (UIP); .45 kg of supplement similar to CON composition and containing 400 g.animal-1 x d-1 of a 50% water and 50% propionic acid mixture (PROP); or .45 kg of supplement similar to CON supplying 200 mg.animal-1 x d-1 of monensin (MON). The hay:straw ratio in each diet was adjusted biweekly, to maintain similar BW gains for heifers fed each dietary treatment. As planned, BW gains were similar (P > .1) for all heifers. The heifers fed MON were 21 d younger (P < .05) at first estrus than heifers fed UIP; CON and PROP were intermediate and similar to heifers fed MON and UIP. The heifers fed UIP were 7 to 8 kg heavier (P < .05) at puberty than CON- or PROP-treated heifers. The heifers fed PROP were 6 kg heavier (P < .1) at puberty than heifers fed MON. Heifers that received UIP required less (P < .05) TDN than did heifers that received CON or PROP to achieve similar gain. Pregnancy rate was similar for all treatment groups. Feeding UIP in excess of NRC CP requirements may improve energy utilization of heifers fed mature roughages but may delay the onset of puberty compared with heifers fed monensin. This study demonstrated that nutrient composition of the diet may influence age of puberty independent of growth rate.

Animal Feed↗

Effect of nutritional management, trace mineral supplementation, and norgestomet implant on attainment of puberty in beef heifers.

We conducted a study to evaluate the influences of nutritional management, trace mineral supplementation, and exogenous progesterone on attainment of puberty in beef heifers. Heifers (n = 180) were assigned at weaning to blocks and treatments. Treatments included two dietary regimens (corn silage vs pasture + oatlage), trace mineral supplementation, and puberty induction strategy (with or without progestin implant). Heifers that received pasture + oatlage were managed on grass-legume pastures from October 14 until December 14 and were then placed in pens and fed an oatlage-based diet through May 1994. Heifers fed the corn silage-based diet were housed in pens throughout the study. Norgestomet was implanted in half of the heifers on April 11 for 10 d. Progestin implant increased (P < .05) the number of heifers that had attained puberty by the end of the study, compared with nonimplanted heifers (89% vs 71%). Trace mineral supplementation did not affect percentage of heifers that reached puberty before the implant period. Plasma copper levels were below recommended levels in heifers fed oatlage-based diets without trace minerals. We conclude that heifers can be placed on regrowth in irrigated pastures during the fall and still make acceptable gains for attainment of puberty the following spring and that progestin treatment can aid in inducing heifers to reach puberty.

Animal Nutritional Physiological Phenomena↗

Germplasm evaluation in beef cattle--Cycle IV: postweaning growth and puberty of heifers.

Postweaning growth, puberty, and pregnancy traits were evaluated for 783 F1 heifers sired by Angus, Hereford, Charolais, Shorthorn, Galloway, Longhorn, Nellore, Piedmontese, and Salers bulls and out of Angus and Hereford dams in Cycle IV of the Germplasm Evaluation (GPE) Program at the U.S. Meat Animal Research Center. The Hereford and Angus sires included a sample of bulls born from 1982 to 1985 (1980s HA) as well as reference sires born from 1963 to 1970 (REF HA) used in previous cycles of the GPE program. Breed group of sire had a significant (P<.01) effect on age and weight at puberty, on 200-, 400-, and 550-d weights, on ADG from 200 to 400 and from 400 to 550 d, and 550-d hip height, but it did not influence (P<.05) pregnancy rate. Mean age and weight at puberty were predicted from the cumulative distribution because of censoring of data in each tail of the distribution. Sire breed group rankings (and predicted means in days) for age at puberty were as follows: Piedmontese (332), Shorthorn (338), Charolais (348), REF HA (348), Galloway (351), 1980s HA (352), Salers (355), Longhorn (357), and Nellore (405). Sire breed group rankings (and predicted means in kilograms) for weight at puberty were Longhorn (283), Piedmontese (298), Galloway (305), REF HA (309), Shorthorn (329), 1980s HA (330), Salers (338), Nellore (341), and Charolais (345). Sire breed group rankings (and least squares means in kilograms) for 200-d weight were Charolais (229), Salers (225), Nellore (221), Shorthorn (220), Piedmontese (215), 1980s HA (215), Galloway (209), REF HA (206), and Longhorn (197), with differences >8.3 kg significant. Rankings for 400-d weight (kilograms) were Charolais (390), Shorthorn (384), Salers (380), 1980s HA (374), Nellore (364), REF HA (356), Piedmontese (353), Galloway (348), and Longhorn (321), with differences >11.5 kg significant. Rankings for 550-d weight (kilograms) were Charolais (445), Salers (430), Shorthorn (429), 80's HA (422), Nellore (420), Piedmontese (401), REF HA (398), Galloway (389), and Longhorn (371), with differences >11.7 kg significant. Rankings for 550-d hip height (centimeters) were Nellore (132.2), Charolais (131.9), Salers (129.9), Shorthorn (129.5), Piedmontese (126.7), 1980s HA (126.1), Longhorn (125.3), Galloway (121.7), and REF HA (121.5), with differences >1.35 cm significant. Breed of sire had significant effects on growth and puberty traits of heifers.

