UMLS:C0848255 - FACTA Search

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Query: UMLS:C0848255 (female puberty)
121 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In normal healthy-weight humans, women have a higher percentage body fat than men, a difference that commences at puberty and continues throughout adult life, suggesting that the mechanism is related to sex steroids. The first half of pregnancy is also a stage of body fat gain in women. From an energy balance point, there is no explanation why women should be fatter than men, as the latter consume more calories proportionately. Moreover, women store fat in early pregnancy when caloric intake does not significantly change. The aim of this review is to focus on evidence supporting one mechanism that may account for these findings. That is, oestrogen reduces postprandial fatty acid oxidation leading to an increase in body fat which may account for the greater fat mass observed in women compared with men and the fat gain in early pregnancy. Therefore, female puberty and early pregnancy could be seen as states of efficient fat storage of energy in preparation for fertility, foetal development and lactation providing an obvious biological advantage. Further research into this mechanism of fat storage may provide further insights into the regulation of body fat.
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PMID:Does oestrogen allow women to store fat more efficiently? A biological advantage for fertility and gestation. 1902 69

Bisphenol-A (BPA), material for polycarbonate and epoxy resin synthesis, has been detected in canned food, among other food containers. In mammal studies, BPA transferred from mother to fetus, caused abnormality of reproductive organs, and advanced female puberty. BPA from canned food and microwave containers was analyzed using high performance liquid chromatography and gas chromatography-mass spectrometry. Population was cohort of mother-son pairs established at Granada University Hospital. Frequency of food consumption (including canned food) was studied with a semi-quantitative questionnaire. The most frequently consumed products were fish and juice cans, consumed 1-3 times/week by 34.7% and 22.3% of the study population, respectively. The women made little use of polymer microwave containers, 52.8% never using them and 45.9% using them <3 times/month. Estimated mean (standard deviation) intake of BPA was 1.1(0.839) microgram/day. No relationship was found between BPA exposure and maternal socio-demographic variables or newborn characteristics. This study offers the first estimate of BPA dietary intake by pregnant women in Southern Spain. The consumption of canned foods and drinks by these women means that their exposure was lower than EFSA estimates for the European population. Nevertheless it remains of concern, given the proven undesirable effects of low-level exposure and higher susceptibility of pregnant women.
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PMID:Dietary exposure assessment of pregnant women to bisphenol-A from cans and microwave containers in Southern Spain. 1912 62

Larynx is responsible for the generation of voice and subsequently impacts on communication, social interaction, personality, and artistic expression. The vocal instrument is comprised of the vibratory body, the respiratory power source, and the oropharyngeal resonating chamber. The lungs are the power supply, the larynx is the vibratory source, and the supraglottal vocal tract (supraglottal pharynx oral cavity, nasal cavity) is the resonator that shapes the sound into words and songs. During the phase of expiration as the diaphragm relaxes and the chest wall recoils, air is pushed through the nearly closed vocal folds. The aerodynamic forces of the air column and myoelastic properties of the vocal folds are responsible for the repeated opening and closing of the glottal tissue that pulses that air column as it flows out. These disruptions in the steady state of tracheal air pressure by glottal activity and vocal fold vibrations result in voice production. Voice is characterized by its frequency intensity and harmonics. The harmonics are hormonally dependent. This is illustrated by changes that occur during male and female puberty. The female voice evolves from childhood to menopause under the varied influences of estrogen, progesterone, and testosterone. These hormones are the dominant factor in determining voice changes throughout life. Female voice has a fundamental frequency one-third lower than that of a child. In males, androgen released at puberty is responsible for the male vocal frequency being an octave lower than that of a child. The females have a reproductive system, which undergoes a regular cyclic change known as the menstrual cycle. Laryngeal changes are evident and fluctuate systematically during the reproductive years with the menstrual cycle. The main objective of this experiment is to provide a solid ground with evidence of changes in voice because of sexual hormones, which will form the base of a multidisciplinary approach to a comprehensive and integrated understanding of premenstrual and menopausal female voice.
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PMID:A study of voice changes in various phases of menstrual cycle and in postmenopausal women. 1918 58

