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PubMed1981

The effect of restricted food intake and refeeding on the ovarian follicle population of the pre-puberal Wistar rat.

A 50 p. 100 restriction of food intake in female Wistar rats from day 21 to day 42 of life prevented ovulation and altered the size distribution and numbers of ovarian follicles. The rate of atresia of non-growing oocytes in primordial follicles was retarded resulting in more oocytes per ovary. The number of follicles initiated to grow was reduced. Semi-starved rats allowed free access to food from day 42 of life achieved the body weight of ad libitum-fed controls at 66 days of age. A delayed puberty occurred. The numbers of non-growing oocytes in primordial follicles per ovary declined but remained significantly greater than control values at 66 days of age. Refeeding increased the numbers of follicles undergoing growth but within the size distribution found in age-matched controls. Thus semi-starvation followed by refeeding rendered the ovary developmentally younger but only in terms of total oocyte numbers. The ovarian response to starvation and refeeding is discussed in relation to pituitary function and provides new information on the potential lability of the oocyte population.

Animals↗
PubMed1988

Short- and long-term effects of manipulation of the pineal/melatonin axis in ewes.

The experiments which have provided insight into the role of the pineal gland and melatonin in sheep reproduction are reviewed. There is now strong evidence that timed daily melatonin administration and continuous administration via implants are equally effective in promoting the same physiological consequences as short daylength. Thus melatonin treatments lasting six weeks can result in an advance of the breeding season and an advance in the seasonal peak in ovulation rate. Much longer periods of exposure to melatonin or long-term pinealectomy result in a different response. In the second part of this review the long-term effects of pineal manipulation in juvenile and pubertal ewes are compared and contrasted. Five years after pinealectomy (at 7.5 months) ewes displayed normal timed breeding seasons without exhibiting a normal annual pattern of LH sensitivity to oestradiol. Pinealectomy at 2.5 months of age resulted in delayed puberty and breeding seasons out of synchrony with normal ewes two years later. These animals maintained an LH sensitivity to oestradiol consistent with their own breeding season. Melatonin implants which delivered melatonin for over a year caused similar effects as pinealectomy at 2.5 months but had essentially opposite effects to pinealectomy in adults. These results generate many questions about the different perception of the melatonin signal in prepubertal versus adult ewes and the factors involved in the onset and offset of the breeding season.

Animals↗
PubMed2001

Impact of lung inflammation on bone metabolism in adolescents with cystic fibrosis.

Deficits in bone mineral density resulting in premature osteopenia and osteoporosis have been documented in cystic fibrosis patients for over 20 years. A high incidence of fractures and kyphosis in the continually increasing adult patient population and in post-lung transplant patients has highlighted the problems associated with poor bone health.The aetiology of osteoporosis in CF is multifactorial but centres on an uncoupling in the normal balance between bone formation and resorption. Delayed puberty, malabsorption and reduced weight-bearing exercise can result in inadequate bone mineral accretion in childhood and adolescence. Corticosteroid use and pro-inflammatory cytokines associated with infective respiratory exacerbations can accelerate bone loss. Dual energy X-ray absorptiometry is the most commonly available technique to measure bone mineral density. All patients should be scanned at least every 2 years from adolescence. The treatment of established disease with bisphosphonates shows encouraging early results.

Adolescent↗
PubMed1976

[Cytogenetic and clinical findings in suspected Turner's syndrome: results of a five-year study of 207 patients (author's transl)].

The hallmark of Turner's syndrome is small stature, primary amenorrhoea with delayed puberty and other congenital defects. Cytogenetic examinations were done over a five-year period of 207 patients of different ages. The diagnosis of Turner's syndrome was confirmed by karyotype in 94 (45.4%), tentatively confirmed by X-chromatin in 11 (5.3%) and in 21 (10.1%) with other disorders involving disturbed sexual development. In 73 cases Turner's syndrome was excluded and in nine the investigation had not been completed by the end of the study. There was a wide spectrum of clinical and cytogenetic findings in the 94 patients with cytogenetically confirmed Turner's syndrome: 50 (53.2%) had karyotype 45,X0; 25 (26.6%) X0/XX mosaic; 19 (20.2%) X-chromosomal structural anomalies with or without additional X0 cell line.