Animals↗

Incidence of puberty in beef heifers fed high- or low-starch diets for different periods before breeding.

Spring-born Hereford x Angus heifers (n = 206) were used to determine effects of energy supplementation programs and amount of starch in the diet on incidence of puberty. In Exp. 1, heifers (205 +/- 5 kg; n = 68) grazing dormant native pasture were fed 0.9 kg/d (as-fed basis) of a 42% CP supplement from November until February 14. Heifers were stratified by weaning weight and allotted randomly to treatment before breeding (May to July). Treatments were 1) 0.9 kg (as-fed basis) of a 42% CP supplement/d and pasture (control); 2) a high-starch (HS) diet (73% corn; 53% starch) fed in a drylot for 60 d (HS-60); 3) a HS diet fed in drylot for 30 d (HS-30); or 4) a low-starch (LS) diet (49% corn; 37% starch) self-fed on pasture for 30 d (LS-30). The HS-60 and HS-30 heifers were limited-fed to gain 0.9 kg/d, and the LS-30 heifers had ad libitum access to the diet. High-starch-60 and LS-30 heifers were heavier (P < 0.05) than control and HS-30 heifers at the beginning of the breeding season. Thirty-one, 25, and 26% more HS-60 heifers were pubertal (P < 0.05) on May 1 compared with LS-30, HS-30, and control heifers, respectively. At puberty, HS-60 heifers were 24 and 22 d younger (P < 0.05) than LS-30 and control heifers, and 31 kg lighter (P < 0.01) than LS-30 heifers. In Exp. 2, heifers grazed dormant pasture and were fed 0.9 kg (as-fed basis) of a 42% CP supplement/d from weaning in October to late February; then heifers were assigned randomly to treatments for 60 d before the breeding season. In two years, control heifers (n = 46) grazed pasture and received 0.9 kg of SBM supplement/d; LS (n = 46) heifers were self-fed a distiller's grain and soybean hull-based diet in drylot; and HS heifers (n = 46) were limited-fed a corn-based diet in drylot. During treatment, HS and LS heifers had greater weight gains than control heifers. Pubertal BW (313 +/- 6 kg) was not influenced by treatment, but HS and LS heifers were younger (P < 0.03) than control heifers at puberty. During a 60-d breeding period, the incidence of puberty was greater (P < 0.05) for HS and LS heifers than for control heifers and was greater (P < 0.05) in HS than in LS heifers in Year 1. Feeding a LS or a HS diet for 30 d before breeding may be inadequate to stimulate puberty in beef heifers, but feeding a diet with a greater amount of starch for 60 d before breeding may increase the incidence of puberty during breeding of heifers that have inadequate yearling weight.

Animal Feed↗

Relationship of growth and puberty in beef heifers fed monensin.

An experiment was designed to determine the effects of dietary monensin on age and weight at puberty in Bos taurus crossbred beef heifers. One hundred and forty heifers were allotted to two weight classes: heavy (H) and light (L) groups, consisting of heifers above and below the average weaning weight, respectively. Heifers within each weight class were assigned to one of three diets during a 203-d winter feeding period: (1) R, 80% roughage: 20% concentrate; (2) M1, R diet plus monensin (200 mg/head daily) with feed intake restricted to produce average daily gains (ADG) similar to R and (3) M2, R diet plus monensin (200 mg/head daily). ADG was higher (P less than .001) for M2 heifers than for R and M1 heifers, which performed similarly. Age and weight at puberty were similar across treatments in L heifers. However, in the H group, HM1 and HM2 heifers were younger (P less than .07) at puberty than HR heifers and this difference was not removed by covariate adjustment of either ADG or body weight. Weigh at puberty was greater (P less than .01) for HM2 heifers than for HM1 or HR heifers; however, this difference was removed by covariate adjustment of either ADG or body weight. Ninety-one percent of LM2 heifers and 100% of all other groups had reached puberty before the breeding season. Pregnancy rates did not differ significantly between treatment groups. Supplementation of a high roughage diet with monensin decreased age at puberty of heifers in the heavy weight class and this decrease was not due to increased body weight or ADG. Perhaps heifers with above average weaning weight possess a greater inherent growth potential than heifers below the average weaning weight and hence are more capable of utilizing monensin to an advantage.

