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Precocious puberty (PP) is a common childhood sexual dysplasia. Central precocious puberty (CPP) is a disease in which the hypothalamic-pituitary-gonadal (HPG) axis is activated in early age, leading to the early release of gonadotrophin releasing hormone, the early development of gonads, and the early onset of puberty. The occurrence of puberty is regulated by gene and environment. Current clinical studies have found that gain-of-function mutations in the KISS1 gene, and loss-of-function mutations in KISS1R (also named GPR54), MKRN3 and DLK1 genes are all important single-gene causes of central precocious puberty. KISS1 is a tumor metastasis suppressor gene. KISS1R codes a G protein-coupled receptor which with its ligand, kisspeptin, forms an excitatory neuroregulator system for GnRH secretion. They play a role in the upstream of the HPG axis. MKRN3 is a maternal-imprinted gene. DLK1 is a gene that regulates the growth of cell. They play a role in the downstream of HPG axis. Recently, the incidence of central precocious puberty has become higher and higher, which is related to the excessive exposure of environmental endocrine disruptors (EEDs) due to the continuous development of social economy. A number of investigations have found that children’s exposure to EEDs is significantly related to the incidence of precocious puberty. In humans, these EEDs also affect the metabolism of gut microbes. This paper aims to review the current studies on the single-gene pathogenesis, epigenetics, gut microbiota and environmental factors of central precocious puberty, so as to provide help for the treatment and prevention of this disease.
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Odontogenesis is a consequence of a complex series of reciprocal signal interactions between odontogenic epithelium and neural crest-derived odontotgenic mesenchyme. These interactions result from a complex interplay of genetic and environmental factors. Given that a fetus develops in the mother, maternal health and environmental exposures have a great influence on tooth development. In this review, we focused on the key issues in the developmental defects of teeth induced by various types of maternal environmental factors, including environmental endocrine disruptors, joint action of two or more chemical exposures, and maternal health status. This review also discussed the adverse effects of maternal environmental factors on tooth development. These effects include enamel developmental defects, molar incisor hypomineralization, dental fluorosis, hyperdontia and hypodontia. Overall, this review provides a theoretical basis for the prevention of tooth defects in early life, assessment of risks from developmental tooth defects, and advancement of pediatric oral health management.
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Insulin-like factor 3 belongs to the insulin superfamily relaxin subfamily.Insulin-like factor 3 is the main product secretion of leydig cells,and its synthetic process totally relies on the state of leydig cells differentiation.Insulin-like factor 3 plays an important role in testicular descent,and has a great clinical value for evaluating function of leydig cells.Meanwhile,insulin-like factor 3 is deemed to play an important role in germ cell survival and regulation of bone metabolism.
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The incidence of aduIt obesity,diabetes,hyperIipidemia and hypertention has been rising dramaticaIIy in recent years. Obesity and overweight have become a significant pubIic heaIth probIem worIdwide. Though obesity is caused by compIex interactions between genetic,behavioraI,and environ-mentaI factors,its etioIogy is stiII uncIear. There is growing evidence that exposure to bisphenoI A(BPA) during prenataI and neonataI or adoIescence periods Ieads to much body mass gain. In addition,in epi-demioIogicaI studies,the association between BPA exposure and obesity and type 2 diabetes has been found. The potentiaI mechanism may be attributed to promoted differentiation and function in adipocytes via aIteration of a number of genes. BPA may act aIso through other mechanisms. It can directIy bind to nucIear receptors acting as agonists or antagonists and indirectIy disrupt hormone IeveIs by inhibiting enzymatic activity or by activating expression of the P450 enzymes. This review is focused on the effects of estrogenic endocrine disrupting chemicaIs such as BPA on the deveIopment of obesity.
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Environmental endocrine disruptors have garnered considerable attention in recent years be-cause of their endocrine disruption on sex development disorders. Kisspeptin system might be a novel target for endocrine disruption at the hypothalamic-pituitary-gonad axis. Environmental endocrine disruptors′estrogenic properties make them capable of interacting with the kisspeptin system,and then confer lifelong consequences in-cluding altered pubertal timing, infertility, and metabolic disorders. To date, three compounds have been well studied for their capacity to interfere with kisspeptin signaling pathways:BPA,PCB mixtures,and the phytoestro-gen GEN.