The excitatory tone to gonadotrophin-releasing hormone (GnRH) neurones is a critical component underlying the pubertal increase in GnRH secretion. However, the homeostatic mechanisms modulating the response of GnRH neurones to excitatory inputs remain poorly understood. A basic mechanism of neuronal homeostasis is the Na(+),K(+)-ATPase-dependent restoration of Na(+) and K(+) transmembrane gradients after neuronal excitation. This activity is reduced in a mouse model of Rett syndrome (RTT), a neurodevelopmental disorder in which expression of FXYD1, a modulator of Na(+),K(+)-ATPase activity, is increased. We now report that the initiation, but not the completion of puberty, is advanced in girls with RTT, and that, in rodents, FXYD1 may contribute to the neuroendocrine regulation of female puberty by modulating GnRH neuronal excitability. Fxyd1 mRNA abundance reaches maximal levels in the female rat hypothalamus by the fourth postnatal week of life (i.e., around the time when the mode of GnRH secretion acquires an adult pattern of release). Although Fxyd1 mRNA expression is low in the hypothalamus, approximately 50% of GnRH neurones contain Fxyd1 transcripts. Whole-cell patch recording of GnRH-EGFP neurones revealed that the neurones of Fxyd1-null female mice respond to somatic current injections with a lower number of action potentials than wild-type cells. Both the age at vaginal opening and at first oestrous were delayed in Fxyd1(-/-) mice, but adult reproductive capacity was normal. These results suggest that FXYD1 contributes to facilitating the advent of puberty by maintaining GnRH neuronal excitability to incoming transsynaptic stimulatory inputs.
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PMID:FXYD1, a modulator of Na,K-ATPase activity, facilitates female sexual development by maintaining gonadotrophin-releasing hormone neuronal excitability. 1918 98

The gender-specific expression pattern of aromatase and 5alpha-reductases (5alpha-R) during brain development provides neurons the right amount of estradiol and DHT to induce a dimorphic organization of the structure. Polychlorinated biphenyls (PCBs) are endocrine disruptive pollutants; exposure to PCBs through placental transfer and breast-feeding may adversely affect the organizational action of sex steroid, resulting in long-term alteration of reproductive neuroendocrinology. The study was aimed at: a) evaluating the hypothalamic expression of aromatase, 5alpha-R1 and 5alpha-R2 in fetuses (GD20), infant (PN12), weaning (PN21) and young adult (PN60) male and female rats exposed to PCBs during development; b) correlating these parameters with the time of testicular descent, puberty onset, estrous cyclicity and copulatory behavior; c) evaluating possible alterations of some non reproductive behaviors (locomotion, learning and memory, depression/anxiety behavior). A reconstituted mixture of four indicator congeners (PCB 126, 138, 153 and 180) was injected subcutaneously to dams at the dose of 10 mg/kg daily from GD15 to GD19 and then twice a week till weanling. The results indicated that developmental PCB exposure produced important changes in the dimorphic hypothalamic expression of both aromatase and the 5alpha-Rs, which were still evident in adult animals. We observed that female puberty onset occurs earlier than in control animals without cycle irregularity, while testicular descent in males was delayed. A slight but significant impairment of sexual behavior and an important alteration in memory retention were also noted specifically in males. We conclude that PCBs might affect the dimorphic neuroendocrine control of reproductive system and of other neurobiological processes.
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PMID:Chronic treatment with polychlorinated biphenyls (PCB) during pregnancy and lactation in the rat Part 2: Effects on reproductive parameters, on sex behavior, on memory retention and on hypothalamic expression of aromatase and 5alpha-reductases in the offspring. 1946 8

The initiation of mammalian puberty requires an increased pulsatile release of gonadotropin-releasing hormone (GnRH) from the hypothalamus. This increase is brought about by changes in transsynaptic and glial-neuronal communication. Coordination of these cellular interactions likely requires the participation of sets of genes hierarchically arranged within functionally connected networks. Using high throughput, genetic, molecular and bioinformatics strategies, in combination with a systems biology approach, three transcriptional regulators of the pubertal process have been identified, and the structure of at least one hypothalamic gene network has been proposed. A genomewide analysis of hypothalamic DNA methylation revealed profound changes in methylation patterns associated with the onset of female puberty. Pharmacological disruption of two epigenetic marks associated with gene silencing (DNA methylation and histone deacetylation) resulted in pubertal failure, instead of advancing the onset of puberty, suggesting that disruption of these two silencing mechanisms leads to activation of repressor genes whose expression would normally decrease at puberty. These observations suggest that the genetic underpinnings of puberty are polygenic rather than specified by a single gene, and that epigenetic mechanisms may provide coordination and transcriptional plasticity to this genetic network.
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PMID:New concepts on the control of the onset of puberty. 1995 55

Towards the end of the 1800 s, chlorosis was a frequently used diagnosis, in Norway as well as in America and the rest of Europe. The physiological basis for the disease was assumed to be decreased levels of haemoglobin and/or red blood cells. Chlorosis was not synonymous with anaemia, but rather a subcategory with a vague symptom-based picture associated with female puberty. The different opinions on causes of the disease can be divided into three main groups: environmental, moral and biological-constitutional. At the time, it was well known that iron was an effective treatment. In a cultural critical perspective the disease was seen both as a phenomenon of degeneration and as a reaction to modern life with its stress and demands. During the first decades of the 1900 s, the chlorotic girl disappeared from medical textbooks and articles. The article points at medical, biological and dietary improvements as explanations for why chlorosis disappeared as a diagnosis, but also considers historical aspects such as new cultural norms for femininity, changed laws and an increasing political understanding of health's role in society.
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PMID:[On chlorosis and anaemic girls in the end of the 19th century]. 2002 78