Acetates↗

The influence of photoperiod on the onset of puberty in the female rabbit.

Seventy-six New Zealand white does born between June 28, 1979 and April 6, 1980 were used in an experiment of 2 X 2 X 2 factorial design to determine if 1) exposure to 18 h (L) or 6 h (D) of light/d beginning at weaning influenced age and body weight at puberty and 2) if mating and(or) hormone treatment at puberty influenced ovulation rate and number of embryos. Beginning at weaning, estrus was checked daily using males known to be fertile. At first expression of estrus, does were either mated or nonmated and were injected iv with either 30 IU human chorionic gonadotropin (hCG), or saline. Means for the L and D groups for age at puberty (d), body weight at puberty (kg), ovarian weight (g) and number of embryos 5 d postcoitus were 105 +/- 3.6 vs 121.9 +/- 4.1 (P less than .01); 2.65 +/- .07 vs 2.87 +/- .08 (P less than .05); .56 +/- .04 vs .78 +/- .04 (P less than .001) and 6.1 +/- .83 vs 3.44 +/- .67 (P less than .01), respectively. Photoperiod did not influence number of ovulations. Number of embryos relative to number of ovulations were higher in rabbits exposed to 18 h of light. Does that were both mated and hormone-treated had more (P less than .025) corpora lutea (11.0 +/- .9) than does that were either hormone-treated (7.7 +/- .86) or mated (7.0 +/- .97) only. Mated does had heavier uteri (10.8 +/- .5 vs 7.9 +/- .5) while hormone treatment increased both ovarian and uterine weights (g) over nontreated does (.74 +/- .04 vs .59 +/- .05; 9.9 +/- .45 vs 8.8 +/- .65). Multiple regression analysis revealed that does born in summer reached puberty later than those born during other seasons. It was concluded that season of birth and exposure of does to 18 h of light from weaning affect onset of puberty. Increasing daily light exposure from 6 to 18 h/d may improve litter size in pubertal does.

Animals↗

Long-day photoperiod that enhances puberty does not limit body growth in Holstein heifers.

Previous research has demonstrated that extended photoperiod accelerates pubescence in dairy heifers thereby limiting time for mammary development, which could be detrimental to future milk yield. We hypothesized that the potential negative effects of rapid growth and puberty through long-day photoperiod (LDPP) exposure could be overcome with a greater supply of metabolizable protein in dairy heifers fed rumen-undegradable protein (RUP). In an initial slaughter study, we compared deuterium oxide (D2O) and direct chemical analysis to assess body composition at 5 and 7 mo of age in heifers (n = 20) exposed to LDPP or short-day photoperiod (SDPP). Before slaughter, D2O dilution was used to estimate body composition and results were compared with actual values determined by direct chemical analysis of body tissue. In 5-mo-old heifers, the correlations between estimates of body protein, water, and mineral contents as determined by D2O dilution and direct chemical analysis of body tissue were 0.86, 0.85, and 0.76, respectively; however, fat content values were not correlated (r = -0.068). In 7-mo-old heifers, we were unable to accurately estimate body composition using the D2O dilution method. A second study was conducted to determine if LDPP, which has previously been shown to hasten puberty, could be combined with RUP to promote lean growth without limiting body stature in prepubertal heifers. Thirty-two weaned heifers (86 +/- 2 d old; 106.2 +/- 17.3 kg of body weight) were assigned to LDPP or SDPP and RUP or control diet in a 2 x 2 factorial arrangement until the onset of puberty. Relative to SDPP, LDPP increased prolactin secretion and promoted lean growth. Exposure to LDPP also enhanced body weight, withers height, and heart girth. Furthermore, RUP supplementation increased withers height and heart girth. There was a significant interaction between LDPP and RUP for hip height. Moreover, LDPP hastened the onset of puberty. In summary, D2O was a feasible method to estimate lean composition in heifers at younger ages; however, it failed to accurately estimate body composition in heifers around puberty. Long-day photoperiod hastened puberty and accelerated lean growth without limiting skeletal growth in dairy heifers.