Adolescent↗
PubMed1993

Leydig cell neoplasia in a patient with Reifenstein syndrome.

We present the rare coincidence of a Leydig cell tumor in both testicles of a patient with partial androgen insensitivity syndrome (PAIS). The clinical picture with perineoscrotal hypospadia, micropenis, gynecomastia and delayed puberty and the serum hormone levels with elevated concentrations of testosterone, luteinising hormone (LH) and follicle-stimulating hormone were entirely consistent with PAIS. Ultimately, the diagnosis was confirmed by determination of genital skin fibroblast androgen receptor binding capacity for 5 beta-dihydrotestosterone, which demonstrated a qualitatively abnormal androgen receptor. At 44 years of age, a nodule in the left testis led to orchidectomy. At that time, the right testis was inconspicuous sonographically. But 3 years later the right testis developed nodules and was removed. Review of testicular histology revealed the presence of Leydig cell hyperplasia (LCH), multifocal nodular hyperplasia and Leydig cell neoplasia (LCN) in both testes. Many micronodules of Leydig cells in transition from hyperplasia to neoplasia were also identified. The simultaneous development of histologically identical nodes of LCN independently from each other and a different sites of both tests indicates the presence of a tumorigenic factor acting on the Leydig cells. Furthermore, the observation of multiple foci of cells in all stages of transition from hyperplasia to neoplasia demonstrates the persistent process of transformation. We speculate, that in this patient the grossly elevated LH levels present over 30 years have enhanced, if not provoked, the formation of LCN. In addition, the defective androgen receptor might have prevented suppressive effects of androgens on the Leydig cells.

Disorders of Sex Development↗
PubMed1999

Hypoleptinaemia in patients with anorexia nervosa and in elite gymnasts with anorexia athletica.

Leptin, the product of the ob-gene, is specifically released by adipocytes. In addition to its metabolic function it seems to affect the feedback-mechanisms of the hypothalamic-pituitary-gonadal-axis. We studied 13 female juvenile elite gymnasts with anorexia athletica (AA) and 9 female patients with anorexia nervosa (AN) regarding the relation between leptin, fat stores, and the reproductive hormone levels. Leptin levels in females with anorexia nervosa (Tanner stage B4 [median]; mean age: 17.8 +/- 1.7 years) were low (2.9 +/- 2.7 microg/L), and were related to body mass index (BMI) (r = 0.71; p = 0.03) and percentage body fat mass (r = 0.78; p = 0.01). Leptin levels of the elite gymnasts were even more decreased (1.2 +/- 0.8 microg/L) caused by the low amount of fat stores. Leptin correlated with BMI (r= 0.77; p = 0.004) and the percentage body fat mass (r = 0.6; p = 0.04). In elite gymnasts leptin levels correlated with CA showing an age-dependent increase (r= 0.59; p = 0.04). Oestradiol was secreted at a low level in both groups (AN: 25.6 +/- 17.4 microg/L; AA: 24.4 +/- 13.5 microg/L). A delay in menarche and a retarded bone maturation occurred in AA. Our results clearly show that leptin levels are low in restrained eaters. Leptin levels represent the fat stores in the body and play a permissive role for female pubertal development. There is evidence that the mechanisms leading to a dysregulation of the reproductive-axis in patients with AN are comparable with those leading to delayed puberty in juvenile elite gymnasts with AA. This implies that AN and AA are overlapping groups and AA can lead to the development of AN.

Adolescent↗
PubMedDate not supplied

[Nephropathy gonadal dysgenesis--or incomplete Drash syndrome?].

This is a report about a phenotypical normal girl with nephropathy and gonadal dysgenesis. At the age of 2 years 8 months she presented with steroid resistant nephrotic syndrome. Focal segmental glomerulosclerosis was found by biopsy. Because of delayed puberty karyotyping was performed, which revealed 46 XY. Thirteen years after onset of proteinuria she reached end stage renal failure. Gonadal dysgenesis and nephropathy are often indistinguishable from incomplete Drash syndrome. Children with early nephropathy of unknown origin or gonadal dysgenesis should be observed for development of Wilms tumor. When chronic nephropathies are present in girls, karyotyping should be considered.