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Objective To explore the relationship of zearalenone (ZEA) and precocious puberty in girls.Methods The peripheral serums from 71 cases of precocious puberty girls and 50 cases of healthy girls were collected respectively and concentrations of ZEA were detected by high performance liquid chromatography.Bone age,body mass index (BMI),volume of uterus and ovaries,concentrations of estradiol (E2),luteinizing hormone (LH) and folliclestimulating hormone (FSH) were detected,and the residence of each subject was recorded as well.Results (1) In 71 patients,52 patients were diagnosed as idiopathic central precocious puberty,others were diagnosed as premature thelarche.(2) In 71 patients,serum ZEA was detected from 51 patients,and undetected in 20 patients.(3)Concentration of ZEA in precocious puberty girls [(318 ±34) ng/L]was significantly increased than that in healthy girls [(143 ± 35) ng/L,P =0.002],but no distinct difference existed between ICPP group and PT group(P =0.326).(4)Compared with uterus volume of ZEA in the undetected patients (1.975 ±0.150) cm3,the uterus volume of ZEA detected patients (2.972 ±0.180) cm3,which was significantly enlarged,there was significant difference (P =0.01) ; Percentage of overweight girls in ZEA detected patients (31.4％,16/51 cases) was lower than which in ZEA undetected patients (65.0％,13/20 cases,P =0.01) ; Although there was no statistical differences in the breast diameter,bone age,value of E2,LH and FSH between ZEA detected patients and undetected patients (all P ＞ 0.05),but the increased tendency in ZEA detected patients existed.(5) ZEA in serum was detected in 53.3％ (16/30 cases) patients living in the cities,and the rate was obviously lower than 82.9％ of the patients (34/41 cases) living in the countryside,there was significant difference (P =0.007).Conclusions ZEA is correlated with precocious puberty in girls.ZEA pollution might be one of reasons for precocious puberty occurrence.
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The definition of environmental endocine disruptors,varieties of chemicals possible to produce endocrine disruptive effects,their possible mechanisms and adverse effects on organisms were briefly introduced in this paper.It suggested that there were many varieties of endocrine disrupting chemical existing in the human environment.The reproductive disorders reported up to date in animal maybe in human,included reduced fertility,reduced hatchability,redcued viability of offspring,impaired hormone secretion or activity and modified reproductive anatomy.Further study should be conducted and relative preventive measures should be adopted.
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Objective To understand whether Imarcaptoacetate dioctyltin(IMA) is a environmental endocrine disruptor or not. Methods The new born Wistar rats were randomly divided into six groups including positive control group, negative control group and four experimental groups. The rats in the experimental groups were given IMA at different concentrations (0.100 0, 0.010 0, 0.001 0, 0.000 1 ?g/10 g) 1/1 000 000 by hypodermic injection, the rats in the negative control group were treated with corn oil and those in the positive control group were treated with dibutyltin dilaurate(DBTD) at concentration of 0.001 ?g/10 g bw. The rats were injected one time each day for five consecutive days. After one and half months, the levels of T, LH and FSH in the blood, the weight of the testicles, ovaries and the sexual organ exponent were determined. The pathological examination on some samples was conducted. Results In both of female and male, the levels of T in IMA treated rats were significantly increased and showed an doge-effect relationship (P0.05). The exponents of the testicles were different among groups (P
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0.05).The body weight and the increase of body weight in 100 mg /kg NP group was significantly lower than those in control group(P
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Objective To study the effects of perinatal exposure to bisphenol A(BPA) on the expression of estrogen receptor ? and ? mRNA in the brain of F1 male offsprings. Methods Pregnant SD rats were given BPA at 2, 20, 100 mg/kg bw per day respectively from eleventh day of gestation throughout the whole lactation by gastric gavage until their pups were weaned on postnatal day 21, F1 male pups from each group were killed on postnatal day 21 respectively, the brain was removed for detecting the expression of estrogen receptor ? and ? mRNA by RT-PCR. Results BPA treatment caused a up-regulation of ER? mRNA and ER? mRNA relative expression in the brain,especially in the middle-dose and low-dose groups it was so obvious. Conclusion Perinatal exposure to BPA can cause a change of ER? mRNA and ER? mRNA expression in the brain of the male offspring,which may be a part of the mechanism of BPA induced brain development damage.