Aging↗

[Precocious puberty in girls depending on choriogonadotropin - case reports and literature review].

A 5-year-old girl presented typical features of isosexual precocity with breast and pubic hair development (Tanner stage 3) and menarche, following a few months history of hirsutism of the back and thighs. Stimulation testing revealed GnRH-independent precocious puberty, secondary hypothyroidism, hyperprolactinemia and mild testosteronemia. The ovaries in ultrasound examination were prepubertal. Tumor markers beta-HCG and AFP were markedly elevated and a suprasellar germ cell tumor 25x15 mm in size was visualized by MRI. Combined chemotherapy followed by radiotherapy resulted in normalization of pubertal features along with estrogen and marker levels. These data indicate a possible development of precocious puberty in girls induced by choriogonadotropin (hCG) released by a supracellar germ cell tumor. Based on our observations and the literature on the subject the authors believe that the autonomous presence of aromatase inside the tumor may be responsible for precocious puberty in girls with hCG-releasing germ cell tumors, regardless of their location. In such cases the rare character of isosexual precocious puberty in girls may result from a unique combination of high hCG-releasing activity and high aromatase activity. In girls with precocious puberty, when discrete androgenization signs develop, the authors postulate to extend the diagnostic management so that hCG-dependent precocious puberty could be ruled out.

English Abstract↗

Effect of prepuberal chronic morphine administration on the onset of puberty in pituitary-grafted female rats.

The effect of morphine on the onset of puberty was studied in female Wistar rats bearing pituitary grafts implanted at 21 days of age, or sham operated (SO). Morphine was given sc, daily, from day 22 until the occurrence of vaginal opening (VO), taken as an index of puberty. Two doses of morphine (2 or 8 mg kg-1 day-1) were used and control animals received saline of the same volume. Morphine (both doses) induced delayed puberty in SO rats, as indicated by age at VO: mean +/- SEM, 36.90 +/- 0.75 and 36.33 +/- 1.08 days vs 33.06 +/- 0.69 days for 2 and 8 mg vs control group. Pituitary graft induced precocious puberty and this effect was reversed by the highest dose of morphine (29.47 +/- 0.84 vs 32.80 +/- 0.59 days for saline vs 8 mg morphine, grafted rats). These data show that chronic administration of morphine during the prepuberal period delayed the onset of puberty and reversed the precocious puberty induced by pituitary graft in the female rat.

Animals↗

[Detection of Porphyromonas gingivalis in the subgingival plaque of puberty gingivitis].

PURPOSE: To detect the presence of Porphyromonas gingivalis (Pg) in the subgingival plaque of puberty gingivitis and to investigate its relationship with gingival health. METHODS: The subjects of 14- to 17-year-old children in this study were divided into two groups, puberty gingivitis group and gingival healthy group, with 36 in each group. Periodontal parameters were recorded. A 16S rRNA-based polymerase chain reaction (PCR) detection method was used to determine the prevalence of Pg in the subgingival plaque samples. The AVG of positive band in the agarose gel electrophoresis was analyzed using the automatic gel documentation and image analyzer software. The relative quantity of Pg was determined. The data were statistically analyzed using SPSS11.5 software. Chi-square test was used to compare the prevalence of Pg in the two groups. Wilcoxon rank sum test was used to analyze the relative quantity of Pg and the severity between the Pg-positive and the Pg-negative subjects. Spearman correlation analysis was used to test the relationship between the relative quantity of Pg and periodontal parameters. RESULTS: The prevalence of Pg in the puberty gingivitis group and gingival healthy group was 47.22% and 25.00%, respectively (P<0.05). The relative quantity of Pg in the two groups was 48.02% and 21.46%, respectively(P<0.01). In all the Pg-positive subjects of puberty gingivitis group, there was positive correlation between the relative quantity of Pg and the gingival index (GI),sulcus bleeding index (SBI) and the probe depth (PD). There were statistically differences between them. The GI and SBI index of the Pg-positive subjects were statistically higher than that of the Pg-negative subjects in the puberty gingivitis group (P<0.01). CONCLUSION: Periodontal pathogens can colonize in the subgingival plaque in puberty subjects and colonization of Pg is relevant to the status of gingival health.

Adolescent↗