Adolescent↗
PubMedDate not supplied

[Parenteral nutrition in treatment of short stature in adolescents with Crohn disease].

Growth retardation and delayed puberty occur in 20-35% of children and adolescents with Crohn's disease. Alternate day corticosteroid treatment, use of azathioprine, enteral or parenteral hyperalimentation and surgery have been advocated to reverse growth failure. Because of nonacceptance of elemental diet 7 patients with Crohn's disease and growth retardation received parenteral nutrition for 2-3 months (maximal for more than 30 months in one patient). All of them exhibited a mean weight gain of 10 kg and a mean increase of their height velocity from 2.4 to 7.1 cm/year. Main problems were bacterial infections and dislocations of the central lines. Surgery was performed in 3 adolescents immediately after parenteral nutrition. One patient showed a catch-up growth during a 30-months nocturnal home parenteral nutrition at a biological age of 21 years. Parenteral nutrition is an effective regimen to manage growth failure in children with Crohn's disease, but has to be performed for larger periods in individual cases.

Adolescent↗
PubMed1992

Convexity meningioma associated with empty sella presenting as primary amenorrhea.

A case of a 30-year-old female seen for a convexity meningioma is presented. History and investigations revealed an empty sella turcica associated with primary amenorrhea. The removal of the convexity meningioma resulted in the disappearance of the amenorrhea and in the rise of plasma gonadotropins. The importance of the consideration of intracranial causes in patients who have a delayed puberty or the absence of a menstrual history is briefly emphasized in the light of literature.

Adult↗
PubMed2000

Delayed diagnoses of Turner's syndrome: proposed guidelines for change.

OBJECTIVE: To measure the delays in diagnosis of Turner's syndrome (TS) and to propose strategies for earlier screening and diagnosis. METHODS: The medical records of 81 girls with TS were reviewed for age at diagnosis, reason(s) for karyotype analysis, and clinical features including growth failure. Delay in diagnosis was calculated as equal to age at diagnosis for children born with lymphedema and/or 2 or more of the following dysmorphic features: webbed neck, nail dysplasia, high palate, and short fourth metacarpal. For all others, delay in diagnosis was calculated as the difference between the age at which height fell below the 5th percentile and the age at which the diagnosis of TS was made. RESULTS: Lymphedema was the key to diagnosis in 97% of the girls diagnosed with TS in infancy, and short stature was the key to diagnosis for 82% of the girls diagnosed in childhood or adolescence. For girls diagnosed in childhood or adolescence, the delay in diagnosis averaged 7.7 +/- 5.4 years. Many had dysmorphic features and/or a history of lymphedema at birth, and diagnosis was made an average of 5.3 years after patients had fallen below the 5th percentile for height. By the time of diagnosis, patients were very short, averaging -2.9 SD in height. CONCLUSIONS: The diagnosis of TS is often delayed. We recommend karyotype analysis for all girls with unexplained short stature, delayed puberty, webbed neck, lymphedema, or coarctation of the aorta. Furthermore, karyotype analysis should be strongly considered for those who remain above the 5th percentile for height but have 2 or more features of TS, including high palate, nail dysplasia, short fourth metacarpal, and strabismus.

Adolescent↗
PubMed2005

Neutral sphingomyelinase 2 (smpd3) in the control of postnatal growth and development.