The hypothalamic peptide, nesfatin-1, derived from the precursor NEFA/nucleobindin 2 (NUCB2), was recently identified as anorexigenic signal, acting in a leptin-independent manner. Yet its participation in the regulation of other biological functions gated by body energy status remains unexplored. We show herein that NUCB2/nesfatin-1 is involved in the control of female puberty. NUCB2/nesfatin mRNA and protein were detected at the hypothalamus of pubertal female rats, with prominent signals at lateral hypothalamus (LHA), paraventricular (PVN), and supraoptic (SON) nuclei. Hypothalamic NUCB2 expression raised along pubertal transition, with detectable elevations of its mRNA levels at LHA, PVN, and SON, and threefold increase of its total protein content between late-infantile and peripubertal periods. Conditions of negative energy balance, such as 48 h fasting or sustained subnutrition, decreased hypothalamic NUCB2 mRNA and/or protein levels in pubertal females. At this age, central administration of nesfatin-1 induced modest but significant elevations of circulating gonadotropins, whose magnitude was notably augmented in conditions of food deprivation. Continuous intracerebroventricular infusion of antisense morpholino oligonucleotides (as-MONs) against NUCB2 along pubertal maturation, which markedly reduced hypothalamic NUCB2 protein content, delayed vaginal opening and decreased ovarian weights and serum luteinizing hormone (LH) levels. In contrast, in adult female rats, intracerebroventricular injection of nesfatin did not stimulate LH or follicle-stimulating hormone secretion; neither did central as-MON infusion alter preovulatory gonadotropin surges, despite suppression of hypothalamic NUCB2. In sum, our data are the first to disclose the indispensable role of NUCB2/nesfatin-1 in the central networks driving puberty onset, a function that may contribute to its functional coupling to energy homeostasis.
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PMID:The anorexigenic neuropeptide, nesfatin-1, is indispensable for normal puberty onset in the female rat. 2053 27

Male odors can influence a female's reproductive physiology. In the mouse, the odor of male urine results in an early onset of female puberty. Several volatile and protein pheromones have previously been reported to each account for this bioactivity. Here we bioassay inbred BALB/cJ females to study pheromone-accelerated uterine growth, a developmental hallmark of puberty. We evaluate the response of wild-type and mutant mice lacking a specialized sensory transduction channel, TrpC2, and find TrpC2 function to be necessary for pheromone-mediated uterine growth. We analyze the relative effectiveness of pheromones previously identified to accelerate puberty through direct bioassay and find none to significantly accelerate uterine growth in BALB/cJ females. Complementary to this analysis, we have devised a strategy of partial purification of the uterine growth bioactivity from male urine and applied it to purify bioactivity from three different laboratory strains. The biochemical characteristics of the active fraction of all three strains are inconsistent with that of previously known pheromones. When directly analyzed, we are unable to detect previously known pheromones in urine fractions that generate uterine growth. Our analysis indicates that pheromones emitted by males to advance female puberty remain to be identified.
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PMID:Analysis of male pheromones that accelerate female reproductive organ development. 2134 29

We previously identified synaptic cell adhesion molecule 1 (SynCAM1) as a component of a genetic network involved in the hypothalamic control of female puberty. Although it is well established that SynCAM1 is a synaptic adhesion molecule, its contribution to hypothalamic function is unknown. Here we show that, in addition to the expected neuronal localization illustrated by its presence in GnRH neurons, SynCAM1 is expressed in hypothalamic astrocytes. Cell adhesion assays indicated that SynCAM is recognized by both GnRH neurons and astrocytes as an adhesive partner and promotes cell-cell adhesiveness via homophilic, extracellular domain-mediated interactions. Alternative splicing of the SynCAM1 primary mRNA transcript yields four mRNAs encoding membrane-spanning SynCAM1 isoforms. Variants 1 and 4 are predicted to be both N and O glycosylated. Hypothalamic astrocytes and GnRH-producing GT1-7 cells express mainly isoform 4 mRNA, and sequential N- and O-deglycosylation of proteins extracted from these cells yields progressively smaller SynCAM1 species, indicating that isoform 4 is the predominant SynCAM1 variant expressed in astrocytes and GT1-7 cells. Neither cell type expresses the products of two other SynCAM genes (SynCAM2 and SynCAM3), suggesting that SynCAM-mediated astrocyte-astrocyte and astrocyte-GnRH neuron adhesiveness is mostly mediated by SynCAM1 homophilic interactions. When erbB4 receptor function is disrupted in astrocytes, via transgenic expression of a dominant-negative erbB4 receptor form, SynCAM1-mediated adhesiveness is severely compromised. Conversely, SynCAM1 adhesive behavior is rapidly, but transiently, enhanced in astrocytes by ligand-dependent activation of erbB4 receptors, suggesting that erbB4-mediated events affecting SynCAM1 function contribute to regulate astrocyte adhesive communication.
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PMID:The synaptic cell adhesion molecule, SynCAM1, mediates astrocyte-to-astrocyte and astrocyte-to-GnRH neuron adhesiveness in the mouse hypothalamus. 2148 31

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