Neutral sphingomyelinases sphingomyelin phosphodiesterase (SMPD)2 and -3 hydrolyze sphingomyelin to phosphocholine and ceramide. smpd2 is expressed ubiquitously, and smpd3 is expressed predominantly in neurons of the CNS. Their activation and the functions of the released ceramides have been associated with signaling pathways in cell growth, differentiation, and apoptosis. However, these cellular responses remain poorly understood. Here we describe the generation and characterization of the smpd3(-/-) and smpd2(-/-)smpd3(-/-) double mutant mouse, which proved to be devoid of neutral sphingomyelinase activity. SMPD3 plays a pivotal role in the control of late embryonic and postnatal development: the smpd3-null mouse develops a novel form of dwarfism and delayed puberty as part of a hypothalamus-induced combined pituitary hormone deficiency. Our studies suggest that SMPD3 is segregated into detergent-resistant subdomains of Golgi membranes of hypothalamic neurosecretory neurons, where its transient activation modifies the lipid bilayer, an essential step in the Golgi secretory pathway. The smpd3(-/-) mouse might mimic a form of human combined pituitary hormone deficiency.

Animals↗
PubMed2006

Mutations in fibroblast growth factor receptor 1 cause both Kallmann syndrome and normosmic idiopathic hypogonadotropic hypogonadism.

Mutations in KAL1 and FGFR1 cause Kallmann syndrome (KS), whereas mutations in the GNRHR and GPR54 genes cause idiopathic hypogonadotropic hypogonadism with normal olfaction (nIHH). Mixed pedigrees containing both KS and nIHH have also been described; however, the genetic cause of these rare cases is unknown. We examined the FGFR1 gene in seven nIHH subjects who either belonged to a mixed pedigree (n = 5) or who had associated midline defects (n = 2). Heterozygous FGFR1 mutations were found in three of seven unrelated nIHH probands with normal MRI of the olfactory system: (i) G237S in an nIHH female and a KS brother; (ii) (P722H and N724K) in an nIHH male missing two teeth and his mother with isolated hyposmia; and (iii) Q680X in a nIHH male with cleft lip/palate and missing teeth, his brother with nIHH, and his father with delayed puberty. We show that these mutations lead to receptor loss-of-function. The Q680X leads to an inactive FGFR1, which lacks a major portion of the tyrosine kinase domain (TKD). The G237S mutation inhibits proper folding of D2 of the FGFR1 and likely leads to the loss of cell-surface expression of FGFR1. In contrast, the (P722H and N724K) double mutation causes structural perturbations in TKD, reducing the catalytic activity of TKD. We conclude that loss-of-function mutations in FGFR1 cause nIHH with normal MRI of the olfactory system. These mutations also account for some of the mixed pedigrees, thus challenging the current idea that KS and nIHH are distinct entities.

Amino Acid Substitution↗
PubMed1999

Dose, timing, and duration of flaxseed exposure affect reproductive indices and sex hormone levels in rats.

Flaxseed ingestion produces large amounts of mammalian lignans. Since lignans have weak estrogenic/antiestrogenic properties, the objective of this study was to determine in rats whether exposure to 5% or 10% flaxseed affects sex hormone levels and reproductive indices when given at different developmental stages. Rats were exposed to either a basal diet (control), 5%, or 10% flaxseed diet starting at weaning on postnatal day (PND) 21 or continuously from gestation to PND 132 for lifetime exposure. Compared to the control, exposure to 5% or 10% flaxseed after weaning produced no marked reproductive effects, whereas lifetime flaxseed exposure caused significant changes that differed depending on the dose. In female rats, lifetime exposure to 5% flaxseed affected the reproductive tract as indicated by delayed puberty onset. In contrast, lifetime exposure to 10% flaxseed caused earlier puberty onset, higher relative ovarian weight, higher serum estradiol levels, and lengthened estrous cycles. In male rats, lifetime 10% flaxseed exposure raised serum testosterone and estradiol levels and produced higher relative sex organ weights and prostate cell proliferation. In contrast, lifetime exposure to 5% flaxseed reduced adult relative prostate weight and cell proliferation, suggesting potential protection against prostatic disease, although sex hormone levels were unaffected. In conclusion, flaxseed can potentially alter reproduction, depending on the dose and timing of exposure.

Animals↗
PubMed2001

Growth deceleration and bone metabolism in nutritional dwarfing rats.

Nutritional status as well as energy and protein intake are critical regulators of IGF-1 and IGFBP-3 and contribute to the modulation of bone remodeling and formation. The purpose of this study was to investigate on an experimental model with nutritional dwarfing (ND), whether the alterations on body growth velocity, energy metabolism and body composition could affect serum concentrations of IGF-1 and IGFBP-3 and bone (tibiae and mandible) histology and histomorphometry. Twenty-one male weanling Wistar rats (body weight = 38.20 +/- 0.94 g) were randomized to three groups: seven of them were killed at day = 0 (CO, n = 7); control (C, n = 7); and experimental 80 (E80, n = 7). During 4 weeks, C was fed ad libitum with a 1:1 carbohydrate to fat diet. E80 was being underfed with the same diet by 80% and the following parameters were measured: weight (Wt) for length (L) ratio z-score; oxygen consumption (VO2); body composition (BC) by EM-SCAN SA 3000. At t = 28, E80 and C were killed. Serum IGF-1 and IGFBP-3 and bone histology and histomorphometry were performed on C0, E80 and C. E80 showed Wt for L z-score between lean and adequate, a decrease in VO2 according to body proportions, a BC of a delayed puberty individual, IGF-1 and IGFBP-3 decreased by 56 and 53%, respectively. Tibiae's hematopoyetic and adipose bone marrow areas were combined, with sealing trabeculae on metaphyseal areas. This study suggests that there is a relationship among growth deceleration in ND rats and structural alterations on tibiae.

Animals↗
PubMed2001

Treatment of risperidone-induced hyperprolactinemia with a dopamine agonist in children.

BACKGROUND: Risperidone, a potent antagonist of both serotonergic (5HT2A) and dopaminergic D2 receptors is associated with hyperprolactinemia in adults and children. Chronically elevated prolactin levels in children with prolactinomas may be associated with arrested growth and development resulting in either delayed puberty or short stature. These possibilities stress the importance of developing a safe and effective approach to drug-induced hyperprolactinemia in youth. We report the successful treatment of risperidone-induced hyperprolactinemia with cabergoline in youth. METHODS: We undertook a retrospective case review of four children with risperidone-induced hyperprolactinemia treated with cabergoline. RESULTS: Four males (age 6-11 years) with Diagnostic and Statistical Manual of Mental Disorders (fourth edition) bipolar disorder or psychoses, with risperidone-induced elevations in serum prolactin levels (57.5-129 ng/mL, normal 5-15 ng/mL), were treated with cabergoline (mean dose 2.13 +/- 0.09 mg/week). When serum prolactin levels normalized in all four subjects (mean 11.2 +/- 10.9 ng/mL), the cabergoline dose was reduced to 1 mg/week in three of four subjects. The mean duration of therapy with cabergoline was 523.5 +/- 129.7 days, and the mean duration of therapy with risperidone was 788.5 +/- 162.5 days. Cabergoline was well tolerated without adverse effects. CONCLUSIONS: Cabergoline may be useful for the treatment of risperidone-induced hyperprolactinemia in youth; however, further research is needed.

Age Factors↗
PubMed2000

Effect of calcium supplementation on bone mineral accretion in gambian children accustomed to a low-calcium diet.

BACKGROUND: Rural Gambian children have poor growth, delayed puberty, a low bone mineral content, and a low calcium intake. OBJECTIVE: We investigated the effect of a calcium supplement on bone mineral accretion in rural Gambian children. DESIGN: A randomized, double-blind, placebo-controlled study was conducted in 160 children (80 boys, 80 girls) aged 8.3-11.9 y. Bone mineral content (BMC), bone mineral density (BMD), and BMC adjusted for bone width, body weight, and height (size-adjusted BMC) were measured at the midshaft and distal radius. Each child received either 1000 mg Ca/d (as calcium carbonate) or a placebo 5 d/wk for 12 mo. Supplementation increased calcium intake from 342 to 1056 mg/d (8.6 to 26.4 mmol/d). RESULTS: Calcium supplementation resulted in a higher BMC, BMD, and size-adjusted BMC (&xmacr; difference +/- SE): midshaft radius-BMC (3.0 +/- 1.4%; P = 0.034), BMD (4.5 +/- 0.9%; P </= 0.0001), and size-adjusted BMC (4.6 +/- 0.9%; P </= 0.0001); distal radius-BMC (8. 4 +/- 3.2%; P = 0.009), BMD (7.0 +/- 2.7%; P = 0.011), and size-adjusted BMC (5.5 +/- 2.7%; P = 0.042). Supplementation had no significant effect on height, weight, or bone width at the midshaft radius or distal radius. At the end of the study, the calcium group had a significantly lower mean plasma osteocalcin concentration than the placebo group after adjustment for baseline concentration, sex, and pubertal status (-21.9 +/- 6.5%; P = 0.001). CONCLUSIONS: Increased calcium intake resulted in increased bone mineral status, possibly in association with a decreased bone remodeling space. Further studies are needed to determine whether an increased calcium intake has long-term benefits in Gambian children.

Anthropometry↗
PubMed2002

Body composition in children with sickle cell disease.

BACKGROUND: Impaired growth, poor nutritional status, and delayed skeletal and sexual maturation are common in children with sickle cell disease (SCD), yet the nature of associated body-composition deficits has not been fully described. OBJECTIVE: The objective was to assess growth, nutritional status, and body composition in 36 African American children with type SS SCD (20 females and 16 males) and 30 healthy control children (15 females and 15 males) of similar age (5-18 y) and ethnicity. DESIGN: Height, weight, bone age, pubertal status, skinfold thickness, and arm circumference were assessed. Height and weight were converted to z scores by comparison with national reference data and skinfold-thickness measurements were converted to z scores by comparison with African American- specific reference data. Fat-free mass (FFM) and fat mass (FM) were estimated by using 4 methods. Prepubertal children, pubertal males, and pubertal females were analyzed separately. RESULTS: Relative to the control subjects and to a national sample, children with SCD had significantly lower z scores for weight, height, arm circumference, and upper arm fat and muscle areas. Relative skeletal maturation was significantly delayed. After adjustment for age, children with SCD had significantly lower FM (prepubertal children and pubertal males only) and FFM (all 3 groups). CONCLUSIONS: Children with SCD have impaired growth, delayed puberty, and poor nutritional status. Low z scores for upper arm fat area indicate deficits in fat (energy) stores, and low FFM coupled with low upper arm muscle area indicate muscle wasting and low protein stores. These body-composition abnormalities suggest that the nutritional needs of the African American children with SCD were not being met.

Adolescent↗
PubMed1999

Exposure to flaxseed or its lignan component during different developmental stages influences rat mammary gland structures.

Reduction of the highly proliferative terminal end bud (TEB) structures in the developing mammary gland by differentiation to alveolar buds (ABs) and lobules has been suggested to be protective against mammary cancer. Flaxseed is high in alpha-linolenic acid (ALA) and secoisolariciresinol diglycoside (SDG). SDG is the precursor of mammalian lignans, which can affect mammary gland structures. Thus, the objective of this study was to determine the effect of lifetime, gestation and lactation or after-weaning exposure to 5 or 10% flaxseed or SDG and flaxseed oil components on the mammary gland structures of virgin female rat offspring at post-natal day 50. Lifetime or gestation and lactation exposure to flaxseed altered mammary gland structure development, whereas exposure to flaxseed after weaning had no effect. Lifetime or gestation and lactation exposure to 5% flaxseed caused endocrine changes, as suggested by delayed puberty onset and reduced number of estrous cycles. These changes reduced exposure to endogenous estrogens, leading to atrophy of mammary TEB structures. SDG, but not flaxseed oil, at the level found in 5% flaxseed produced similar effects as 5% flaxseed. This suggested that the lignans were the component in flaxseed responsible for the observed effects. Lifetime or gestation and lactation exposure to 10% flaxseed also caused endocrine changes, as suggested by early puberty onset and lengthened cycles due to prolonged estrus. This increased exposure to endogenous estrogens and stimulated mammary gland differentiation, as indicated by fewer TEBs and more ABs. Thus, lifetime or gestation and lactation exposure to 5 or 10% flaxseed induced structural changes in the mammary gland that may potentially reduce mammary cancer risk.

Animal Feed↗